BACKGROUND: Although coagulopathy can be very common in severe traumatic shock patients, the exact incidence and mechanism remain unclear. In this study, a traumatic shock rabbit model with special abdomen injuries was developed and evaluated by examining indicators of clotting and fi brinolysis.METHODS: Forty New Zealand white rabbits were randomly divided into four groups: group 1(sham), group 2(hemorrhage), group 3(hemorrhage-liver injury), and group 4(hemorrhage-liver injury/intestinal injury-peritonitis). Coagulation was detected by thromboelastography before trauma(T0), at 1 hour(T1) and 4 hours(T2) after trauma.RESULTS: Rabbits that suffered from hemorrhage alone did not differ in coagulation capacity compared with the sham group. The clot initiations(R times) of group 3 at T1 and T2 were both shorter than those of groups 1, 2, and 4(P<0.05). In group 4, clot strength was decreased at T1 and T2 compared with those in groups 1, 2, and 3(P<0.05), whereas the R time and clot polymerization were increased at T2(P<0.05). The clotting angle signifi cantly decreased in group 4 compared with groups 2 and 3 at T2(P<0.05).CONCLUSION: This study suggests that different abdominal traumatic shock show diverse coagulopathy in the early phase. Isolated hemorrhagic shock shows no obvious effect on coagulation. In contrast, blunt hepatic injury with hemorrhage shows hypercoagulability, whereas blunt hepatic injury with hemorrhage coupled with peritonitis caused by a ruptured intestine shows a tendency toward hypocoagulability. BACKGROUND: Although coagulopathy can be very common in severe traumatic shock patients, the exact incidence and mechanism remain unclear. In this study, a traumatic shock rabbit model with special abdomen injuries was developed and evaluated by examining indicators of clotting and fi brololysis. METHODS: Forty New Zealand white rabbits were randomly divided into four groups: group 1 (sham), group 2 (hemorrhage), group 3 (hemorrhage-liver injury), and group 4 (hemorrhage-liver injury / intestinal injury-peritonitis). Coagulation was detected by thromboelastography before trauma (T0), at 1 hour (T1) and 4 hours (T2) after trauma .RESULTS: Rabbits that suffered from hemorrhage individually did not differ in coagulation capacity compared with the sham group. The clot initiations (R times ) of group 3 at T1 and T2 were both shorter than those of groups 1, 2, and 4 (P <0.05). In group 4, clot strength was decreased at T1 and T2 compared with those in groups 1, 2, and 3 (P <0.05), while the R time and clot polyme The clotting angle signifi cantly decreased in group 4 compared with groups 2 and 3 at T2 (P <0.05). CONCLUSION: This study suggests that different abdominal traumatic shock show diverse coagulopathy in the early phase. Isolated hemorrhagic shock shows no obvious effect on coagulation. In contrast, blunt hepatic injury with hemorrhage shows hypercoagulability, and blunt hepatic injury with hemorrhage coupled with peritonitis caused by a ruptured intestine shows a tendency toward hypocoagulability.