Gosselin Andrew R, Bargoud Christopher G, Sawalkar Abhishek, Mathew Shane, Toussaint Ashley, Greenen Matthew, Coyle Susette M, Macor Marie, Krishnan Anandi, Goswami Julie, Hanna Joseph S, Tutwiler Valerie
bioRxiv. 2024 Jan 19:2024.01.16.575945. doi: 10.1101/2024.01.16.575945.
Traumatic injury is a leading cause of death for those under the age of 45, with 40% occurring due to hemorrhage. Severe tissue injury and hypoperfusion lead to marked changes in coagulation, thereby preventing formation of a stable blood clot and increasing hemorrhage associated mortality.
We aimed to quantify changes in clot formation and mechanics occurring after traumatic injury and the relationship to coagulation kinetics, and fibrinolysis.
Plasma was isolated from injured patients upon arrival to the emergency department. Coagulation kinetics and mechanics of healthy donors and patient plasma were compared with rheological, turbidimetric and thrombin generation assays. ELISA's were performed to determine tissue plasminogen activator (tPA) and D-dimer concentration, as fibrinolytic markers.
Sixty-three patients were included in the study. The median injury severity score (ISS) was 17, median age was 37.5 years old, and mortality rate was 30%. Rheological, turbidimetric and thrombin generation assays indicated that trauma patients on average, and especially deceased patients, exhibited reduced clot stiffness, increased fibrinolysis and reduced thrombin generation compared to healthy donors. Fibrinogen concentration, clot stiffness, D-dimer and tPA all demonstrated significant direct correlation to increasing ISS. Machine learning algorithms identified and highlighted the importance of clinical factors on determining patient outcomes.
Viscoelastic and biochemical assays indicate significant contributors and predictors of mortality for improved patient treatment and therapeutic target detection.
Traumatic injury may lead to alterations in a patient's ability to form stable blood clotsA study was performed to assess how trauma severity affects coagulation kineticsKey alterations were observed in trauma patients, who exhibit weaker and slower forming clotsPaired with machine learning methods, the results indicate key aspects contributing to mortality.
创伤性损伤是45岁以下人群的主要死因，其中40%的死亡是由出血导致的。严重的组织损伤和低灌注会导致凝血发生显著变化，从而妨碍稳定血凝块的形成，并增加与出血相关的死亡率。
我们旨在量化创伤性损伤后血凝块形成和力学的变化，以及与凝血动力学和纤维蛋白溶解的关系。
在受伤患者抵达急诊科后分离血浆。通过流变学、比浊法和凝血酶生成试验比较健康供体和患者血浆的凝血动力学和力学。进行酶联免疫吸附测定以确定组织纤溶酶原激活物（tPA）和D-二聚体浓度，作为纤维蛋白溶解标志物。
63名患者纳入研究。损伤严重程度评分（ISS）中位数为17，年龄中位数为37.5岁，死亡率为30%。流变学、比浊法和凝血酶生成试验表明，与健康供体相比，创伤患者总体上，尤其是死亡患者，表现出血凝块硬度降低、纤维蛋白溶解增加和凝血酶生成减少。纤维蛋白原浓度、血凝块硬度、D-二聚体和tPA均与ISS升高呈显著正相关。机器学习算法识别并突出了临床因素在确定患者预后方面的重要性。
粘弹性和生化检测表明，这些因素对死亡率有显著影响，是改善患者治疗和检测治疗靶点的预测指标。
创伤性损伤可能导致患者形成稳定血凝块的能力发生改变进行了一项研究以评估创伤严重程度如何影响凝血动力学在创伤患者中观察到关键变化，他们表现出血凝块形成较弱且较慢结合机器学习方法，结果表明了导致死亡的关键因素。
