The Use of Tranexamic Acid in Hip and Pelvic Fracture Surgeries

John D. Adams, Jr, MD, FAAOS; William A. Marshall, MD


J Am Acad Orthop Surg. 2021;29(12):e576-e583. 

In This Article

Mechanism of Action of Tranexamic Acid

Fibrinolytic mechanisms are essential for maintaining vascular hemostasis and patency. The foundation of these mechanisms is regulated by the conversion of inactive plasminogen to plasmin, which is an enzyme that cleaves fibrin and leads to clot degradation. Several regulatory pathways modulate plasmin activation under physiologic conditions. Tissue injury disrupts this equilibrium, which may result in coagulopathy and bleeding.[10] Pharmacologic interventions have been developed that focus on these derangements in efforts to reduce blood loss and transfusion rates secondary to trauma.

TXA is a drug that competitively inhibits plasminogen activation and reduces plasmin activity, thus limiting fibrinolysis. It achieves this by occupying lysine-binding sites on plasminogen, which prevents binding to lysine residues located on the molecule fibrin (Figure 1). By reducing fibrinolysis, existing clot is stabilized without the promotion of new clot formation. Subsequently, other parameters such as platelet counts and coagulation have been shown to be unaffected by this process.[11,12]

Figure 1.

Mechanism of action of tranexamic acid (TXA). A, Plasminogen is activated to plasmin by binding to tissue plasminogen activator (t-PA). B, Fibrinolysis occurs when plasmin binds to fibrin. C, TXA occupies the lysine binding site of fibrin to plasmin, thus (D) inhibiting fibrinolysis by preventing the binding of plasmin and fibrin.