Tranexamic acid

Breakdown · detail · Lysine analogue Within 3 hours

A synthetic lysine analogue that saturates the lysine-binding kringle sites of plasminogen, so plasminogen and t-PA can no longer dock onto fibrin. Plasmin is therefore never generated at the clot surface and the clot is protected from lysis. It is an antifibrinolytic, not a procoagulant.

Traced from the start

  1. Tissue factor and the extrinsic triggerVitamin K cycle and gamma-carboxylation
  2. Contact activation system (factor XII, prekallikrein, high-molecular-weight kininogen)
  3. Subendothelial collagen and von Willebrand factor
  4. Tissue factor-factor VIIa complex (extrinsic tenase)Factor IXaFactor VIIIa and its von Willebrand factor carrierActivated platelet phospholipid surface
  5. Factor XaFactor VaProthrombin (factor II)
  6. Thrombin (factor IIa)
  7. Plasminogen and tissue plasminogen activator
  8. Tranexamic acid

Detail

Mechanism
Competitive blockade of the lysine-binding sites of plasminogen, preventing its binding to fibrin
Trauma evidence
CRASH-2 showed reduced death from bleeding in trauma when given within 3 hours of injury, without excess vascular occlusive events
Obstetric evidence
The WOMAN trial showed reduced death from bleeding in postpartum haemorrhage when given within 3 hours of delivery
Other uses
Menorrhagia, dental extraction in haemophilia and von Willebrand disease, epistaxis, and prophylaxis in hereditary angioedema
Cautions
Avoid in upper urinary tract bleeding, where clot retention can obstruct the ureter; seizures occur at high doses in cardiac surgery

When it goes wrong

Tranexamic acid given more than 3 hours after injury or after delivery

No mortality benefit and possible harm — the entire benefit lies within the first 3 hours, which is why it is given at the roadside or on arrival rather than after imaging

Practise this structure

1 question in the bank tagged Fibrinolysis.