Darlington Daniel N, Kheirabadi Bijan S, Delgado Angel V, Scherer Michael R, Martini Wenjun Z, Dubick Michael A
Damage Control Resuscitation Program, US Army Institute of Surgical Research, Fort Sam Houston, Texas 78234-6315, USA.
J Trauma. 2011 Nov;71(5):1271-7. doi: 10.1097/TA.0b013e318214f522.
As part of our overall interest in the mechanisms and treatment related to the development of the lethal triad of hypothermia, acidosis, and coagulopathy seen in trauma patients, the purpose of this study was to determine whether acidosis, inducible either by HCl infusion or hemorrhage/hypoventilation, leads to coagulopathy, and if correction of the acidosis will alleviate this coagulopathy.
In two separate experiments, acidosis was induced in anesthetized swine by (1) HCl infusion (n = 10) or (2) hemorrhage/hypoventilation (n = 8). Arterial blood samples were taken before HCl infusion or hemorrhage (arterial pH 7.4), after HCl infusion or hemorrhage (pH 7.1), and after bicarbonate infusion to return pH to 7.4. Arterial pH and blood gases were measured every 15 minutes.
Acidosis (arterial pH 7.1) led to a hypocoagulation as measured by several coagulation parameters. In both experiments, acidosis was associated with a significant decrease in the maximum strength of the clot and the rate at which the clot formed. There was a significant decrease in endogenous thrombin potential and maximum thrombin concentration after acidosis in both groups (thrombin generation assay). However, the activated clotting time, prothrombin time, and activated partial thromboplastin time were significantly elevated only in the HCl-infused group. Fibrinogen concentration and platelet count were significantly reduced in both groups after acidosis. The hypocoagulation that was induced by either hemorrhage/hypoventilation or HCl infusion was not immediately corrected after returning pH to 7.4 with bicarbonate injection.
These data suggest that acidosis induced by HCl infusion or by hemorrhage/hypoventilation leads to hypocoagulation. Simple correction of the arterial pH with bicarbonate is not sufficient to correct this coagulopathy.
作为我们对创伤患者中出现的低体温、酸中毒和凝血功能障碍这一致死三联征的发生机制及治疗方法总体研究兴趣的一部分，本研究的目的是确定由盐酸输注或出血/通气不足诱导的酸中毒是否会导致凝血功能障碍，以及酸中毒的纠正是否会减轻这种凝血功能障碍。
在两项独立实验中，通过以下方式在麻醉猪中诱导酸中毒：（1）盐酸输注（n = 10）或（2）出血/通气不足（n = 8）。在盐酸输注或出血前（动脉pH 7.4）、盐酸输注或出血后（pH 7.1）以及输注碳酸氢盐使pH恢复至7.4后采集动脉血样本。每15分钟测量一次动脉pH和血气。
通过多个凝血参数测量，酸中毒（动脉pH 7.1）导致凝血功能低下。在两项实验中，酸中毒均与血凝块最大强度及血凝块形成速率的显著降低相关。两组在酸中毒后内源性凝血酶潜力和最大凝血酶浓度均显著降低（凝血酶生成测定）。然而，仅在盐酸输注组中活化凝血时间、凝血酶原时间和活化部分凝血活酶时间显著升高。酸中毒后两组纤维蛋白原浓度和血小板计数均显著降低。通过出血/通气不足或盐酸输注诱导的凝血功能低下在注射碳酸氢盐使pH恢复至7.4后并未立即得到纠正。
这些数据表明，由盐酸输注或出血/通气不足诱导的酸中毒会导致凝血功能低下。用碳酸氢盐单纯纠正动脉pH不足以纠正这种凝血功能障碍。
