A trauma patient receiving protocolised massive transfusion has a core temperature of 32.8 degrees Celsius with diffuse microvascular oozing despite adequate product ratios. The dominant mechanism by which hypothermia produces this coagulopathy is:
- A Impairment of temperature-dependent enzymatic activity in the coagulation cascade and platelet dysfunction ✓
- B Accelerated hepatic synthesis of tissue plasminogen activator
- C Increased clearance of fibrinogen by the reticuloendothelial system
- D Autoantibody-mediated destruction of von Willebrand factor
Explanation
Coagulation is optimised at 37 degrees Celsius: serine protease reactions of the cascade slow dramatically below 35 degrees, and platelet adhesion and aggregation become impaired, so standard tests run at 37 degrees underestimate the true in vivo coagulopathic state. This makes hypothermia part of the lethal trauma triad with acidosis and coagulopathy, and active rewarming is itself a definitive haemostatic intervention. Enhanced fibrinolysis, altered fibrinogen clearance and acquired inhibitors play no established role here.
Reference: Miller's Anesthesia, 9th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.