Acute traumatic coagulopathy (ATC) develops within minutes of severe injury, present in 25-35% of critically injured patients on arrival and associated with 4x increased mortality. ATC is driven by three mechanisms: (1) Tissue injury releases tissue factor and damage-associated molecular patterns (DAMPs), activating coagulation massively while simultaneously triggering protein C activation that consumes factors V and VIII and promotes fibrinolysis through tPA release. (2) Shock-induced tissue hypoperfusion causes endothelial glycocalyx shedding, releasing syndecan-1 and heparan sulfate which have auto-anticoagulant properties. (3) Hypothermia and acidosis further impair enzymatic function of the coagulation cascade (each 1°C drop below 37°C reduces clotting factor activity by ~10%; pH <7.2 reduces thrombin generation by >50%). The lethal triad (hypothermia, acidosis, coagulopathy) creates a self-perpetuating cycle. Damage control resuscitation (DCR) addresses all three components simultaneously: preventing hypothermia (warm fluids, Bair Hugger), correcting acidosis (restoring perfusion, avoiding crystalloid excess), and replacing coagulation factors through balanced blood product transfusion. The PROPPR trial established that a 1:1:1 ratio of pRBC:FFP:platelets more closely mimics whole blood reconstitution and is superior to higher pRBC ratios (reduced death from exsanguination at 24...