[Traumatic emergencies and hemostasis].

Abstract

The occurrence of bleeding in trauma patients is a life-threatening problem which can be explained by different mechanisms. The infusion of cristalloids, colloids, packed red blood cells, or even fresh frozen plasma is very rarely responsible for bleeding but it can contribute to dilute the patient's platelet pool, and especially dilutional thrombocytopenia is the first cause of bleeding after massive transfusion. Blood coagulation factor activity is decreased after a massive fluid infusion is performed but it has to reach a dramatically low plasma level in order to induce troubles. It has to be emphasized that colloids and especially dextrans can impair the patient's haemostasis by interfering the same way with the factor VIII-von Willebrand complex and fibrin formation. Gelatins do not interfere with platelets or with the coagulation system. A third mechanism that can explain the strong link between haemostasis and haemodilution is the haemostatic role of red cells. It has been shown in experimental models that red cells play a definite function in promoting platelet accretion on the damaged vessel surface. Higher values of haematocrit (Ht) are responsible for a better platelet adhesion On the opposite, platelet adhesion decreases when low values of Ht (< 20%) are reached. Hypothermia can also impair platelet function and worsen the bleeding. A simplified monitoring of haemostasis can be proposed with platelet count, whole blood coagulation clotting time, immediately available activated partial thromboplastin time and prothrombin time with bedside portable monitors and thromboelastography. Haematocrit and body temperature have to be monitored as well.