A time course study of acute traumatic coagulopathy prior to resuscitation: from hypercoagulation to hypocoagulation caused by hypoperfusion?

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.