24th July 2024

Disseminated intravascular coagulation

In normal homeostasis, coagulation and fibrinolysis are under control and activated in an ordered fashion. In DIC, these processes are overactive, leading to both increased coagulability and increased bleeding. There is release of large volumes of tissue factor, which activates the clotting cascade. Coagulation factors are used up quicker than they are able to be produced. Fibrin degradation products are produced and interfere with clot formation and platelet aggregation, leading to an increased bleeding state. DIC can present acutely or chronically.

DIC can be caused by infection, cancer (importantly APML), trauma and obstetric complications such as preeclampsia.

Clinical features of DIC

FBC will show low Hb and platelets; schistocytes will be present on blood film; coagulation studies will show prolonged PT and APTT; fibrinogen can be low and d-dimer elevated.

Management of DIC

Treatment of the underlying cause of DIC is paramount. Blood products to correct clotting derangements are indicated when patients are actively bleeding. This includes platelets, FFP and cryoprecipitate.