Kaipeng Duan1, Wenkui Yu1, Zhiliang Lin1, Shanjun Tan1, Xiaowu Bai1, Lin Xu1, Yi Dong1, Ning Li2. 1. Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, PR China. 2. Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, PR China. Electronic address: liningnju@126.com.
Abstract
INTRODUCTION: Coagulopathy 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. METHODS: Twelve 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. RESULTS: Multi-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. CONCLUSION: After traumatic hemorrhagic shock, hypercoagulation turned into hypocoagulation in a short period, which was probably caused by hypoperfusion.
INTRODUCTION:Coagulopathy after sever injury predicts the requirements of blood products, organ failure and mortality in traumaticpatients. 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. METHODS: Twelve 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. RESULTS:Multi-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. CONCLUSION: After traumatic hemorrhagic shock, hypercoagulation turned into hypocoagulation in a short period, which was probably caused by hypoperfusion.
Authors: Julia R Coleman; Annika B Kay; Ernest E Moore; Hunter B Moore; Eduardo Gonzalez; Sarah Majercik; Mitchell J Cohen; Thomas White; Fredric M Pieracci Journal: Am J Surg Date: 2019-09-10 Impact factor: 2.565
Authors: H B Moore; E E Moore; M P Chapman; E Gonzalez; A L Slaughter; A P Morton; A D'Alessandro; K C Hansen; A Sauaia; A Banerjee; C C Silliman Journal: J Thromb Haemost Date: 2015-09-22 Impact factor: 5.824