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.