Disseminated Intravascular Coagulation

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Disseminated Intravascular Coagulation (DIC)
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Concept
Concept
DIC represents a continuum in clinical
pathological severity, characterized by the
increasing loss of localization or compensated
control in intravascular activation of
coagulation. It is characterized by
the activation of the coagulation system
with resultant consumption of a variety of
coagulation proteins and platelets, which results
in hemorrhagic diathesis and ischemic injury to
various tissues.
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• Infectious disease---the most common clinical
  condition associated with DIC
• Severe trauma---acute DIC is often seen with
  serious injuries and burns caused by the release
  of thromboplastic material
• Neoplasia---both solid tumor and cancer
• Vascular disorder---large aortic aneurysms may
  result in local activation of coagulation
• Obstetric accidents---includes amniotic
  fluidembolism and placental abruption, the fetus,
  the placenta, and the amniotic fluid are rich in
  thromboplastic substances.

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Blood coagulation
?a ?a PLCa2
TFPI
?a ?a PLCa2
(-)
AT
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Blood coagulation
coagulation inhibitory systems
Body fluid anticoagulation system
Cell anticoagulation system
Monocyte-macrophage Vascular endothelial cell(VEC)
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Pathogenesis
Pathogenesis of DIC
excessive generation of thrombin defects in
inhibitors of coagulation generation of
systemic plasmin and fibrinolytic defect
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Pathogenesis
Excessive generation of thrombin
Severe tissue injury
Trauma?Obstetrical calamities?Tumours
Tissue necrosis TF?? ? a
??abnormal activation of the extrinsic
coagulation system
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1. Severe tissue injury

• Introduction into the circulation of substances
  with tissue thromboplastic activity may initiate
  the extrinsic clotting reactions.
• This can occur with severe trauma, wounds, major
  operation, malignant necrosis and by the actions
  of uterine contents in patients with obstetrical
  complications.

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Pathogenesis
Extensive damage of vascular endothelial
cells VEC has the normal anticoagulant
effect, damage VEC has a procoagulant effect.
infection, ET, hypoxia, acidosis
VEC injury TF?
collagen fibers exposed
micro-thrombosis ?a ?platelet adhesion
and aggregation DIC
coagulation increased
M ?? PMN activated cytokines, completment,
ROS?
Indirect way
Direct way
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• 2. Extensive damage of vascular
  endothelial cells
• Infection, shock , hypoxia and immune reactions
  can damage the vascular endothelial cells.

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• Blood contacts with exposed collagen to trigger
  intrinsic clotting cascade through activation of
  factor ? and to aggregate platelets. In
  infection, gram-negative bacterial endotoxin can
  cause clotting in many animal species and
  endotoxinemia is a major cause of intravascular
  clotting.

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Antithrombin ,protein C, and tissue
factor-pathway inhibitor appear to be affected in
DIC. Plasma levels of AT are markedly reduced as
a result of the ongoing coagulation, degradation
by elastase released from activated
neutrophils. Then the protein C system is
impaired. Nature coagulation inhibitors,
including AT, protein C, are consumed thus
contributing to the increased generation of
thrombin and fibrin.
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The plasma level of plasminogen-activator
inhibitor thpe 1 is increased, which inhibits
the fibrinolytic system.
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Predisposing factors
Predisposing factors to DIC
Inappropriately conditioned monocytes-macrophages
Liver injury Hypercoagulable state Dysfunction
of microcirculation
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Predisposing factors
Inappropriately conditioned monocytes-macrophages
The reticuloendothelial system can remove most of
the products of introvascular coagulation and
various initiators of the process from the
circulation.
Hypercoagulable state of blood
The platelets and several kinds of clotting
factors (F?,?,?, ?, ?, ?, ?, etc.) in blood are
increased. The activity of anticoagulant
materials and or fibrinolysis are decreased.
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Predisposing factors
Dysfunction of microcirculation
Stasis of the microcirculation permits
activated clotting factors to accumulate in blood
capillary making it easier to develop into DIC.
Severe hepatic dysfunction
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Consequences
Consequences of DIC
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Consequences
Bleeding
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Consequences
Bleeding mechanisms

• Consumption of clotting factors and platelets
• Activation of secondary fibrinolytic system
• Production of fibrin degradation products

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Consequences
Disturbance of circulation---Shock
? Microthromobus
blood returning to heart ?
DIC bleeding blood volume?
? Bradykinin,histamine? vasodilation
blood pressure? FDP can increased to
dilates vessels that cause hypotension

? Heart function??
cardiac output? blood
pressure?
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Consequences
Microangiopathic hemolytic anemia (MHA)
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