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Войти в исследования Trauma surgery & acute care open · 2025
Tranexamic acid as an adjunct to resuscitative endovascular balloon occlusion of the aorta does not worsen outcomes in a porcine model of hemorrhage.
СтатьяНазвание и аннотация: Перевод в очереди
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Neidert Leslie E, Morgan Clifford G, Lonowski Dominic, Castro Cecilia, Hemond Peter J, Lozano Valeria R, Tiller Michael M, Cardin Sylvain, Glaser Jacob J
Аннотация
BACKGROUND: Non-compressible torso hemorrhage (NCTH) represents a leading cause of preventable mortality in trauma. Resuscitative endovascular balloon occlusion of the aorta (REBOA) stabilizes NCTH but may predispose patients to thrombus generation. REBOA must therefore be prospectively evaluated for coagulation risks with concomitant usage of anti-fibrinolytic tranexamic acid (TXA). Using a porcine model of hemorrhage, it was hypothesized that TXA with REBOA would worsen coagulation outcomes and organ damage.
MATERIALS AND METHODS: Thirty-two male Yorkshire swine underwent 30% blood volume hemorrhage with randomization to vehicle control (VC; normal saline), VC+REBOA, TXA, or TXA+REBOA. At T0, animals received 10 mL/minute of group-specific infusion (GSI) followed at T10 by 500 mL of whole blood (WB), second GSI at 13 mL/hour, and Zone 1 REBOA inflation in REBOA groups. At T40, REBOA was deflated, with additional 500 mL WB, and continuation of GSI for 3 hours. Physiological, coagulation, and inflammatory parameters were measured throughout the protocol, with postmortem histopathology.
RESULTS: After REBOA deflation at T40, lactate was significantly higher for the REBOA groups versus the non-REBOA groups, and pH, bicarbonate, and base excess were all significantly lower than the non-REBOA groups. There were no significant differences observed between groups in coagulation, inflammatory, metabolic, or histopathologic parameters.
CONCLUSIONS: Administration of TXA with REBOA did not cause more deleterious coagulation outcomes. All significant changes were expected results of REBOA ischemia, and not attributable to TXA treatment. This suggests NCTH can safely be treated with both hemorrhage control methods without exacerbating clotting outcomes.
LEVEL OF EVIDENCE: Not applicable-basic animal research.
MATERIALS AND METHODS: Thirty-two male Yorkshire swine underwent 30% blood volume hemorrhage with randomization to vehicle control (VC; normal saline), VC+REBOA, TXA, or TXA+REBOA. At T0, animals received 10 mL/minute of group-specific infusion (GSI) followed at T10 by 500 mL of whole blood (WB), second GSI at 13 mL/hour, and Zone 1 REBOA inflation in REBOA groups. At T40, REBOA was deflated, with additional 500 mL WB, and continuation of GSI for 3 hours. Physiological, coagulation, and inflammatory parameters were measured throughout the protocol, with postmortem histopathology.
RESULTS: After REBOA deflation at T40, lactate was significantly higher for the REBOA groups versus the non-REBOA groups, and pH, bicarbonate, and base excess were all significantly lower than the non-REBOA groups. There were no significant differences observed between groups in coagulation, inflammatory, metabolic, or histopathologic parameters.
CONCLUSIONS: Administration of TXA with REBOA did not cause more deleterious coagulation outcomes. All significant changes were expected results of REBOA ischemia, and not attributable to TXA treatment. This suggests NCTH can safely be treated with both hemorrhage control methods without exacerbating clotting outcomes.
LEVEL OF EVIDENCE: Not applicable-basic animal research.