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Tranexamic acid stops hyperfibrinolysis in dogs with hemorrhagic shock: a randomized, controlled clinical trial
Erin Long Mays1, Bernie Hansen1, Laura Culbreth1
11College of Veterinary Medicine, North Carolina State University, Raleigh, NC.
Objective:
To determine the effect of tranexamic acid (TXA) on clot hyperfibrinolysis (HF), defined as excessive clot lysis at 30 minutes (LY30%), with rapid thromboelastography (rTEG) or rTEG samples spiked with tissue plasminogen activator (tPA-stressed rTEG), in dogs with hemorrhagic shock.
Methods:
Prospective blinded clinical trial at 2 teaching hospitals, March 16, 2018, to May 20, 2022. Twenty-five dogs with hemorrhagic shock and HF were treated with standard care plus either TXA (20 mg/kg; TXA group) or saline (SAL group) over 20 minutes followed by an infusion of the same dose over 8 hours. Rapid TEG and tPA-stressed rTEG assays were performed immediately before study drug administration and at 8, 12, and 24 hours afterwards (T0, T8, T12, and T24, respectively).
Results:
4 dogs died or were euthanized before the end of the study period due to disease/injury severity. All survivors had normal rTEG LY30% values after T0; the value for 1 nonsurvivor increased at T8. The tPA-stressed LY30% normalized in all TXA (n = 14) and 8 of 11 SAL dogs at T8; TXA dogs had lower median tPA-stressed rTEG LY30% values at T8 and T12 than SAL dogs (P = .001 and .02, respectively). There was no treatment effect on blood product administration or survival, and no adverse effects were attributed to TXA administration.
Conclusions:
Resuscitation with or without TXA reduced HF identified by tPA-stressed rTEG. Hyperfibrinolysis was completely suppressed at the conclusion of the 8-hour TXA infusion.
Clinical Relevance:
Although TXA treatment stopped HF, there was no effect on survival or transfusion requirements.
