Zhou Bo, Wang Gang, Peng Nanhai, He Xiandi, Guan Xiaoxiang, Liu Yun
Department of Nursing, Huangshan Vocational Technical College and Jinling Hospital, China.
Research Institute of General Surgery, Jinling Hospital, China.
Adv Clin Exp Med. 2015 Jul-Aug;24(4):571-8. doi: 10.17219/acem/29044.
Extensive preclinical evidence suggests that induced hypothermia can protect tissues from ischemia-reperfusion injury, reduce organ damage, and improve survival in the advanced stages of shock.
We assessed the effects of induced hypothermia on the hemodynamic parameters and coagulation capacity during hemorrhagic shock (HS) and fluid resuscitation, in a pig model of HS with multiple intestinal perforations.
Pigs (n=16) were randomized into 2 groups: a hypothermia (HT) group (n=8, 34°C) and a normothermia (NT) group (n=8, 38°C). Hypothermia to 34°C was induced with a cold blanket at the pre-hospital stage. Traumatic HS shock was induced using multiple intestinal perforations. Pulse indicator continuous cardiac output (PiCCO) was used to monitor hemodynamic changes. Coagulation capacity was measured using thromboelastography (TEG) at baseline as well as during resuscitation periods. Survival was documented for 72 h post-trauma.
Mortality in the hypothermic HS group was low, but there were no significant differences in mortality between the groups (mortality=2/8 HT vs. 5/8 NT, p=0.137). During hypothermia, the heart rate, extravascular lung water index (EVLWI), oxygen uptake index (VO2), and oxygen delivery index (DO2) in the HT group were significantly lower than those in the NT group. There were no significant differences between the 2 groups in the other hemodynamic indices or prothrombin time. Analyses of thromboelastometry at 34°C during hypothermia showed significant differences for reaction time (R) and alpha angle, but not for maximal amplitude (MA).
Rewarming reversed the coagulation changes induced by hypothermia. Induced mild hypothermia (34°C) in the pre-hospital stage affects hemodynamic parameters and the coagulation system but does not worsen outcomes in a pig HS model. The hypothermia-induced coagulation changes were reversed during rewarming without evidence of harmful effects. Our results suggest that pre-hospital induced hypothermia can be performed carefully following major trauma.
大量临床前证据表明,诱导性低温可保护组织免受缺血再灌注损伤,减少器官损害,并提高休克晚期的生存率。
在多肠穿孔出血性休克(HS)猪模型中,我们评估了诱导性低温对HS及液体复苏期间血流动力学参数和凝血能力的影响。
将猪(n = 16)随机分为2组:低温(HT)组(n = 8,34°C)和正常体温(NT)组(n = 8,38°C)。在院前阶段用冷毯诱导体温降至34°C。通过多肠穿孔诱导创伤性HS休克。使用脉搏指示连续心输出量(PiCCO)监测血流动力学变化。在基线以及复苏期间使用血栓弹力图(TEG)测量凝血能力。记录创伤后72小时的生存率。
低温HS组的死亡率较低,但两组之间的死亡率无显著差异(死亡率=2/8 HT对VS 5/8 NT,p = 0.137)。在低温期间,HT组的心率、血管外肺水指数(EVLWI)、氧摄取指数(VO2)和氧输送指数(DO2)显著低于NT组。两组在其他血流动力学指标或凝血酶原时间方面无显著差异。低温期间34°C时的血栓弹力测定分析显示反应时间(R)和α角有显著差异,但最大振幅(MA)无显著差异。
复温逆转了低温引起的凝血变化。院前阶段诱导轻度低温(34°C)会影响血流动力学参数和凝血系统,但不会使猪HS模型的预后恶化。复温期间低温诱导的凝血变化被逆转,且无有害影响的证据。我们的结果表明,在重大创伤后可谨慎进行院前诱导性低温治疗。