Trebuian Cosmin Iosif, Popa Daian, Buleu Florina, Sutoi Dumitru, Williams Carmen Gabriela, Crintea Iulia Najette, Chioibas Raul Daniel, Iancu Aida, Ciolac Livia, Mederle Ovidiu Alexandru
Department of Surgery I, "victor Babes" University of Medicine and Pharmacy, Timișoara, Romania.
Emergency County Hospital, Reșita, Romania.
Int J Gen Med. 2024 Jul 29;17:3337-3347. doi: 10.2147/IJGM.S464892. eCollection 2024.
Coronavirus disease-2019 (COVID-19)-related severe acute respiratory distress syndrome (ARDS) differs pathophysiological from other pulmonary septic shock-related ARDS. Thus, we assessed whether all-cause in-hospital mortality differs for severe COVID-19-related and classical severe ARDS and which inflammatory biomarkers can predict mortality among these patients.
This single-center, retrospective, observational cohort study included pulmonary septic shock patients (n = 114) with COVID-19-related and classical severe ARDS admitted in the Intensive Care Unit.
Patients with a mean age of 73 (IQR 62-82), predominantly male (63%), were divided into two groups based on outcomes: survivors (n = 50) and non-survivors (n = 64). COVID-19-related severe ARDS (n = 48) accounts for 75% of deaths. Present comorbidities like heart disease (p = 0.043), neurologic disorders (p = 0.018), and liver disease (p = 0.038) were associated with in-hospital mortality, as well. Regarding inflammatory biomarkers, the AUC/-statistic was 0.656 (95% CI: 0.53-0.759) for leukocytes, 0.613 (95% CI: 0.509-0.717) C-reactive protein (CRP) and 0.651 (95% CI: 0.548-0.753) for procalcitonin in predicting all-cause in-hospital mortality among patients with pulmonary septic shock and severe ARDS.
Patients with pulmonary septic shock and with COVID-19-related severe ARDS had a higher incidence of in-hospital mortality than those with classical severe ARDS. The high value of leukocytes, C-reactive protein, and procalcitonin were predictive for all-cause in-hospital mortality in patients with pulmonary septic shock and ARDS. Infection with COVID-19 was an independent predictor of in-hospital mortality in the presence of ARDS.
2019年冠状病毒病(COVID-19)相关的严重急性呼吸窘迫综合征(ARDS)在病理生理学上与其他肺部感染性休克相关的ARDS不同。因此,我们评估了COVID-19相关严重ARDS和经典严重ARDS的全因住院死亡率是否存在差异,以及哪些炎症生物标志物可以预测这些患者的死亡率。
这项单中心、回顾性、观察性队列研究纳入了入住重症监护病房的肺部感染性休克患者(n = 114),这些患者患有COVID-19相关和经典严重ARDS。
平均年龄为73岁(四分位间距62 - 82岁)、男性占主导(63%)的患者根据结局分为两组:幸存者(n = 50)和非幸存者(n = 64)。COVID-19相关严重ARDS(n = 48)占死亡人数的75%。当前的合并症如心脏病(p = 0.043)、神经系统疾病(p = 0.018)和肝脏疾病(p = 0.038)也与住院死亡率相关。关于炎症生物标志物,白细胞预测肺部感染性休克和严重ARDS患者全因住院死亡率的曲线下面积(AUC)/统计量为0.656(95%置信区间:0.53 - 0.759),C反应蛋白(CRP)为0.613(95%置信区间:0.509 - 0.717),降钙素原为0.651(95%置信区间:0.548 - 0.753)。
肺部感染性休克且患有COVID-19相关严重ARDS的患者住院死亡率高于经典严重ARDS患者。白细胞、C反应蛋白和降钙素原的高值可预测肺部感染性休克和ARDS患者的全因住院死亡率。COVID-19感染是存在ARDS时住院死亡率的独立预测因素。