Campbell James Eric, Aden James Keith, Cap Andrew Peter
From the Joint Inflammation Modulation of Trauma Program (J.E.C.), Tri-Services Research Laboratories; and Coagulation and Blood Research Program (J.K.A., A.P.C.), US Army Institute of Surgical Research, Fort Sam Houston, San Antonio, Texas.
J Trauma Acute Care Surg. 2015 May;78(5):955-61. doi: 10.1097/TA.0000000000000586.
Thrombelastography (TEG) is suggested as an optimal instrument for the identification of acute traumatic coagulopathy-induced alterations in coagulation status. Patient whole blood (WB) used in TEG analysis is generally collected from a large blood vessel containing representative systemic blood, often close to 40% hematocrit (Hct). Trauma patients often exhibit bleeding from the microvasculature. This study examines early coagulation function changes at the simulated microvascular level based on altered Hct and pH in vitro through TEG analyses of normal donor blood.
Anticoagulated normophysiologic fresh human blood was centrifuged. Individual component effects on coagulation were investigated through variable recombination groups: platelet-rich plasma (PRP), platelet-poor plasma (PPP), and red blood cells (RBCs), which were compared with WB. Acute traumatic coagulopathy-induced acidic microvascular environment was simulated and investigated using tissue factor-activated TEG analysis of variable Hct (40%, 30%, 20%, and 0%) samples and variable [H]. Incremental replacement of RBC with either PPP or normal saline (NS) simulated resuscitation in vitro was also conducted under similar conditions.
Only acidified PRP reflected loss of clot strength. Acidified PRP and PPP were delayed equally in clot time. In all groups, inclusion of RBCs normalized clot time. RBC replacement with PPP significantly delayed clot time when samples were acid-challenged, signifying greater acid effect in low Hct microvascular beds. NS simulated resuscitation incurred even greater clotting delays.
Acidemia-induced coagulopathy at the level of the capillary Hct (1) is more severe than at higher Hct levels (larger blood vessels), (2) shows that simulated resuscitation with NS causes greater increases in clot time and decreases in clot strength beyond that which occurs with plasma replacement, and (3) may not accurately be portrayed through common TEG practice of testing systemic WB of greater than 30% Hct.
血栓弹力图（TEG）被认为是识别急性创伤性凝血病引起的凝血状态改变的最佳工具。TEG分析中使用的患者全血（WB）通常从含有代表性全身血液的大血管采集，血细胞比容（Hct）通常接近40%。创伤患者常表现为微血管出血。本研究通过对正常献血者血液进行TEG分析，在体外基于改变的Hct和pH值，研究模拟微血管水平的早期凝血功能变化。
将抗凝的正常生理状态的新鲜人血离心。通过可变重组组研究各成分对凝血的影响：富血小板血浆（PRP）、贫血小板血浆（PPP）和红细胞（RBC），并与全血进行比较。使用组织因子激活的TEG分析可变Hct（40%、30%、20%和0%）样本和可变[H]，模拟并研究急性创伤性凝血病诱导的酸性微血管环境。在相似条件下，还进行了用PPP或生理盐水（NS）逐步替代RBC的体外模拟复苏。
只有酸化的PRP反映出凝块强度的丧失。酸化的PRP和PPP在凝血时间上延迟程度相同。在所有组中，加入RBC可使凝血时间正常化。当样本受到酸挑战时，用PPP替代RBC显著延迟凝血时间，表明在低Hct微血管床中酸效应更大。NS模拟复苏导致的凝血延迟甚至更大。
毛细血管Hct水平的酸血症诱导的凝血病（1）比更高Hct水平（较大血管）更严重，（2）表明用NS模拟复苏导致的凝血时间增加和凝块强度降低比血浆替代更明显，（3）通过检测Hct大于30%的全身WB的常规TEG操作可能无法准确描述。
