Disseminated intravascular coagulopathy

Disseminated intravascular coagulopathy

It is a disorder arising as a secondary manifestation of various diseases where there are consumption of platelets, clotting factors in wide spread area of circulation as well as secondary activation of plasminogen fibrinolytic system.

Etiology:

1.       Massive tissue trauma

2.       Sepsis

3.       Obstructive complications: abruption placenta,

Dead fetus, amniotic fluid embolism

4.       Incompatible blood transfusion

5.       Fat embolism

6.       Cardio pulmonary bypass surgery

7.       Advance malignancy

8.       Autoimmune diseases

9.       Shock, heatstroke ,burn

10.   Snake venom

Sites: in decreasing order of frequency

1.       Brain

2.       Heart

3.       Lungs

4.       Kidneys

5.       Adrenal glands

6.       Spleen

7.       Liver

Pathophysiology:

Wide spread activation of the inflammatory

Cells due to the predisposing Factor

Causes release of cytokines (IL-1, 6, 8, TNF, Plasminogen

Activator factor, amino acid metabolites)

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When there is large amount of cytokines released

Its causes endothelial damage and cytokines

Exposed to sub endothelial matrix

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at the same time it causes activation of both arm

of coagulation pathway (intrinsic & extrinsic) in

wide spread area of the body.

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Formation of micro thrombi

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(A.)Vascular occlusion of various organ-

1. microangiopathic hemolytic anemia(due to fragmentation of red cell )

2. Ischemic tissue damage

(B.)Activision of plasmin

1.       Proteolysis of clotting factors

2.       Fibrinolysis- inhabit thrombin, platelet aggregations, fibrin polymerization

Consumption of clotting factors and platelet ;hence it also called CONSUMPTION COAGULOPATHY

NOTE:

The predisposing factors are often multiple and interrelated

TWO MAJOR MECHANISM TRIGGERED DIC:

1.       Release of tissue factors or thromboplastic substances into the

Circulation

2.       Wide spread injury to the endothelial cell

TWO CONSEQUENCES OF DIC:

1.       Widespread deposition of fibrin within the microcirculation

Leads to ischemia

2.       Consumption of platelet and clotting factors and the activation of

Plasminogen leads to hemorrhagic diathesis.

As there is consumption of platelet so there is increase of  BLEEDING TIME & PT

As there is consumption of clotting factors so there is increase of  CLOTTING TIME & APTT