Objective
The two sides of Trauma Induced Coagulopathy (TIC), the hypo- and the hyper- coagulable states, are poorly understood. To identify potential mechanisms for venous thromboembolism and bleeding after acute trauma, we estimated changes in circulating procoagulant MPs and thrombin activity during hospitalization for trauma.
Methods
Whole blood was collected by venipuncture into 3.2% trisodium citrate at 0, 6, 12, 24 and 72 hours after injury, and discharge. Platelet poor plasma was harvested and stored at −80°C until analysis. Thrombin generation was determined using the calibrated automated thrombogram (CAT), reported as lagtime (minutes), peak height (nM thrombin) and time to reach peak height (ttPeak - minutes). The concentration of total procoagulant MPs (number/uL]) was measured by flow cytometry. Data are presented as median [interquartile range].
Results
Among 443 trauma patients (1734 samples; ISS=13.0 [6.0, 22.0], hospital LOS=4.0 [2.0, 10.0] days, age=48 [28, 65] years, 70.7% male, 95% with blunt mechanism, mortality 3.2%), no discernable patterns in thrombin generation or MP concentration were observed over time. The peak height and MPs were significantly different from healthy volunteers and were 337 [285, 395] nM and 400 [211, 772] per uL plasma, respectively. Extreme (defined as highest or lowest 5%) values reflecting a possible “hypercoagulable state” (lagtime ≤ 1.98, peak height ≥ 486.2, ttPeak ≤ 3.61, and total procoagulant MP ≥ 2278) were reached within 12 hours after acute trauma, while extreme values representing a possible “hypocoagulable state” (lagtime ≥ 18.6, peak height ≤ 17.8 and ttPeak ≥ 29.45) were not reached until 1-3 days.
Conclusion
Although there was no predictable pattern of coagulopathy observed in each patient after trauma, those who reached extreme values did so relatively early after injury. These findings should be taken into account when designing risk model tools involving coagulation laboratory parameters.