Hypothermic coagulopathy in trauma: Effect of varying levels of hypothermia on enzyme speed, platelet function and fibrinolytic activity

Abstract

Purpose. The coagulopathy noted in hypothermic trauma patients has been variously theorized to be caused by either enzyme inhibition, platelet alteration, or fibrinolytic processes, but no study has examined the possibility that all three processes may work in conjunction. The purpose of this study was to determine the interrelationship of these three mechanisms as the causes of coagulopathy in adult trauma patients at varying levels of clinically common hypothermia (33.0 degrees C-36.9 degrees C). Methods. Of 232 consecutive adult trauma patients presenting to a Level I Trauma Center, n = 112 met the inclusion criteria of an Injury Severity Score of 9 or greater and time since injury of less than 2 hours. Patients with frank DIC at presentation were excluded. Of the included patients, 40 were normothermic and 72 were hypothermic (>=37 degrees C, n = 40, 36 superscript 9-36 degrees C, n = 29; 35 superscript 9-35 degrees C, n = 20; 34 superscript 9-34 degrees C, n = 16; 33 superscript 9-33 degrees C, n = 7). Included patients were prospectively studied with thrombelastography adjusted to core body temperature. Thrombelastography measures the shear elasticity of blood and is sensitive to interacting cellular and plasmatic components. Six parameters of blood clotting were analyzed (two each for enzyme speed, platelet activity, and fibrinolysis), and an overall index of coagulation was calculated. Additionally, PT, aPTT, platelets, CO2, hemoglobin, hematocrit, and ISS were measured. Results. Analysis by MANOVA of the relationship between coagulation and temperature demonstrated that in hypothermic trauma patients, 34 degrees C was the critical point where enzyme activity slowed significantly (p<.0001), and significant alteration in platelet activity was seen (p<.001). Fibrinolysis was not signifcantly different at an of the measured temperatures (p>.25). The coagulation index was also significantly lower for the patients with temperatures below 34 degrees C (p<.001). Conclusions. Enzyme activity slowing and decreased platelet function individually contribute to hypothermic coagulopathy in trauma patients, particularly below 34.0 degrees C. All three coagulation measure affected are part of the polymerization process of platelets and fibrin, and this may be the mechanism by which the alteration in coagulation occurs.