目的: 探讨创伤出血性休克后急性呼吸窘迫综合征(acute respiratory distress syndrome，ARDS)的危险因素。方法: 回顾性研究2012年12月至2021年8月期间共314名创伤出血性休克患者，其中男性患者152名，女性患者162名，年龄中位数为63.00 (49.75~82.00)岁。记录患者住院期间的各项临床指标，根据入院7 d内是否发生ARDS将患者分为两组，即ARDS组(n=89)和非ARDS组(n=225)，通过判定差异寻找ARDS的危险因素，并建立预测是否出现ARDS的回归模型。结果: 创伤出血性休克后ARDS的发生率为28.34%，Logistic回归模型分析发现创伤出血性休克后ARDS的独立危险因素包括男性、冠状动脉粥样硬化性心脏病(简称冠心病)史、高急性生理与慢性健康评分Ⅱ(acute physiology and chronic health evaluation Ⅱ，APACHE Ⅱ)、受伤原因为车祸伤和肌钙蛋白Ⅰ升高，各独立危险因素的OR值及95%可信区间(confidence intervals，CI)分别为4.01(95%CI：1.75~9.20)、5.22(95%CI：1.29~21.08)、1.07(95%CI：1.02~1.57)、2.53(95%CI：1.21~5.28)和1.26(95%CI：1.02~1.57)，P值分别为0.001、0.020、0.009、0.014和0.034。预测创伤出血性休克后ARDS的受试者工作特征(receiver operating characteristic，ROC)曲线下面积(area under curve，AUC)分别为：男性0.59 (95%CI：0.51~0.68)、冠心病史0.55(95%CI：0.46~0.64)、APACHE Ⅱ评分0.65(95%CI：0.57~0.73)、受伤原因为车祸伤0.58(95%CI：0.50~0.67)、肌钙蛋白Ⅰ 0.73(95%CI：0.66~0.80)，总体预测值为0.81(95%CI：0.74~0.88)。结论: ARDS在创伤出血性休克患者中发生率较高，男性、冠心病史、高APACHE Ⅱ评分、受伤原因为车祸伤和肌钙蛋白Ⅰ升高是创伤出血性休克后ARDS的独立危险因素，及时监测这几项指标有利于早期识别和治疗创伤出血性休克后ARDS。

Objective: To investigate the risk factors of acute respiratory distress syndrome (ARDS) after traumatic hemorrhagic shock. Methods: This was a retrospective cohort study of 314 patients with traumatic hemorrhagic shock at Trauma Medicine Center, Peking University People's Hospital from December 2012 to August 2021, including 152 male patients and 162 female patients, with a median age of 63.00 (49.75-82.00) years. The demographic data, past medical history, injury assessment, vital signs, laboratory examination and other indicators of these patients during hospitalization were recorded. These patients were divided into two groups, ARDS group (n=89) and non-ARDS group (n=225) according to whether there was ARDS within 7 d of admission. Risk factors for ARDS were identified using Logistic regression. The C-statistic expressed as a percentage [area under curve (AUC) of the receiver operating characteristic (ROC) curve] was used to assess the discrimination of the model. Results: The incidence of ARDS after traumatic hemorrhagic shock was 28.34%. Finally, Logistic regression model showed that the independent risk factors of ARDS after traumatic hemorrhagic shock included male, history of coronary heart disease, high acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score, road traffic accident and elevated troponin Ⅰ. The OR and 95% confidence intervals (CI) were 4.01 (95%CI: 1.75-9.20), 5.22 (95%CI: 1.29-21.08), 1.07 (95%CI: 1.02-1.57), 2.53 (95%CI: 1.21-5.28), and 1.26 (95%CI: 1.02-1.57), respectively; the P values were 0.001, 0.020, 0.009, 0.014, and 0.034, respectively. The ROC curve was used to analyze the value of each risk factor in predicting ARDS. It was found that the AUC for predicting ARDS after traumatic hemorrhagic shock was 0.59 (95%CI: 0.51-0.68) for male, 0.55 (95%CI: 0.46-0.64) for history of coronary heart disease, 0.65 (95%CI: 0.57-0.73) for APACHE Ⅱ score, 0.58 (95%CI: 0.50-0.67) for road traffic accident, and 0.73 (95%CI: 0.66-0.80) for elevated troponin Ⅰ, with an overall predictive value of 0.81 (95%CI: 0.74-0.88). Conclusion: The incidence of ARDS in patients with traumatic hemorrhagic shock is high, and male, history of coronary heart disease, high APACHE Ⅱ score, road traffic accident and elevated troponin Ⅰ are independent risk factors for ARDS after traumatic hemorrhagic shock. Timely monitoring these indicators is conducive to early detection and treatment of ARDS after traumatic hemorrhagic shock.