Evaluating Casual and Inferential Association Across the Clinical Care Spectrum Between Extra-Cranial Injury and Suicidality After Moderate to Severe TBI

摘要 与轻度至重度TBI相关的先天性和损伤特异性异质性使其具有挑战性， 确定临床和治疗目标，在这些目标中，干预可以有意义地减少损伤的急性影响 并改善长期恢复轨迹。一个因素既导致了 与TBI损伤复合体和恢复相关的是多发性创伤的存在或不存在，沿着 创伤护理的复杂性需要管理与损伤相关的程序和出现的并发症。小 有关于多发伤后心理社会结果的数据，但现有报告表明结果更糟 与单纯创伤性脑损伤相比，我们之前的研究表明， 脑外损伤（ECI）会增加长期自杀倾向（SE）， 接受住院康复治疗的个人。这个项目的长期目标是提高效率 TBI和ECI患者的心理健康监测、资源获取和治疗效率 通过早期识别SE风险最大且最需要更密集随访的人- 向上服务。在实现这一目标的过程中，我们相信干预将改善健康，功能和生活质量。我们 长期假设是，确定急性到慢性护理恢复途径将允许个性化 筛查、分诊和治疗策略，以减少SE、增加生活角色参与和改善健康- TBI后的生活质量为了解决这些假设，我们建议1）描述人口统计学特征 (age/性别）、急性护理复杂性（并发症、手术、住院时间）和结局（SE、就业， 在TBI患者中，无/有ECI。2)确定人口统计学（性别、年龄）和心理社会学 （就业、药物滥用）影响TBI后ECI和SE之间关系的因素。第三章 确定急性护理复杂性因素是否可以解释ECI和心理社会因素之间的关系。 TBI后的结局和SE。拟议的研究利用了一个独特的大型TBI数据库， 国家创伤数据库（NTDB）和TBI-MS国家数据库的合并， 时间，一项关于急性创伤因素如何影响长期心理社会结果的全面调查 在TBI之后这个新颖的合并数据集已经允许ECI和自杀倾向的关联被 确定并提供动力，以进一步表征重要的因果和推理因素， SE.在项目结束时，我们将说明一个急性到慢性护理的因果关系路径， 相关的先天性、共同发生的急性护理复杂性和心理社会因素导致TBI后SE。工作 将为未来的监测、预防和治疗提供信息，为心理健康提供个性化的方法。 服务访问和TBI后的恢复。这些数据将支持未来研究个人生物学的工作， 与环境和心理社会因素的相互作用，与TBI后的抑郁和自杀病因。

ABSTRACT The innate and injury specific heterogeneity associated with mild to severe TBI has made it challenging to identify clinical and therapeutic targets where intervention can meaningfully reduce the acute effects of injury and improve the long term recovery trajectory. One factor that contributes both to the heterogeneity associated with the TBI injury complex and recovery is the presence or absence of polytrauma, along with the complexity of trauma care required to manage injury related procedures and complications that arise. Little data exists regarding psychosocial outcomes after polytrauma, but existing reports suggest worse outcomes for those with polytrauma recovering from TBI versus TBI alone. Our previous works show that severe extracerebral injury (ECI) increases the propensity for suicidal endorsement (SE) over the long term among individuals who receive inpatient rehabilitation. The long-term goal of this project is to improve effectiveness and efficiency of mental health monitoring, resource access, and treatment for individuals with TBI and ECI through early identification of those at greatest risk for SE and with the greatest need for more intensive follow- up services. In attaining this goal we believe intervention will improve health, function, and quality of life. Our long-term hypothesis is that identifying acute to chronic care recovery pathways will allow for personalized screening, triage, and treatment strategies to reduce SE, increase life role participation, and improve health- related life quality after TBI. To address these hypotheses, we propose 1) to characterize demographics (age/sex), acute care complexity (complications, procedures, length of stay), and outcomes (SE, employment, substance use) among those with TBI, without/with ECI. 2) Identify demographic (sex, age) and psychosocial (employment, substance abuse) factors that influence the relationship between ECI and SE after TBI. 3) determine whether acute care complexity factors explain relationships between ECI and psychosocial outcomes and SE after TBI. The proposed research utilizes a unique large TBI database derived from a merger of the National Trauma Data Bank (NTDB) and the TBI-MS National Database allowing, for the first time, a comprehensive investigation of how acute trauma factors can affect long-term psychosocial outcomes after TBI. This novel, merged dataset has already allowed the association of ECI and suicidality to be ascertained and provides the impetus to further characterize important causal and inferential factors that drive SE. At project conclusion, we will illustrate an acute to chronic care causal pathway by which ECI, and associated innate, co-occurring acute care complexity, and psychosocial factors lead to SE after TBI. The work will inform future monitoring, prevention, and treatments that provide a personalized approach to mental health service access, and recovery after TBI. These data will support future work examining personal biology, and its interaction with environmental and psychosocial factors, with depression and suicidality etiologies after TBI.