Disseminated Intravascular Coagulation

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Basics

Description

  • Normal coagulation: Series of local reactions among blood vessels, platelets, and clotting factors
  • Disseminated intravascular coagulation (DIC) is systemic activation of coagulation and fibrinolysis by some other primary disease process.
  • Coagulation system activation results in systemic circulation of thrombin and plasmin.
  • Role of thrombin in DIC:
    • Tissue factor/factor VIII(a) activate the extrinsic pathway, leads to thrombin formation.
    • Thrombin circulates and converts fibrinogen to fibrin monomer.
    • Fibrin monomer polymerizes into fibrin (clot) in the circulation.
    • Clots cause microvascular and macrovascular thrombosis with resultant peripheral ischemia and end organ damage.
    • Platelets become trapped in clot with resultant thrombocytopenia.
  • Role of plasmin in DIC:
    • Plasmin circulates systemically converting fibrinogen into fibrin degradation products (FDPs).
    • FDPs combine with fibrin monomers.
    • FDP-monomer complexes interfere with normal polymerization and impair hemostasis.
    • FDPs also interfere with platelet function.
  • Role of impaired anticoagulation in DIC.
    • Failure of physiologic anticoagulation is necessary for DIC to occur.
    • Antithrombin III, protein C system, and tissue factor pathway inhibitor all impaired.
  • Acute DIC—uncompensated form:
    • Clotting factors used more rapidly than body can replace them
    • Hemorrhage predominant clinical feature, which overshadows ongoing thrombosis
  • Chronic DIC—compensated form:
    • Body able to keep up with pace of clotting factor consumption
    • Thrombosis predominant clinical feature

Etiology

  • Precipitated by many disease states
  • Complications of pregnancy:
    • Retained fetus
    • Amniotic fluid embolism
    • Placental abruption
    • Abortion
    • Eclampsia
    • HELLP syndrome
  • Sepsis:
    • Gram negative (endotoxin-mediated meningococcemia)
    • Gram positive (mucopolysaccharide-mediated)
    • Other microorganisms (e.g., viruses, parasites)
  • Trauma:
    • Crush injury
    • Severe burns
    • Severe head injury
    • Fat embolism
  • Malignancy:
    • Solid tumor or metastatic disease
    • Hematologic malignancy (e.g., leukemia)
  • Intravascular hemolysis:
    • Transfusion reactions
    • Massive transfusion
  • Organ destruction:
    • Severe pancreatitis
    • Severe hepatic failure
  • Vascular abnormalities:
    • Kasabach–Merritt syndrome
    • Large vascular aneurysm
  • Thrombocytopenia:
    • Thrombotic thrombocytopenic purpura
    • Idiopathic thrombocytopenic purpura
  • Miscellaneous:
    • Snake bites
    • Recreational drugs

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Basics

Description

  • Normal coagulation: Series of local reactions among blood vessels, platelets, and clotting factors
  • Disseminated intravascular coagulation (DIC) is systemic activation of coagulation and fibrinolysis by some other primary disease process.
  • Coagulation system activation results in systemic circulation of thrombin and plasmin.
  • Role of thrombin in DIC:
    • Tissue factor/factor VIII(a) activate the extrinsic pathway, leads to thrombin formation.
    • Thrombin circulates and converts fibrinogen to fibrin monomer.
    • Fibrin monomer polymerizes into fibrin (clot) in the circulation.
    • Clots cause microvascular and macrovascular thrombosis with resultant peripheral ischemia and end organ damage.
    • Platelets become trapped in clot with resultant thrombocytopenia.
  • Role of plasmin in DIC:
    • Plasmin circulates systemically converting fibrinogen into fibrin degradation products (FDPs).
    • FDPs combine with fibrin monomers.
    • FDP-monomer complexes interfere with normal polymerization and impair hemostasis.
    • FDPs also interfere with platelet function.
  • Role of impaired anticoagulation in DIC.
    • Failure of physiologic anticoagulation is necessary for DIC to occur.
    • Antithrombin III, protein C system, and tissue factor pathway inhibitor all impaired.
  • Acute DIC—uncompensated form:
    • Clotting factors used more rapidly than body can replace them
    • Hemorrhage predominant clinical feature, which overshadows ongoing thrombosis
  • Chronic DIC—compensated form:
    • Body able to keep up with pace of clotting factor consumption
    • Thrombosis predominant clinical feature

Etiology

  • Precipitated by many disease states
  • Complications of pregnancy:
    • Retained fetus
    • Amniotic fluid embolism
    • Placental abruption
    • Abortion
    • Eclampsia
    • HELLP syndrome
  • Sepsis:
    • Gram negative (endotoxin-mediated meningococcemia)
    • Gram positive (mucopolysaccharide-mediated)
    • Other microorganisms (e.g., viruses, parasites)
  • Trauma:
    • Crush injury
    • Severe burns
    • Severe head injury
    • Fat embolism
  • Malignancy:
    • Solid tumor or metastatic disease
    • Hematologic malignancy (e.g., leukemia)
  • Intravascular hemolysis:
    • Transfusion reactions
    • Massive transfusion
  • Organ destruction:
    • Severe pancreatitis
    • Severe hepatic failure
  • Vascular abnormalities:
    • Kasabach–Merritt syndrome
    • Large vascular aneurysm
  • Thrombocytopenia:
    • Thrombotic thrombocytopenic purpura
    • Idiopathic thrombocytopenic purpura
  • Miscellaneous:
    • Snake bites
    • Recreational drugs

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