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Outcomes in mechanically ventilated patients with hypoxaemic respiratory failure caused by COVID-19

2020; Elsevier BV; Volume: 125; Issue: 6 Linguagem: Inglês

10.1016/j.bja.2020.08.047

1471-6771

Luigi Camporota, Barnaby Sanderson, Alison Dixon, Francesco Vasques, Andrew Jones, Manu Shankar‐Hari,

Pneumothorax, Barotrauma, Emphysema

Editor—Acute hypoxaemic respiratory failure (AHRF) is a key manifestation of acute coronavirus disease 2019 (COVID-19), caused by severe acute respiratory distress syndrome due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. COVID-19-related AHRF ranges from a mild self-limiting condition to severe progressive hypoxaemia requiring mechanical ventilation, with or without radiological evidence of bilateral consolidation and diffuse ground-glass lesions,1Shi H. Han X. Jiang N. et al.Radiological findings from 81 patients with COVID-19 pneumonia in Wuhan, China: a descriptive study.Lancet Infect Dis. 2020; 20: 425-434Abstract Full Text Full Text PDF PubMed Scopus (2437) Google Scholar fulfilling the Berlin acute respiratory distress syndrome (ARDS)2Ranieri V.M. Rubenfeld G.D. Thompson B.T. et al.Acute respiratory distress syndrome: the Berlin definition.JAMA. 2012; 307: 2526-2533Crossref PubMed Scopus (7009) Google Scholar criteria. The severity of hypoxaemia in COVID-19 is often disproportionate to the reduction in lung volumes,3Gattinoni L. Coppola S. Cressoni M. Busana M. Rossi S. Chiumello D. COVID-19 does not lead to a "typicalˮ acute respiratory distress syndrome.Am J Respir Crit Care Med. 2020; 201: 1299-1300Crossref PubMed Scopus (902) Google Scholar which may be a consequence of the effects of SARS-CoV-2 on pulmonary vascular tone, inflammation, and thrombosis.4Ackermann M. Verleden S.E. Kuehnel M. et al.Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19.N Engl J Med. 2020; 388: 120-128Crossref Scopus (3475) Google Scholar, 5Helms J. Tacquard C. Severac F. et al.High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study.Intensive Care Med. 2020; 46: 1089-1098Crossref PubMed Scopus (1831) Google Scholar, 6McGonagle D. O'Donnell J.S. Sharif K. Emery P. Bridgewood C. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia.Lancet Rheumatol. 2020; 2: e460-461Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar The aim of this study was to compare respiratory parameters and outcomes for COVID-19 patients with ARDS from other causes of similar severity of hypoxaemia using aggregate data from the LUNG-SAFE (Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure) study.7Bellani G. Laffey J.G. Pham T. et al.Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries.JAMA. 2016; 315: 788-800Crossref PubMed Scopus (2869) Google Scholar We present the clinical characteristics, lung mechanics, gas exchange, and outcomes of a cohort of critically ill COVID-19 patients with AHRF receiving invasive mechanical ventilation with partial pressure of oxygen/inspired oxygen concentration ratio (Pao2/Fio2 ratio) <300 mm Hg during their first critical care admission in a format similar to that of the LUNG-SAFE study.7Bellani G. Laffey J.G. Pham T. et al.Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries.JAMA. 2016; 315: 788-800Crossref PubMed Scopus (2869) Google Scholar We grouped (COVID-19 vs LUNG-SAFE) patients based on the severity of oxygenation alone based on the Berlin definition of ARDS.2Ranieri V.M. Rubenfeld G.D. Thompson B.T. et al.Acute respiratory distress syndrome: the Berlin definition.JAMA. 2012; 307: 2526-2533Crossref PubMed Scopus (7009) Google Scholar Chest radiogram characteristics were not considered in the inclusion criteria. The study was a single-centre, retrospective, observational cohort study of adult patients admitted with confirmed COVID-19 AHRF to the Critical Care Department at Guy's and St Thomas' Hospital (GSTT) in London, UK, between March 3 and May 22, 2020. The study had institutional approval and with waiver of individual informed consent (reference number 10796). Baseline patient data, clinical characteristics, lung mechanics, gas exchange, and outcomes were obtained from clinical information systems (CareVue Rev.F.01, Philips, Eindhoven, The Netherlands; and other electronic patient records) using Microsoft SQL Server Management Studio v18.4 (Microsoft, Redmond, WA, USA). Actual or temperature-corrected partial pressure of carbon dioxide (Paco2), Pao2, and pH were merged with contemporaneous ventilation parameters and measurements. We used the worst Pao2/Fio2 ratio on critical care admission day to categorise hypoxaemia into mild (Pao2/Fio2 ratio 200–300 mm Hg), moderate (Pao2/Fio2 ratio 100–200 mm Hg) and severe (Pao2/Fio2 ratio ≤100 mm Hg) as per the Berlin ARDS definition.2Ranieri V.M. Rubenfeld G.D. Thompson B.T. et al.Acute respiratory distress syndrome: the Berlin definition.JAMA. 2012; 307: 2526-2533Crossref PubMed Scopus (7009) Google Scholar There were no missing data. All analyses were conducted in R version 3.6.1 (http://www.R-project.org). Amongst the 317 critical care admissions over the study period attributable to COVID-19, 213 patients met our inclusion criteria of AHRF receiving invasive mandatory mechanical ventilation with Pao2/Fio2 ratio <300 mm Hg, during their first critical care admission. We excluded patients receiving noninvasive respiratory support (n=48) or extracorporeal membrane oxygenation (ECMO; n=51), or readmissions (n=9). The mean (95% confidence interval [CI]) age of the cohort was 56 (54–57) yr, 72.8% (n=155) were male, 40.4% (n=86) had hypertension, and 33.8% (n=72) had diabetes mellitus as comorbidities. There were 23 (10.8%) patients with mild, 122 (57.3%) with moderate, and 68 (31.9%) with severe ARDS, based on Pao2/Fio2 ratio categories. Mean tidal volumes were ∼7 ml kg−1 of predicted body weight (PBW) for all three severity categories, with similar total minute ventilation. Mean PEEP was 10 (95% CI, 9.6–10.4) cm H2O, which increased from 8 (95% CI, 7.4–9.1) cm H2O in mild disease to 11 (95% CI, 10.5–11.9) cm H2O in severe disease. Values of peak inspiratory pressure and driving pressure increased with disease severity, with peak inspiratory pressures of 21 (95% CI, 19.4–22.6) cm H2O in mild, 24 (95% CI, 23.6–25.1) cm H2O in moderate, and 28 (95% CI, 26.4–28.7) cm H2O in severe disease. Delta pressure was 13 (95% CI, 11.3–14.4) cm H2O in mild, 14.7 (95% CI, 14.2–15.3) cm H2O in moderate, and 15.4 (95% CI, 14.6–16.3) cm H2O in severe disease. The majority of patients in all categories of severity had a peak airway pressure <30 cm H2O and received tidal volumes 40 ml cm H2O−1 (Fig. 1b). Overall, the mean (95% CI) duration of mechanical ventilation was 15 (13.5–16.5) days, with longer duration of mechanical ventilation associated with more severe disease (Fig. 1c). The critical care length of stay was longer in the moderate and severe categories compared with the mild category, but similar in the moderate and severe categories owing to higher and earlier mortality in the severe category. ICU mortality was 9% in mild disease, 27.5% in moderate disease, and 55.7% in severe disease, with significant differences among the three severity categories (P<0.01 log-rank; Fig. 1d). Overall ICU mortality of 34.2% in our cohort was similar to the overall mortality reported in the LUNG-SAFE (35.3%)7Bellani G. Laffey J.G. Pham T. et al.Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries.JAMA. 2016; 315: 788-800Crossref PubMed Scopus (2869) Google Scholar cohort and in the COVID-19 cohort receiving mechanical ventilation (35%).8Auld S.C. Caridi-Scheible M. Blum J.M. et al.ICU and ventilator mortality among critically ill adults with coronavirus disease 2019.Crit Care Med. 2020; 48: e799-804Crossref PubMed Scopus (26) Google Scholar Similar to the LUNG-SAFE cohort and the Berlin ARDS predictive validity analyses, there was a dose–response relationship between mortality and severity of hypoxaemia, albeit with lower mortality in the mild category. These results illustrate that although the characteristics of the COVID-19 AHRF population largely overlap with the LUNG-SAFE cohort, the COVID-19 cohort had a greater predominance of moderate (57% vs 47%) and severe (31% vs 23%), and a lower proportion of patients with mild hypoxaemia (10.8% vs 30%) compared with the LUNG-SAFE cohort.7Bellani G. Laffey J.G. Pham T. et al.Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries.JAMA. 2016; 315: 788-800Crossref PubMed Scopus (2869) Google Scholar Despite the greater severity of hypoxaemia compared with LUNG-SAFE, a greater proportion of patients with COVID-19 were ventilated within protective boundaries. In conclusion, despite initial data showing high mortality in mechanically ventilated COVID-19 patients, our data show that with comparable degrees of hypoxaemia and lung mechanics to ARDS from other causes, the mortality is similar to ARDS as survival is high in mild disease. More detailed characterisations of patient phenotypes may help us understand the factors associated with severity of hypoxaemia and lung parenchymal involvement. The authors declare that they have no conflict of interests. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research, or the Department of Health and Social Care.