Martini Wenjun Zhou
Hemostasis Program, US Army Institute of Surgical Research, Fort Sam Houston, Texas 78234, USA.
J Trauma. 2009 Jul;67(1):202-8; discussion 208-9. doi: 10.1097/TA.0b013e3181a602a7.
Although the lethal triad of hypothermia, acidosis, and coagulopathy has been recognized for a decade, the underlying mechanisms related to the development of coagulopathy are not fully understood. Consequently, current strategy in treating trauma patients with coagulopathy is limited to "staying out of the trouble" instead of "getting out of trouble." A better understanding of the underlying mechanisms will facilitate the search for effective therapeutic approaches when this lethal triad cannot be avoided.
Reviewing recent studies that explored alterations of thrombin generation and fibrinogen availability caused by hypothermia and acidosis.
Hypothermia and acidosis compromise thrombin-generation kinetics via different mechanisms. Hypothermia primarily inhibits the initiation phase, whereas acidosis severely inhibits the propagation phase of thrombin generation. Similarly, hypothermia and acidosis affect fibrinogen metabolism differently. Hypothermia inhibits fibrinogen synthesis, whereas acidosis accelerates fibrinogen degradation, leading to a potential deficit in fibrinogen availability. In addition, coagulation complications caused by acidosis cannot be immediately corrected by pH neutralization alone.
Hypothermia and acidosis impair thrombin generation and fibrinogen availability via different mechanisms. Current data indicate that pH correction alone cannot immediately correct acidosis-induced coagulation impairments. Future studies are warranted to test the effects of pH neutralization in conjunction with fibrinogen supplementation in normalizing acidosis-induced clotting complications.
尽管低体温、酸中毒和凝血功能障碍这一致死三联征已被认识十年，但与凝血功能障碍发生相关的潜在机制尚未完全明确。因此，目前治疗创伤性凝血功能障碍患者的策略仅限于“避免麻烦”而非“解决麻烦”。更好地理解潜在机制将有助于在无法避免这一致死三联征时寻找有效的治疗方法。
回顾近期探讨低体温和酸中毒引起的凝血酶生成及纤维蛋白原可用性改变的研究。
低体温和酸中毒通过不同机制损害凝血酶生成动力学。低体温主要抑制起始阶段，而酸中毒严重抑制凝血酶生成的传播阶段。同样，低体温和酸中毒对纤维蛋白原代谢的影响不同。低体温抑制纤维蛋白原合成，而酸中毒加速纤维蛋白原降解，导致纤维蛋白原可用性潜在不足。此外，仅通过pH中和不能立即纠正酸中毒引起的凝血并发症。
低体温和酸中毒通过不同机制损害凝血酶生成和纤维蛋白原可用性。目前数据表明，仅pH纠正不能立即纠正酸中毒引起的凝血功能障碍。未来有必要开展研究，测试pH中和联合补充纤维蛋白原对纠正酸中毒引起的凝血并发症的效果。
