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DISSEMINATED
INTRAVASCULAR
COAGULATION
P.GIRISH KUMAR
ROLL NO.89
Other names :
1.Consumption coagulopathy
2.Defibrination syndrome
Types :
1) Acute DIC
2) CHRONIC DIC
NORMAL HEMOSTASIS
What is dic ?
PATHOGENESIS :
1. Generation of a hyperthrombinemic state.
2. Alteration of the physiological anticoagulants levels.
3. Im...
Generation of hyperethrombinemic state
1. The exposing of the tissue factors thromboplastins and
factor3 during injury cau...
The cascade goes as follows :
Thrombin in turn activates :
Alteration of the physiological
anticoagulant levels:
There are 3 most common Anticoagulants in the body :
1. Antithrombin...
• Consumption of the elaborated thrombin.
• Elastase release from neutrophils (seen in
case of septicemia and anoxic liver...
Impaired fibrinolysis at the onset of DIC:
1. PAI-1 a neurohumoral compound released from endothelial cells.
2. It suppres...
Activation and liberation of inflammatory
cytokines in DIC :
Clinical features :
•Microangiopathic hemolytic
anemia
•Dyspnea
•Cyanosis and respiratory failure
•Convulsions and coma
•O...
DIFFERENTIAL DIAGNOSIS :
1. Severe liver disease :lab
parameters won’t change
rapidly and presence of
portal hypertension....
Lab investigations of DIC :
CBC and blood
smear
Clotting times
Fibrin related
markers
Coagulation factors
• Decreased may
not be in acute
but in severe
dic.
• D-dimer
elevated.norm
al level rules
out DIC
• PT Prolonged.
• PTT pr...
International society on
Thrombosis and
Hemostasis scoring
system for diagnosis of
DIC
A score below 5 is suggestive
as a ...
disseminated intravascular coagulation
disseminated intravascular coagulation
disseminated intravascular coagulation
disseminated intravascular coagulation
disseminated intravascular coagulation
disseminated intravascular coagulation
disseminated intravascular coagulation
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disseminated intravascular coagulation

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disseminated intravascular coagulation

  1. 1. DISSEMINATED INTRAVASCULAR COAGULATION P.GIRISH KUMAR ROLL NO.89
  2. 2. Other names : 1.Consumption coagulopathy 2.Defibrination syndrome Types : 1) Acute DIC 2) CHRONIC DIC
  3. 3. NORMAL HEMOSTASIS
  4. 4. What is dic ?
  5. 5. PATHOGENESIS : 1. Generation of a hyperthrombinemic state. 2. Alteration of the physiological anticoagulants levels. 3. Impaired fibrinolysis at the onset of DIC. 4. Activation and liberation of inflammatory cytokines in the pathogenesis of DIC.
  6. 6. Generation of hyperethrombinemic state 1. The exposing of the tissue factors thromboplastins and factor3 during injury causes a cascade activation of a factor pathway that has a dominant role in the hyperthrombinemic state in DIC. 2. Cytokines and the bacterial endotoxins are all triggers to the formation of endothelial cell tissue factor. 3. In severe trauma also tissue phospholipids initiates the clotting cascade.
  7. 7. The cascade goes as follows :
  8. 8. Thrombin in turn activates :
  9. 9. Alteration of the physiological anticoagulant levels: There are 3 most common Anticoagulants in the body : 1. Antithrombin 2. Active protein C 3. Tissue factor pathway inhibitor (TFPI) In DIC : 1. Anti thrombin 2. Active protein C
  10. 10. • Consumption of the elaborated thrombin. • Elastase release from neutrophils (seen in case of septicemia and anoxic liver impairement) Causes of decrease in antithrombin levels • Thrombomodulin(integral membrane protein of endothelial cells) combines with protein C to form active protein C.This is done in activation of thrombomodulin by thrombin. • In case of liver injury and or a down regulation thrombomodulin expression on the vascular surface. Causes of decrease in active protein C levels
  11. 11. Impaired fibrinolysis at the onset of DIC: 1. PAI-1 a neurohumoral compound released from endothelial cells. 2. It suppresses fibrinolysis normally 3. In some DIC individuals , PAI -1gene mutation shown leading to increased PAI-1 levels
  12. 12. Activation and liberation of inflammatory cytokines in DIC :
  13. 13. Clinical features : •Microangiopathic hemolytic anemia •Dyspnea •Cyanosis and respiratory failure •Convulsions and coma •Oliguria and acute renal failure •Sudden or progressive circulatory failure and shock •Petechiae •Bleeding , possibly from multiple sites of body SITES OF THROMBOSIS IN DECREASING ORDER OF FREQUENCY •Brain •Heart •Kidney •Adrenals •Spleen •Lungs •Liver
  14. 14. DIFFERENTIAL DIAGNOSIS : 1. Severe liver disease :lab parameters won’t change rapidly and presence of portal hypertension. 2. Microangiopathic disorders(TTP) :no consumption of clotting factors or hyperfibrinolysis.
  15. 15. Lab investigations of DIC : CBC and blood smear Clotting times Fibrin related markers Coagulation factors
  16. 16. • Decreased may not be in acute but in severe dic. • D-dimer elevated.norm al level rules out DIC • PT Prolonged. • PTT prolonged • TT increased due to consumption of fibrinogen • Thrombocyt openia. • Schistocytes . Complete blood counting And blood smear Clotting times Coagulation factors(fibrinogen) Fibrin degradation products(most sensitive test)
  17. 17. International society on Thrombosis and Hemostasis scoring system for diagnosis of DIC A score below 5 is suggestive as a diagnosis but not the definite; hence the test must be repeated.

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