Recent data have associated improved survival after hemorrhagic shock with the early use of plasma-based resuscitation. Our laboratory has shown that FFP5 has decreased hemostatic potential compared with freshly thawed plasma (FFP0). We hypothesized that FFP5 would increase bleeding and mortality compared with FFP0 in a rodent bioassay model of uncontrolled liver hemorrhage.
Hemostatic potential of plasma was assessed with the Calibrated Automated Thrombogram (CAT) assay. Rats underwent isovolemic hemodilution by 15% of blood volume with the two human plasma groups (FFP0 and FFP5) and two controls (sham and lactated Ringers). A liver injury was created by excising a portion of liver resulting in uncontrolled hemorrhage. Rats that lived for 30 minutes after liver injury were resuscitated to their baseline blood pressure and followed for 6 hours. Hemostasis was assessed by thromboelastography.
Hemostatic potential of FFP5 decreased significantly in all areas measured in the CAT assay as compared with FFP0 (p < 0.01). In the FFP5 group, overall survival was 54%, compared with 100% in the FFP0 and sham group (p = 0.03). For animals that survived 30 minutes and were resuscitated, there was no difference in bleeding and/or coagulopathy between groups. Irrespective of treatment, animals that died after resuscitation demonstrated increased intraperitoneal fluid volume (14.85 mL ± 1.9 mL vs. 7.02 mL ± 0.3 mL, p < 0.001).
In this model of mild preinjury hemodilution with plasma, rats that received FFP5 had decreased survival after uncontrolled hemorrhage from hepatic injury. There were no differences in coagulation function or intraperitoneal fluid volume between the two plasma groups.
From the Center for Translational Injury Research (P.A.L., M.M., S.P., C.E.W., J.B.H.), University of Texas Health Science Center, Houston, Texas; and Department of Surgery (P.A.L., K.S., W.W., Y.W., N.M., S.P., C.E.W., J.B.H.), University of Texas Medical School at Houston, Houston, Texas.
Submitted for publication January 14, 2011.
Accepted for publication August 12, 2011.
Supported by NIH Grant T32 GM 0879201, the Texas Emerging Technology Fund, the Memorial Hermann Hospital Fund.
Presented at the 41st Annual Meeting of the Western Trauma Association, February 27–March 5, 2010, Big Sky, Montana.
Address for reprints: John B. Holcomb, MD, Center for Translational Injury Research, 6410 Fannin St., UTPB 11.23, Houston, TX 77007; email: John.Holcomb@uth.tmc.edu.