Background
Tranexamic Acid
Tranexamic acid (trans‐4‐(aminomethyl) cyclohexanecarboxylic acid) (TXA) is a synthetic derivative of the amino acid lysine that competitively inhibits the activation of plasminogen to the serine protease, plasmin, via binding to kringle domains. TXA also acts as a competitive inhibitor of tissue plasminogen activator. It blocks the lysine‐binding sites of plasminogen, resulting in inhibition of plasminogen activation and fibrin binding to plasminogen and therefore impairment of fibrinolysis.
TXA directly inhibits plasmin activity, but higher doses are required to reduce plasmin formation. TXA is about ten times more potent in vitro than aminocaproic acid and binds more strongly than aminocaproic acid to the strong and weak receptor sites of the plasminogen molecule, in a ratio corresponding to the difference in potency between the compounds. TXA is distributed throughout all body tissues and the plasma half‐life is 120 min.1
Over the last decade there has been an explosion of interest in the use of TXA in reducing bleeding, fuelled, in particular, by the publication of CRASH‐2. Here’s a summary of recent papers relevant to its use in the ED.