Coagulopathy in the Critically Injured Patient

Conclusion

The pathophysiology of coagulopathy in the trauma patient is complex and multifactorial. The term ‘DIC’ is incorrectly used to define trauma-related coagulopathy. Although the routine laboratory results resemble those of DIC because they detect activation of coagulation and fibrinolysis and consumption of platelets and coagulation factors, the pathophysiology of the coagulopathy is quite different. While DIC reflects a hypercoagulable state with loss of localization of the coagulation process, leading to diffuse deposition of fibrin, trauma-related coagulopathy is a hypocoagulable state with fibrin deposition limited to the site of injury. The use of the right terms is not only a semantic issue but has major implications for treatment. In fact this was the main reason for the delay in introduction of rFVIIa to trauma patients a few years after its introduction to hemophilia and bleeding disorders: The use of agents markedly enhancing hemostasis, such as rFVIIa, in patients already suffering from a hypercoagulable state seemed to be risky. Much of the early data in the literature are not applicable due to the change of blood components and transfusion policy in the modern area of trauma patient resuscitation. A multidisciplinary approach involving anesthesiologists, transfusion specialists, hematologists, laboratory specialists and surgeons is required for the diagnosis and treatment of traumatic bleeding.