• Kaipeng Duan, Wenkui Yu, Zhiliang Lin, Shanjun Tan, Xiaowu Bai, Lin Xu, Yi Dong, and Ning Li.
• Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, PR China.
• Transfus Apher Sci. 2014 Jun 1;50(3):399-406.

IntroductionCoagulopathy after sever injury predicts the requirements of blood products, organ failure and mortality in traumatic patients. The early onset and complexity of traumatic coagulopathy preclude the understanding the underlying mechanism. The aim of the study is to characterize the early coagulation alteration in a swine model with multi-trauma and shock.MethodsTwelve pigs were subjected to multi-trauma (femur fracture, laparotomy, 10 cm intestine resection and grade III injury of liver) and hemorrhaged to a mean arterial pressure (MAP) of 40 mmHg. Physiologic parameters and coagulation variables (prothrombin time (PT), international normalized ratio (INR), fibrinogen, antithrombin-III (AT-III) activity, D-dimer and thromboelastography (TEG)) were measured after instrumentation (baseline), 5 min after multi-trauma (after trauma), 10 min (early shock) and 40 min (late shock) after hemorrhage. A group of 6 instrumented pigs were used as control.ResultsMulti-trauma and hemorrhage caused significant increase of base excess (BE) and lactate (p<0.05). PT shortened after multi-trauma but increased significantly at late shock (p<0.05). Fibrinogen reduced greatly after trauma and at early shock (p<0.05), while remained stable afterwards. AT-III activity decreased throughout the experiment. Reaction time (R) shortened after trauma and at early shock (both p<0.05). Maximal amplitude (MA) decreased significantly during the shock period.ConclusionAfter traumatic hemorrhagic shock, hypercoagulation turned into hypocoagulation in a short period, which was probably caused by hypoperfusion.Copyright © 2014 Elsevier Ltd. All rights reserved.

23 keywords...

hide…