From Plasma Transfusion to Individualized, Goal-directed Coagulation Factor Administration

摘要

In the evolution of the understanding of hemostasis in recent years, it became apparent that fibrinogen is in a central position.1 During primary hemostasis, platelets become activated,2 resulting in an inside-out activation of platelet glyco-protein nb/HIa complex (GpHb-IIIa) receptors that enables inter-platelet Unking by fibrinogen3 (Fig 1). In addition, these activated platelets present highly efficacious surfaces for plasma coagulation to take place according to the cell-based model,4'5 resulting in a thrombin burst6 (Fig 2). This thrombin burst results in the conversion of fibrinogen to soluble fibrin and in the activation of factor XIII to cross-link the soluble fibrin into solid fibrin strands.In many bleeding situations, including trauma and cardiac surgery, fibrinogen is the first coagulation element that may become critically low. This is because the fibrinogen concentration is relatively low to start with in these situations8'9 and because there is no fibrinogen stored in the human body that might be mobilized.10 Early testing for fibrinogen concentration— and even more so, for fibrinogen activity—has been proposed in Europe and implemented in many centers.