伴有和不伴有长骨骨折的创伤人群的急性呼吸窘迫综合征和急性肺损伤

Julia Larson, H. Robertson, S. Grey, S. Schobel, B. Potter, E. Elster
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摘要

引言:创伤是45岁以下人群死亡的主要原因。在最初的创伤中幸存下来的患者的康复往往会因损伤后遗症而变得复杂,这会增加感染和炎症的易感性。失控的炎症会发展成危及生命的器官衰竭,包括急性呼吸窘迫综合征(ARDS)。急性呼吸窘迫综合征病因中确定的生物标志物与骨折急性炎症和愈合阶段确定的生物标记物之间存在相似性。本研究调查了长骨骨折对急性呼吸窘迫综合征发展的影响,假设长骨骨折患者与无长骨骨折的患者相比,具有不同的生物标志物特征,并增加了肺损伤的发展。方法:这是对来自三个创伤中心的观察数据库中的患者进行的回顾性数据分析。匹配和分析患有和不患有长骨骨折的创伤患者是否存在急性呼吸窘迫综合征的已知生物标志物以及急性呼吸窘迫综合症的发展。结果:急性呼吸窘迫综合征的总体发展或住院结果没有差异,但长骨骨折患者在住院前10天的急性呼吸窘迫综合症风险比高2.35倍。长骨骨折患者的IL-6水平有统计学意义的增加(p=0.0007)。结构方程建模表明,IL-6受到长骨骨折和IL-8的积极影响。结论:长骨骨折的存在并没有导致急性呼吸窘迫综合征的总体发展或住院结果的差异,尽管发现在最初10天内急性呼吸窘迫综合症发展的风险比增加。需要进一步的研究来更好地描述创伤人群中不同细胞因子谱与急性呼吸窘迫综合征发展之间的关系。
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Acute respiratory distress syndrome and acute lung injury in a trauma population with and without long bone fractures
Introduction: Trauma is the leading cause of death in persons under the age of 45. Recovery in patients who survive initial trauma are frequently complicated by sequelae of injury that increases susceptibility to infection and inflammation. Uncontrolled inflammation can advance into life-threatening organ failure, including acute respiratory distress syndrome (ARDS). Similarities exist between biomarkers established in the etiology of acute respiratory distress syndrome and those identified in the acute inflammatory and healing phase of bone fractures. This study investigates the impact of long bone fractures on the development of acute respiratory distress syndrome where it is hypothesized that patients with long bone fractures would have different biomarker profiles and increased development of lung injury compared to patients without long bone fractures. Methods: This is a retrospective data analysis of patients from an observational data repository from three trauma centers. Trauma patients with and without long bone fractures were matched and analyzed for the presence of known biomarkers of acute respiratory distress syndrome and for the development of acute respiratory distress syndrome. Results: There were no differences in overall acute respiratory distress syndrome development or hospital outcomes, however long bone fracture patients had a 2.35-fold higher hazard ratio of acute respiratory distress syndrome in the first 10 hospital days. There was a statistically significant increase in the levels of IL-6 in patients with long bone fractures (p = .0007). Structural equations modeling demonstrated that IL-6 was positively influenced by long bone fractures and IL-8. Conclusion: The presence of long bone fractures did not result in differences in the overall development of acute respiratory distress syndrome or hospital outcomes, though was found to have an increased hazard ratio for acute respiratory distress syndrome development in the first 10 days. Further research is needed to better characterize the relationship between varying cytokine profiles and the development of acute respiratory distress syndrome in a trauma population.
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