EComment. Is the maintenance of haemostasis possible without fibrinogen?

Abstract

Although fibrinogen is a key factor in thrombosis, its role in the pathogenesis of haemostatic disturbances after cardiac surgery is often underestimated. Therefore we were glad to read the article by Gielen et al. [1]. Apparently during the postoperative period, decrease in fibrinogen often coincides with the deficiency of other clotting factors and platelet dysfunction, and the level of postoperative blood loss does not depend only on the fibrinogen concentration. Thus, there are no linear connections between blood loss and the level of fibrinogen. However, we cannot underestimate the contribution of this clotting factor in the mechanical stability of clots, which also depends on platelets, coagulation factor XIII and von Willebrand factor. The deficiency of those factors, primarily fibrinogen, leads to the decrease in the fibrin monomer and its polymerization, which further results in delayed thrombus formation along with increase of fibrinolysis sensitivity and blood loss. Based on thromboelastography data, a feedback loop exists between the fibrinogen level and maximum lysis [2]. Therefore, the fibrinogen level serves as an integral value of the formation and stabilization of the clot. It is necessary to note that the velocity of fibrin formation may be affected by the absolute quantity of fibrinogen and its concentration, therefore hypofibrinogenaemia may be the result either of fibrinogen loss or haemodilution. The main target of haemodilution is the formation and stability of the clot, but not the thrombin formation [3]. We tested the connection between pre- and postoperative coagulation values and the level of blood loss after cardiac surgical procedures in children. For patients with congenital heart disease, we consider a threshold fibrinogen concentration of 2.5 g/l to be necessary for prevention of bleeding. In cases with lower concentrations of fibrinogen, we observed postoperative blood losses of 0.75 ml/kg/h to 1.27 ml/kg/h [4]. Hypofibrinogenaemia in children may be caused by hypotrophy due to social (early artificial feeding) and medical factors, impaired hepatic protein synthesis, and a decrease in terminal elimination half-life in cyanotic patients. A postoperative level of fibrinogen less than 2 g/l led to blood loss of 0.61 to 0.85 ml/kg/h [2]. Indeed, there is insufficient evidence to prove that the use of fibrinogen concentrate after cardiac surgery is successful. However, a controlled replacement therapy of blood loss via the use of fibrinogen concentrate in hypofibrinogenaemia is efficient and abolishes the deficiency of other haemostasis components without the risk of thrombosis development. On the other hand, based on stoichiometry, a possible way to circumvent a low level of fibrinogen concentration may be the optimization of the circulating blood volume via the application of ultrafiltration. Conflict of interest: none declared