Background: 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.
Methods: 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.
Results: 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.
Conclusion: 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.