- Auteur(s) : Yves Ozier, Marc Samama
, Service d’anesthésie-réanimation chirurgicale, Université René-Descartes, Paris 5, groupe hospitalier Cochin, 123, boulevard de Port-Royal, 75674 Paris Cedex.
- Mots-clés : blood component transfusion, plasma substitutes, hemostasis, blood coagulation, hemorrhage.
- Page(s) : 191-7
- Année de parution : 2000
Massive blood transfusion is usually defined as the replacement of at least one blood volume within 24 hours. This broad definition encompasses different situations with regard to underlying diseases states, bleeding rates and consequences. Coagulopathy and microvascular bleeding are well-known life-threatening complications of such situations.
The pathogenesis of impaired hemostasis is multifactorial. Both blood replacement strategies and factors related to the underlying conditions may be involved. Whereas dilution thrombocytopenia was underlined as the primary cause of coagulopathy in the whole blood transfusion era, dilution of coagulation factors may be a more significant contributor with modern resuscitation strategies based on cristalloids/colloids and plasma-poor red blood cells. Hypothermia, disseminated intravascular coagulation in relation with tissue injury and circulatory failure are likely to play a significant role in trauma patients. Moreover, synthetic colloid solutions used for blood volume expansion may have specific adverse effects on hemostasis. Hydroxyethyl starch (HES) solutions are frequently used and differ in their pharmacological properties. An acquired von Willebrand syndrome may result from the infusion of high molecular weight (MW) or of large volumes of medium MW HES solutions.
Prevention and treatment of massive blood transfusion coagulopathy should be based on aggressive treatment of shock and hypothermia, and on blood component therapy. HES solutions infusions should be restricted according to recommended dose limits. In the past, prophylactic fresh-frozen plasma (FFP) and platelets transfusion has been said to have no place. However, relying on a specific biological diagnosis of the hemostatic defect is an unrealistic view in high bleeding rate situations. Considering the time scale for laboratory screening and blood components availability, the use of FFP is advocated as soon as one blood volume has been replaced. If platelet counts and units may be more easily obtained, platelets transfusion may be guided by repeatedly determined platelet counts.