Role of fibrinogen in trauma-induced coagulopathy

Abstract

Coagulation defects related to severe trauma, trauma-induced coagulopathy (TIC), have a number of causal factors including: major blood loss with consumption of clotting factors and platelets, and dilutional coagulopathy after administration of crystalloids and colloids to maintain blood pressure. In addition, activation of the fibrinolytic system or hyperfibrinolysis, hypothermia, acidosis, and metabolic changes can also affect the coagulation system. All of these directly affect fibrinogen polymerization and metabolism. Other bleeding-related deficiencies usually develop later in massive bleeding related to severe multiple trauma. In major blood loss, fibrinogen reaches a critical value earlier than other procoagulatory factors, or platelets. The question of the critical threshold value is presently the subject of heated debate. A threshold of 100 mg dl(-1) has been recommended, but recent clinical data have shown that at a fibrinogen level of <150-200 mg dl(-1), there is already an increased tendency to peri- and postoperative bleeding. A high fibrinogen count exerts a protective effect with regard to the amount of blood loss. In multiple trauma patients, priority must be given to early and effective correction of impaired fibrin polymerization by administering fibrinogen concentrate.