Medical

Trauma-Induced Coagulopathy (TIC)

The complex acquired bleeding disorder that develops within minutes of severe trauma, driven by tissue injury, shock, inflammation, and consumption of clotting factors. TIC is distinct from dilutional coagulopathy caused by aggressive crystalloid resuscitation and is present on hospital arrival in a substantial fraction of severely injured patients. TIC drives much of the preventable mortality from hemorrhagic shock.

In the Field
TIC is what changed trauma resuscitation in the 21st century. The old model treated coagulopathy as a late complication of crystalloid dilution that you addressed after the bleeding stopped. The TIC model recognizes that the bleeding patient is already coagulopathic when you start, and that aggressive crystalloid makes it worse. The response is damage control resuscitation: minimize crystalloid, use whole blood or balanced 1:1:1 component therapy, give TXA early (within 3 hours), correct hypothermia and acidosis aggressively. TCCC doctrine reflects this: blood products are preferred over crystalloid, TXA is given for casualties likely to need transfusion, and the lethal triad of hypothermia-acidosis-coagulopathy is treated as the operationally critical complication.
Common Mistake
Treating coagulopathy as an end-stage problem rather than a present-on-arrival problem. The patient with severe trauma already has TIC physiology by the time they reach you; the question is how much you make it worse before you start to correct it. Aggressive crystalloid is the classic mistake - it dilutes clotting factors that are already low and shifts pH toward acidosis. The other mistake is delayed TXA administration. TXA given within 1 hour has the strongest evidence; given within 3 hours still benefits; given after 3 hours has no benefit or may harm. Time matters.

Technical Detail

TIC mechanisms: tissue injury releases tissue factor, activating both clotting and fibrinolytic pathways; protein C pathway activation produces anticoagulant effect; shock and hypoperfusion drive endothelial dysfunction and acidosis; consumption coagulopathy depletes platelets and clotting factors; hyperfibrinolysis (excessive clot breakdown) contributes to ongoing bleeding. Drivers of TIC: severe tissue injury (Injury Severity Score over 15), hypoperfusion and shock, acidosis (pH under 7.2), hypothermia (under 35 degrees C), hemodilution from crystalloid resuscitation. Diagnosis: standard coagulation studies (PT, PTT, INR) detect late-stage TIC; thromboelastography (TEG) or rotational thromboelastometry (ROTEM) detect TIC patterns at point of care and guide component therapy. Treatment: damage control resuscitation - whole blood or balanced 1:1:1 component therapy, minimal crystalloid, aggressive hypothermia prevention, early TXA (2 grams IV/IO push within 3 hours of injury), early surgical control of bleeding, calcium replacement after transfusion. TCCC 2026 explicitly addresses TIC physiology through fluid resuscitation hierarchy and TXA recommendation.