The CRASH-2 trial established the mortality benefit of tranexamic acid (TXA) in trauma. Which time window for TXA administration shows maximum benefit, and what is its mechanism?

• A Within 3 hours; TXA inhibits thrombin directly, preventing clot formation
• B Within 1 hour of injury — anti-fibrinolytic effect; TXA inhibits plasminogen activation by blocking lysine-binding sites on plasminogen, preventing fibrin clot degradation ✓
• C Within 6 hours; TXA activates protein C pathway, reducing coagulopathy
• D TXA should be given only after blood transfusion; timing relative to injury is not significant

Explanation

The CRASH-2 trial (20,000+ patients) demonstrated that TXA within 3 hours of injury reduced all-cause mortality; within 1 hour provided the greatest mortality benefit (~32% relative reduction). TXA (tranexamic acid) is a lysine analogue that binds to lysine-binding sites on plasminogen and plasmin, blocking their attachment to fibrin and thereby inhibiting fibrinolysis. Trauma-induced fibrinolysis activation contributes to the acute coagulopathy of trauma. Administration beyond 3 hours from injury was associated with increased mortality (possibly pro-thrombotic in late fibrinolysis shutdown), making the time window clinically critical.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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