Tranexamic acid stops hyperfibrinolysis in dogs with hemorrhagic shock: a randomized, controlled clinical trial

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.