Let’s review: DIC is a condition that often develops under extreme physiologic stress, such as sepsis, malignancy, surgery/trauma, pregnancy, burns, or snake bites, even. Clotting factors get stuck together and form micro-thrombi which leads to two ironic pathways:
- Tissue factor activation, thrombin activation, which causes clotting
- Because the clotting factors are used up and FDP’s are released, oozing is also a problem
The #1 way to treat DIC: treat the underlying cause!
The treatments for DIC are divided into blood products for coagulation, and anticoagulation.
Vitamin K: often first-line therapy, can be given orally or IV. While factor VII may increase within 4 hours, the more important increase in factor II takes at least 24 hours (and the PO form takes even longer than that).
Fresh frozen plasma: FFP contains factors II, VII, IX, X, XIII (all vitamin-K dependent), as well as prothrombin complex concentrates. However, it has significant potential side effects, including volume overload and TRALI.
Prothrombin complex concentrate: PCC contains either three (II, IX, X) or four (II, VII, IX, X) clotting factors, along with C and S. It is faster-acting than FFP and has a better safety profile with less risk of overload, TRALI because of the cleansing process, and no increased risk of thrombotic events.
For DIC: Vitamin K is often given, although FFP should be added on at a rate of 15 ml/kg. Because of the risk of transfusing too much volume, small amounts of PCC can be added on. DIC is characterized by low fibrinogen and so replacement with pure fibrinogen or cryoprecipitate may be helpful.
All patients with DIC should receive at least prophylactic doses of heparin. LWMH has better evidence than UFH. If a patient has thrombosis-type DIC, therapeutic doses of heparin should be considered. There’s no evidence right now showing that other anticoagulants like fondaparinux are more effective.