Disseminated intravascular coagulation Hematology Medicine Physiotherapy

Pathophysiology of Disseminated Intravascular Coagulation (DIC)

In this article we will discuss the Pathophysiology of Disseminated Intravascular Coagulation (DIC)

In this article, we will discuss the Pathophysiology of Disseminated Intravascular Coagulation (DIC). So, let’s get started.


The following are the steps in pathogenesis of DIC:

(1) Thrombin generation that overpowers its controlling mechanism: In most forms of DIC, the tissue factor TF (thromboplastin) is released, e.g. from leukemic cells in leukemia and from placenta in obstetric conditions which activates the extrinsic pathway of coagulation by interacting with factor VII thereby initiating coagulation. The sepsis, cytokines, endotoxin, trauma, ischemia, tumor cells can initiate DIC by release of TF. In DIC, thrombin formation is excessive, uncontrolled and overcomes the factors (antithrombin III, activated protein C) which normally inhibits thrombin formation.

(2) Fibrin deposition in microcirculation: Large amounts of thrombin generated leads to fibrin formation from fibrinogen leading to its deposition in the microvasculature. Widespread microvasculature thrombosis produces tissue ischemia and organ damage. Microangiopathic hemolytic anaemia is a consequence of DIC as RBCs are sheared by the intravascular fibrin strands.

(3) Consumption of platelets and coagulation factors: As DIC continues, the platelets and coagulation factors are trapped and consumed beyond the capacity of the body to compensate. This contributes to bleeding.

(4) Secondary fibrinolysis and production of fibrinogen degradation products (FDPs): Protein C, antithrombin (AT), proteins plasmin inhibitors provide defence against fibrinolysis. A lack of these inhibitors would favour DIC and its worsening. In response to thrombosis, endothelial cells secret plasminogen activators to initiate fibrinolysis (secondary fibrinolysis). Plasmin formed from activation of plasminogen degrades both the fibrinogen and fibrin leading to the formation of FDPs, thus, dissolves clots thereby increasing the risk of bleeding. FDPs interferes with fibrin polymerization, thrombin activity and platelet function that further aggravate bleeding tendency.

(5) Role of chemical mediators such a cytokines: DIC in different diseases result from release of various cytokines that act through activation of coagulation pathway. DIC occurs as chemical mediators are released from macrophages, monocytes and endothelial cells. Tissue necrosis factor (TNF) and IL-1 can cause production of TF which initiates DIC. Many of the effects of DIC such as hypotension or acute lung injury may be due to the effects of these cytokines.

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