Watts D D, Trask A, Soeken K, Perdue P, Dols S, Kaufmann C
Department of Trauma Services, Inova Regional Trauma Center, Falls Church, Virgina 22042-3300, USA.
J Trauma. 1998 May;44(5):846-54. doi: 10.1097/00005373-199805000-00017.
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 simultaneously contribute to coagulopathy, but are perhaps triggered at different levels of hypothermia. The purpose of this study was to determine whether, at clinically common levels of hypothermia (33.0-36.9 degrees C), there are specific temperature levels at which coagulopathic alterations are seen in each of these processes.
Of 232 consecutive adult trauma patients presenting to a Level I trauma center, 112 patients met the inclusion criteria of an Injury Severity Score of 9 or greater and time since injury of less than 2 hours. Of the included patients, 40 were normothermic and 72 were hypothermic (> or =37 degrees C, n = 40; 36.9-36 degrees C, n = 29; 35.9-35 degrees C, n = 20; 34.9-34 degrees C, n = 16; 33.9-33 degrees C, n = 7). Included patients were prospectively studied with thrombelastography adjusted to core body temperature. Additionally, PT, aPTT, platelets, CO2, hemoglobin, hematocrit, and Injury Severity Score were measured.
Analysis by multivariate analysis of variance of the relationship between coagulation and temperature demonstrated that in hypothermic trauma patients, 34 degrees C was the critical point at which enzyme activity slowed significantly (p < 0.0001), and at which significant alteration in platelet activity was seen (p < 0.001). Fibrinolysis was not significantly affected at any of the measured temperatures (p > 0.25).
Patients whose temperature was > or =34.0 degrees C actually demonstrated a significant hypercoagulability. Enzyme activity slowing and decreased platelet function individually contributed to hypothermic coagulopathy in patients with core temperatures below 34.0 degrees C. All the coagulation measures affected are part of the polymerization process of platelets and fibrin, and this process may be the mechanism by which the alteration in coagulation occurs.
关于低温创伤患者出现的凝血病，有多种理论认为其是由酶抑制、血小板改变或纤维蛋白溶解过程引起的，但尚无研究探讨这三种过程可能同时导致凝血病，且可能在不同低温水平下被触发的可能性。本研究的目的是确定在临床常见的低温水平（33.0 - 36.9摄氏度）下，是否存在特定温度水平，在这些温度下这些过程中的每一个都会出现凝血病性改变。
在一家一级创伤中心就诊的232例连续成年创伤患者中，112例患者符合损伤严重度评分9分或更高且受伤时间小于2小时的纳入标准。在纳入的患者中，40例体温正常，72例体温过低（体温≥37摄氏度，n = 40；36.9 - 36摄氏度，n = 29；35.9 - 35摄氏度，n = 20；34.9 - 34摄氏度，n = 16；33.9 - 33摄氏度，n = 7）。对纳入患者进行前瞻性研究，采用根据核心体温调整的血栓弹力图检查。此外，还测量了凝血酶原时间（PT）、活化部分凝血活酶时间（aPTT）、血小板、二氧化碳、血红蛋白、血细胞比容和损伤严重度评分。
通过对凝血与温度关系的多变量方差分析表明，在低温创伤患者中，34摄氏度是酶活性显著减慢（p < 0.0001）以及血小板活性出现显著改变（p < 0.001）的临界点。在任何测量温度下，纤维蛋白溶解均未受到显著影响（p > 0.25）。
体温≥34.0摄氏度的患者实际上表现出显著的高凝状态。酶活性减慢和血小板功能降低分别导致核心体温低于34.0摄氏度患者的低温凝血病。所有受影响的凝血指标都是血小板和纤维蛋白聚合过程的一部分，这个过程可能是凝血发生改变的机制。
