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به نام خدا
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Disseminated Intravascular Coagulation
M.Bahmanpour MDAssistant professor
IUMS
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Algorithm for Diagnosis of DIC“DIC Score”
factor scorePresence of known underlying disorder No= 0 yes=2Coagolation testPlatelets >100k=0 <100k=1 <50k=2D-dimer level increased No=0 moderate=2 strang=3Pt prolongation (sec) <3=0 >3but<6 =1 >6=2 Fibrinogen (mg/dl) >100=0 <100=1
Total score >= 5 compatible with overt DIC < 5 suggestive of nonovert DIC
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DIC
An acquired syndrome characterized by systemicintravascularcoagulation
Coagulation is always the initial event.
Most morbidity and mortality depends on extent of intravascular thrombosis
Multiple causes
WWW. Coumadin.com
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Hemostasis Review
Coagulation cascade Vascular Endothelium Anticlotting Mechanisms Fibrinolytic System Platelets Blood Flow Dynamics
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Vascular Endothelium
Vascular endothelium expresses: Thrombomodulin Tissue Plasminogen
Activator Tissue
thromboplastin/Tissue factor
www.Coumadin.com
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Coagulation
Intrinsic Pathway Extrinsic Pathway Common Pathway Contact Pathway Tissue Factor Pathway
Primary factor in DIC
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Anticlotting Mechanisms Antithrombin III (ATIII):
The major inhibitor of the coagulation cascade. Inhibits Thrombin Inhibits activated Factors IX, X,
XI, and XII. Activity is enhanced by heparin.
Tissue factor pathway inhibitor TFPI
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Anticlotting Mechanisms
Protein C Activated by
Thrombin/Thrombomodulin Anticoagulant and fibrinolytic
activity. Vitamin K and Protein S are
cofactors
Protein S
Www.coumadin.com
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Fibrinolytic System Plasmin
Produced from Plasminogen by Tissue Plasminogen activator (TPA)
Degrades Fibrin and Fibrinogen (Fibrin degradation products, FDP)
Degrades Factors V, VIII, IX, XI, and XII.
Activity is inhibited by Antiplasmin.
Www.coumadin.com
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Fibrinolytic Inhibitors Antiplasmin
Inactivates plasmin rapidly. Acts slowly on plasmin
sequestered in the fibrin clot. Inactivates factors XI and XII
slowly.
Plasminogen -Activator Inhibitor-1(PAI-1) Inhibits the function of TPA Also has some inhibitory
activity against urokinase, plasmin, thrombin, activated Protein C, factors and XII, and kallikrein
Www.coumadin.com
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Hemostatic Balance
ATIIIClotting Factors
Tissue factor*
PAI-1
AntiplasminTFPI
Prot. CProt. S
Procoagulant Anticoagulant
Fibrinolytic System
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DIC
An acquired syndrome characterized by systemicintravascularcoagulation
Coagulation is always the initial event
SYSTEMIC ACTIVATION OF COAGULATION
Intravascular deposition of
fibrin
Depletion of platelets and coagulation
factors
Thrombosis of small and midsize
vesselsBleeding
Organ failure DEATH
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Pathophysiology of DIC
Activation of Blood Coagulation Suppression of Physiologic Anticoagulant
Pathways Impaired Fibrinolysis Cytokines
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Pathophysiology of DIC
Activation of Blood CoagulationTissue factor/factor VIIa mediated thrombin
generation via the extrinsic pathway complex activates factor IX and X
TF endothelial cellsmonocytesExtravascular:
• lung• kidney• epithelial cells
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Pathophysiology of DIC
Suppression of Physiologic Anticoagulant Pathwaysreduced antithrombin III levels reduced activity of the protein C-protein S systemInsufficient regulation of tissue factor activity by
tissue factor pathway inhibitor (TFPI) inhibits TF/FVIIa/Fxa complex activity
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Pathophysiology of DIC Impaired Fibrinolysis
relatively suppressed at time of maximal activation of coagulation due to increased plasminogen activator inhibitor type 1
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Pathophysiology of DIC - Cytokines
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
CoagulationInflamation
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Diagnosis of DIC
Presence of disease associated with DICAppropriate clinical settingClinical evidence of thrombosis, hemorrhage or both.
Laboratory studiesno single test is accurateserial test are more helpful than single test
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Conditions Associated With DIC
Malignancy LeukemiaMetastatic disease
Cardiovascular Post cardiac arrestAcute MI Prosthetic devices
Hypothermia/Hyperthermia
PulmonaryARDS/RDS Pulmonary embolism
Severe acidosis Severe anoxia Collagen vascular disease Anaphylaxis
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Conditions Associated With DIC
Infectious/Septicemia Bacterial
Gm - / Gm +
Viral CMV Varicella Hepatitis
Fungal Intravascular hemolysis Acute Liver Disease
Tissue Injury trauma extensive surgery tissue necrosis head trauma
ObstetricAmniotic fluid emboli Placental abruption EclampsiaMissed abortion
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Clinical Manifestations of DICORGAN ISCHEMIC HEMOR.Skin Pur. Fulminans
GangreneAcral cyanosis
PetechiaeEchymosisOozing
CNS Delirium/ComaInfarcts
Intracranialbleeding
Renal Oliguria/AzotemiaCortical Necrosis
Hematuria
Cardiovascular MyocardialDysfxn
Pulmonary Dyspnea/HypoxiaInfarct
Hemorrhagiclung
GIEndocrine
Ulcers, InfarctsAdrenal infarcts
Massivehemorrhage.
Ischemic Findingsare earliest!
Bleeding is the most obvious
clinical finding
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Clinical Manifestations of DIC
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Microscopic findings in DIC
Fragments Schistocytes Paucity of platelets
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Laboratory Tests Used in DIC
D-dimer* Antithrombin III* F. 1+2* Fibrinopeptide A* Platelet factor 4* Fibrin Degradation Prod Platelet count Protamine test
Thrombin time Fibrinogen Prothrombin time Activated PTT Protamine test Reptilase time Coagulation factor levels
*Most reliable test
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Laboratory diagnosis Thrombocytopeniaplat count <100,000 or rapidly declining
Prolonged clotting times (PT, APTT) Presence of Fibrin degradation products or
positive D-dimer Low levels of coagulation inhibitorsAT III, protein C
Low levels of coagulation factorsFactors V,VIII,X,XIII
Fibrinogen levels not useful diagnostically
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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 process .The only proven treatment!
Supportive therapy No specific treatmentsPlasma and platelet substitution therapyAnticoagulantsPhysiologic coagulation inhibitors
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Plasma therapy Indications
Active bleeding Patient requiring invasive procedures Patient at high risk for bleeding complications
Prophylactic therapy has no proven benefit. Cons: Fresh frozen plasma(FFP):
provides clotting factors, fibrinogen, inhibitors, and platelets in balanced amounts.
Usual dose is 10-15 ml/kg
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Platelet therapy
IndicationsActive bleeding Patient requiring invasive procedures Patient at high risk for bleeding complications
Platelets approximate dose 1 unit/10kg
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Blood
Replaced as needed to maintain adequate oxygen delivery.Blood loss due to bleedingRBC destruction (hemolysis)
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Coagulation Inhibitor Therapy
Antithrombin III Protein C concentrate Tissue Factor Pathway Inhibitor (TFPI) Heparin
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The major inhibitor of the coagulation cascade Levels are decreased in DIC.Anticoagulant and antiinflammatory properties
Therapeutic goal is to achieve supranormal levels of ATIII (>125-150%). Experimental data indicated a beneficial effect in preventing or
attenuating DIC in septic shock reduced DIC scores, DIC duration, and some improvement in organ
function
Clinical trials have shown laboratory evidence of attenuation of DIC and trends toward improved outcomes.
A clear benefit has not been established in clinical trials.
Antithrombin III
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Protein C Concentrates
Inhibits Factor Va, VIIa and PAI-1 in conjunction with thrombomodulin.
Protein S is a cofactor Therapeutic use in DIC is experimental and is based on
studies that show: Patients with congenital deficiency are prone to
thromboembolic disease. Protein C levels are low in DIC due to sepsis. Levels correlate with outcome. Clinical trials show significantly decreased morbidity and
mortality in DIC due to sepsis.
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Tissue Factor Pathway Inhibitor
Tissue factor is expressed on endothelial cells and macrophages
TFPI complexes with TF, Factor VIIa,and Factor Xa to inhibit generation of thrombin from prothrombin
TF inhibition may also have antiinflammatory effects Clinical studies using recombinant TFPI are promising.
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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.
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Antifibrinolytic Therapy
Rarely indicated in DIC Fibrinolysis is needed to clear thrombi from the micro
circulation.Use can lead to fatal disseminated thrombosis.
May be indicated for life threatening bleeding under the following conditions: bleeding has not responded to other therapies and: laboratory evidence of overwhelming fibrinolysis. evidence that the intravascular coagulation has ceased.
Agents: tranexamic acid, EACA
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Summary
DIC is a syndrome characterized systemic intravascular coagulation.
Coagulation is the initial event and the extent of intravascular thrombosis has the greatest impact on morbidity and mortality.
Important link between inflammation and coagulation. Morbidity and mortality remain high. The only proven treatment is reversal or control of the
underlying cause.
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Thanks