Disseminated intravascular coagulation
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| Excessive activation of haemostatic process results in DIC |
Inappropriate and excessive systemic activation of the haemostatic process results in disseminated intravascular coagulation (DIC), factor deficiencies, thrombocytopenia, platelet dysfunction and anaemia.
The main causes of DIC include septicaemia, malignancy, obstetric disorders (eg, eclampsia, abruptio placentae, fetal death in utero), and ABO-incompatible blood transfusion.
There is an overall reduction in levels of all coagulation factors, particularly factors V, VIII and fibrinogen.
Hepatic synthesis of coagulation factors is unable to compensate fully for their consumption, due to an ongoing activation of the coagulation cascade.
The bone marrow is also unable to maintain a normal platelet count and thrombocytopenia ensues.
The combination of coagulation factor deficiency, thrombocytopenia and inhibitory actions of raised fibrin degradation products causes generalised and continued bleeding tendency, which is characteristic of DIC.
In approximately 5%–10% of cases, microthrombotic lesions are present as initial clinical features. Gangrene of fingers and toes may also occur.
