Disseminated Intravascular Coagulopathy

Changes in the haemostatic system during pregnancy and the local activation of the clotting system at parturition carry a risk not only of thromboembolism, but also of DIC, consumption of clotting factors and platelets, leading to severe bleeding. One of the problems with DIC is its definition. It is always secondary to some general stimulation of the coagulation system. Table 1 shows the DIC trigger mechanisms. DIC is manifested in several forms, from a compensated state with no clinical manifestations, but evidence ofincreased production and breakdown of coagulation factors to the condition of massive uncontrollable haemorrhage with very low levels of plasma fibrino-gen, raised levels of fibrin degradation products (FDPs), and variable degrees of thrombocytopaenia. Fibrinolysis is stimulated by DIC, and

Table 1. Trigger Mechanisms for DIC in Pregnancy

Pre-eclampsia

Septicaemia

Hypovolaemia

Abruptio placenta Amniotic fluid embolism Retained dead foetus Abortion induced with hypertonic fluids Intrauterine sepsis Placenta accreta Hydatidiform mole

Intravascular haemolysis Incompatible blood transfusion Large foeto-maternal bleed Septicaemia

Endothelial injury

Thromboplastin,

Endothelial injury

Collagen

Xlla XIa IXa

Phospholipid

Collagen

Xlla XIa IXa

VIII

Xa V IIa

Fibrinogen -

-Fibrin

FDPs resulting from the process interfere with the formation of firm fibrin clots. A vicious cycle is established, leading to further bleeding.

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