Birmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK
Birmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
BMJ Open Respir Res. 2020 Nov;7(1). doi: 10.1136/bmjresp-2020-000731.
Acute respiratory distress syndrome (ARDS) is the major cause of mortality in patients with SARS-CoV-2 pneumonia. It appears that development of 'cytokine storm' in patients with SARS-CoV-2 pneumonia precipitates progression to ARDS. However, severity scores on admission do not predict severity or mortality in patients with SARS-CoV-2 pneumonia. Our objective was to determine whether patients with SARS-CoV-2 ARDS are clinically distinct, therefore requiring alternative management strategies, compared with other patients with ARDS. We report a single-centre retrospective study comparing the characteristics and outcomes of patients with ARDS with and without SARS-CoV-2.
Two intensive care unit (ICU) cohorts of patients at the Queen Elizabeth Hospital Birmingham were analysed: SARS-CoV-2 patients admitted between 11 March and 21 April 2020 and all patients with community-acquired pneumonia (CAP) from bacterial or viral infection who developed ARDS between 1 January 2017 and 1 November 2019. All data were routinely collected on the hospital's electronic patient records.
A greater proportion of SARS-CoV-2 patients were from an Asian ethnic group (p=0.002). SARS-CoV-2 patients had lower circulating leucocytes, neutrophils and monocytes (p<0.0001), but higher CRP (p=0.016) on ICU admission. SARS-CoV-2 patients required a longer duration of mechanical ventilation (p=0.01), but had lower vasopressor requirements (p=0.016).
The clinical syndromes and respiratory mechanics of SARS-CoV-2 and CAP-ARDS are broadly similar. However, SARS-CoV-2 patients initially have a lower requirement for vasopressor support, fewer circulating leukocytes and require prolonged ventilation support. Further studies are required to determine whether the dysregulated inflammation observed in SARS-CoV-2 ARDS may contribute to the increased duration of respiratory failure.
急性呼吸窘迫综合征（ARDS）是 SARS-CoV-2 肺炎患者死亡的主要原因。似乎 SARS-CoV-2 肺炎患者中“细胞因子风暴”的发展促使 ARDS 进展。然而，入院时的严重程度评分并不能预测 SARS-CoV-2 肺炎患者的严重程度或死亡率。我们的目的是确定 SARS-CoV-2 ARDS 患者是否在临床上与其他 ARDS 患者不同，因此需要采用不同的管理策略。我们报告了一项单中心回顾性研究，比较了 SARS-CoV-2 与非 SARS-CoV-2 ARDS 患者的特征和结局。
分析了伯明翰伊丽莎白女王医院的两个重症监护病房（ICU）队列的患者：2020 年 3 月 11 日至 4 月 21 日期间收治的 SARS-CoV-2 患者，以及 2017 年 1 月 1 日至 2019 年 11 月 1 日期间因细菌性或病毒性感染导致社区获得性肺炎（CAP）并发 ARDS 的所有患者。所有数据均常规收集于医院的电子病历系统。
SARS-CoV-2 患者中，亚洲裔患者比例较高（p=0.002）。SARS-CoV-2 患者入院时外周血白细胞、中性粒细胞和单核细胞计数较低（p<0.0001），C 反应蛋白（CRP）较高（p=0.016）。SARS-CoV-2 患者机械通气时间较长（p=0.01），但血管加压素需求较低（p=0.016）。
SARS-CoV-2 和 CAP-ARDS 的临床综合征和呼吸力学相似。然而，SARS-CoV-2 患者初始时血管加压素支持需求较低，外周血白细胞计数较低，需要长时间的通气支持。需要进一步的研究来确定 SARS-CoV-2 ARDS 中观察到的失调炎症是否会导致呼吸衰竭时间延长。
