Study on coagulation profiles and platelet function in trauma-induced coagulopathy caused by three types of injury

Abstract Background : Traumatic coagulopathy is a major public health issue globally with undefined mechanisms. We established rat models of hemorrhagic shock (HS), multiple injury (MI) and traumatic brain injury (TBI) to investigate the diversity of traumatic coagulopathy, especially platelet dysfunction. Methods : Seventy male SD rats were divided randomly into seven groups(n=10): control, HS30min, HS3h, MI30min, MI3h, TBI30min and TBI3h. Plasma or whole blood was collected for conventional coagulation tests, thromboelastography and platelet mapping. X-ray, 7T magnetic resonance imaging and hematoxylin-eosin staining of injured tissues were conducted to confirm the injuries of rats model. Results : The activated partial thromboplastin time (aPTT) prolonged significantly in HS30min and MI3h groups, compared with those in control (P=0.0403 and P=0.0076, respectively). R values decreased in HS30min and HS3h groups, compared with those in control (P Conclusion : These results demonstrated that it might be the failure of forming a strong clot instead of the prolonged clot time, which contributed to traumatic coagulopathy. The platelet dysfunctions might contribute to trauma-induced coagulopathy in different ways. The loss of platelets might be the main reason for HS-induced coagulopathy. While, AA-dependent pathway inhibition might account for MI-induced coagulopathy. ADP-dependent pathway inhibition might be the major contributor for TBI-induced coagulopathy.