Hemodilution is not critical in the pathogenesis of the acute coagulopathy of trauma

Abstract

Background: The acute coagulopathy of trauma is multifactorial, but generally believed to be aggravated by coexisting acidosis, hypothermia, and hemodilution. While acidosis and hypothermia have been extensively evaluated, there is a paucity of data on the independent role of hemodilution in this scenario. We therefore hypothesized that hemodilution will impair coagulation following experimental trauma and hemorrhagic shock.

Methods: Adult male Spraque-Dawley rats underwent trauma and hemorrhagic shock, followed by resuscitation with 2 × SBV using normal saline (NS). Thrombelastography (TEG) was performed before and after shock.

Results: In this trauma model, resuscitation resulted in a hemodilution of 50% (43% ± 4.05% versus 19.8% ± 3.96% Hct pre-shock versus post-shock , P < 0.0001). Despite the substantial hemodilution, there was no significant change in clot strength (12.96 ± 2.84 versus 11.79 ± 1.28 dynes/cm(2) G pre-shock versus post-shock, P = 0.13). Similarly, the onset of coagulation (R time) was not impaired (1.68 ± 1.74 s versus 1.75 ± 0.63 s R time pre-shock versus post-shock, P = 0.45).

Conclusion: In the absence of hypothermia and acidosis, hemodilution (≤ 50%) has a trivial effect on coagulation following trauma and hemorrhagic shock. These data call to question the commonly held belief that hemodilution per se is critical in the development of post-injury coagulopathy.

Figure 1. TEG diagram

The following TEG parameters were recorded from standard tracings: reaction time (R, minutes), coagulation time (K, minutes), angle (α, degrees), maximum amplitude (MA, mm), clot strength (G, dynes/cm²), and estimated percentage lysis (LY30, Lysis at 30 min,%).