Coagulopathy of massive transfusion

Coagulopathy of massive transfusion is unusual with transfusions less than 1 to 1.5 BVs, assuming the patient has a normal coagulation profile, platelet count, and platelet function initially.

1. Thrombocytopenia. Diffuse oozing and failure to form clots after massive transfusion may be precipitated in part by thrombocytopenia, which is typically due to the transfusion of platelet-poor blood products. However, clinically significant bleeding is unlikely with platelet counts above 50,000 cells/mm³. If the loss of one BV or more is expected, platelets should be transfused to maintain a count of 50,000 cells/mm³ or greater.
2. Coagulation factor deficiencies. The normal human body has tremendous reserves of clotting factors. In addition, the patient receives small amounts of the most stable clotting factors in the plasma of each unit of red cells. Bleeding from factor deficiency in the face of massive transfusion is therefore typically due to decreased levels of fibrinogen and labile factors with shorter storage half-lives (especially factors V, VIII, or IX). Bleeding from hypofibrinogenemia is unusual unless the fibrinogen level is below 75 mg/dL. In some patients, factor VIII levels increase with massive transfusion because of increased release from endothelial cells. Additional labile clotting factors are best repleted in the form of FFP. Six units of platelets contain coagulation factor levels equivalent to 1 unit of FFP. Cryoprecipitate may also provide a source of concentrated fibrinogen for the patient who cannot tolerate FFP owing to volume overload.