Fibrinolytic dysregulation is an important mechanism in traumatic coagulopathy. It is an incompletely understood process that consists of a spectrum ranging from excessive breakdown (hyperfibrinolysis) and the shutdown of fibrinolysis. Both hyperfibrinolysis and shutdown are associated with excess mortality and post-traumatic organ failure. The pathophysiology appears to relate to endothelial injury and hypoperfusion, with several molecular markers identified in playing a role. Although there are no universally accepted diagnostic tests, viscoelastic studies appear to offer the greatest potential for timely identification of patients presenting with fibrinolytic dysregulation. Treatment is multimodal, involving prompt hemorrhage control and resuscitation, with controversy surrounding the use of antifibrinolytic drug therapy. This review presents the current evidence on the pathophysiology, diagnostic challenges, as well as the management of this hemostatic dysfunction. Level of evidence: Level III.
- Acute coagulopathy of trauma
- Fibrinolysis shutdown