Ferraro F J, Spillert C R, Swan K G, Lazaro E J
Department of Surgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103.
Am Surg. 1992 Jun;58(6):355-7.
Injury severity score and hypothermia can lead to a high level of mortality when combined clinically. In acute trauma, the presence of a coagulopathy is difficult to treat and the aim is prevention. Aliquots of whole blood from healthy human volunteers (n = 9) were added to saline (control) and saline plus endotoxin (activated). The control and activated groups were divided and subjected to 60 minutes of normothermia (24 degrees C) or hypothermia (0 degrees C). The samples were returned to 37 degrees C; then the recalcification times were determined using fibrin formation and the viscous drag as the determining factors. The activated hypothermic group showed a decreased recalcification time of 345 (+/- 48.9) seconds compared to 405 (+/- 60.8) for the activated normothermic group (P less than 0.001). When the normothermic and hypothermic groups were compared without endotoxin added, the differences were not significant. The authors conclude that the effects of endotoxin on clotting time are worsened by hypothermia in vitro and act synergistically to possibly cause the coagulopathy seen in trauma patients.
损伤严重程度评分和体温过低在临床上合并出现时可导致高死亡率。在急性创伤中，凝血病难以治疗，目标是预防。将来自健康人类志愿者（n = 9）的全血等分试样添加到生理盐水（对照组）和生理盐水加内毒素（激活组）中。将对照组和激活组分开，使其经历60分钟的正常体温（24摄氏度）或低温（0摄氏度）。将样品恢复到37摄氏度；然后以纤维蛋白形成和粘性阻力作为决定因素来测定再钙化时间。激活的低温组的再钙化时间减少至345（±48.9）秒，而激活的正常体温组为405（±60.8）秒（P < 0.001）。当比较未添加内毒素的正常体温组和低温组时，差异不显著。作者得出结论，在体外，体温过低会加剧内毒素对凝血时间的影响，二者协同作用可能导致创伤患者出现凝血病。
