LAUSR

zation of diagnosis and treatment of diseases through genetic, biomarker and phenotypic characteristics. This emphasis on phenotype allows traumatologists to utilize VETs to classify trauma patients – who have been recently described within a spectrum of fibrinolysis as hyperfibrinolytic, physiologic or hypofibrinolytic – by their fibrinolytic phenotype. Emphasis on the fibrinolytic spectrum and the ability of VETs to detect ‘phenotype switching’ in trauma patients during resuscitation is seen by supporters of PBM as a rudimentary but real opportunity to detect the ‘signal from the noise’ of those patients who require VET-guided BCT and prohaemostatic therapy. These results and other clinical studies, which are observational or perspective non-RCTs, as well as some RCTs reveal that goal-directed haemostatic resuscitation for trauma-induced coagulopathy can maintain haemostasis. The availability of new generation devices should enhance the feasibility of earlier testing and, ultimately, the proven benefit. The future significance of trauma-induced coagulopathy and fibrinolysis in trauma will require that epidemiologists and traumatologists adopt both Platonic and Aristotelian mindsets as they refine the benefits of TXA in trauma proposed by the CRASH-2 trial and adopt the classical cause-and-effect Aristotelian analysis of non-RCTs. This can be accomplished, for example, by the prehospital administration of TXA to all shocked patients in trauma with subsequent TXA guided by VETs. The level of inquiry following the important discovery by the CRASH-2 trial that TXA is effective in trauma resuscitation has been refined by those who use PBM to apply those lessons learned in this landmark trial.