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Background: Gas exchange abnormalities in COVID-19 survivors might involve impairment of the transfer through alveolar-capillary membrane and/or loss of capillary bed. Membrane diffusing capacity (Dm) and capillary volume (Vc) can be calculated from combined DLCO-DLNO. Aim(s): To investigate the values of Dm and Vc after COVID-19. Method(s): We retrospectively included all the patients (Pts) having performed DLCO-DLNO after COVID-19 in 4 French centres between 2020/04/20 and 2021/12/16. We excluded Pts with known history of COPD, severe asthma, interstitial lung disease, pulmonary hypertension, and congestive heart failure. We collected data from clinical records, pulmonary function test (PFT), and CT-scan when performed +/-1.5 months from PFT. Result(s): Data from 132 Pts have been analysed yet (over a total of about 500): 72 men (55%), mean age 57.7+/-13 years, mean BMI 30+/-5.7. 25 Pts (19%) were grade 1-4 on COVID-19 WHO scale (no oxygen), 45 (34%) were grade 5 (oxygen), 44 (33%) were grade 6 (NIV or high-flow oxygen), and 18 (14%) were grade 7-9 (mechanical ventilation). Median time between COVID-19 and PFT was 4.4 months [3.1-6.1]. 58 Pts (44%) had DLCO < lower limit of normal (LLN), with a significant correlation between initial COVID-19 severity and later DLCO. Mean Dm and Vc were 48.7% +/-15.1 and 80.2% +/-21. The most frequent pattern was Dm < LLN and normal Vc, in 78 Pts (59%). Only 1 (1%) had isolated Vc < LLN with normal Dm. Among the 37 (28%) with both Dm and Vc < LLN, 36 performed a CT-scan that showed fibrosing sequellae in 26 (72%). Conclusion(s): Dm was the most decreased variable, suggesting delayed healing after COVID-19. Decreased Vc was frequently associated with pulmonary fibrosis.
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Declaration de liens d'interets: Les auteurs declarent ne pas avoir de liens d'interets. Copyright © 2022
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Introduction La COVID-19 peut être responsable d’une pneumonie sévère pouvant entraîner une fibrose séquellaire, mais présente également un tropisme vasculaire. L’objectif principal de cette étude était de décrire les parts respectives d’altération du facteur membranaire (Dm) et du volume capillaire pulmonaire (Vc) dans les suites d’une COVID-19, à l’aide de la technique de double diffusion DLCO-DLNO. Méthodes Étude rétrospective observationnelle monocentrique. Tous les patients majeurs ayant réalisé une EFR avec double diffusion dans le cadre d’une réévaluation post-COVID au CHU Avicenne entre le 20/04/2020 et le 24/08/2021 étaient éligibles. Ont été exclus les patients avec BPCO, PID, HTAP préexistante. Les données cliniques ont été recueillies, la première EFR de réévaluation et la TDM thoracique si réalisée à±1 mois des EFR. Résultats Au total, 41 hommes et 29 femmes ont été inclus (59 %/41 %), d’âge moyen 58,2 ans±13,3 et d’IMC 30,1±6,5 (Tableau 1). Ils ont été divisés en 3 groupes selon la sévérité de l’épisode initial : COVID-19 ambulatoire (groupe 1 ;n=18), hospitalisation en salle (groupe 2 ;n=24), hospitalisation en soins intensifs (groupe 3 ;n=28). L’EFR a été réalisée en moyenne 5,2 mois±2,9 après la COVID-19. La fonction était significativement plus altérée au sein du groupe 3 : 14 patients (20 %) présentaient un trouble ventilatoire restrictif, dont 12 appartenaient au groupe 3 ;26 patients (37 %) avaient une DLCO<limite inférieure de la normale, dont 22 appartenaient au groupe 3. Sur l’ensemble de la cohorte, les Dm et VC moyens étaient : 45,4 %±13,9 et 80,2 %±23 (Tableau 1). Le profil le plus fréquent était une altération isolée du Dm (38 patients ;54 %). Aucune altération isolée du Vc n’a été observée. Parmi 22 patients avec diminution des 2 variables, 20 avaient réalisé une TDM : 12 présentaient des signes de fibrose d’étendue>5 % avec bronchectasies par traction, 4 des réticulations sous-pleurales et 4 du verre dépoli. Conclusion Le Dm était la variable fonctionnelle la plus altérée. Elle peut être diminuée malgré une DLCO normale. Ce profil évoque préférentiellement un mécanisme de cicatrisation longue, y compris pour des COVID-19 initialement peu sévères. L’altération du Vc était fréquemment associée à une fibrose séquellaire. Cette étude va se poursuivre en incluant des patients supplémentaires, afin de décrire l’évolution longitudinale chez les patients ayant réalisé plusieurs mesures, et d’étudier les corrélations avec les autres variables fonctionnelles et avec les images de la TDM thoracique.
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Introduction: COVID-19 is a respiratory disease with clinical manifestation, severity, and outcomes heterogeneity, from asymptomatic presentation to an acute hypoxemic respiratory failure. Clinical characteristics and comorbidities may affect susceptibility to a more severe COVID-19. We hypothesize that obstructive sleep apnea (OSA) may be a significant factor that mitigates COVID-19 severity. Methods: A prospective multicentric cohort "Co-survivors" with a sample size of 400 patients was set and started recruiting in June 2020. Patients with a respiratory presentation of COVID-19 were selected. All severities of COVID-19 were allowed from outpatients to patients requiring prolonged invasive mechanical ventilation. At 3-months follow-up, patients underwent a cardio-respiratory clinical investigation. Initial and actual clinical manifestations and comorbidities were collected. All patients underwent a full polysomnography (PSG) or respiratory polygraphy (PG). Results: At the time of the analysis, 121 patients were included in the cohort. OSA was diagnosed before COVID-19 and already treated in 10 patients, and 23 were waiting for investigation. Full PSG was performed in 88 patients (80 PSG and 8 PG). OSA was absent in 15 (17%) patients, while mild, moderate, and severe OSA was present in 30 (34.1%), 21 (23.9%) and 22 (25%), respectively. Outpatient COVID-19 was reported in 30 (34.1%), hospitalization was needed without and with acute respiratory failure in 13 (14%) and 45 (51%) patients, respectivelly. These later were predominantly male and older, did not exhibit more comorbidity but metabolic characteristics with significant higher body mass index and waist circumference. Sleep recordings revealed an AHI of 7.4 [1.7;15.4], 15.7 [8.3;48.9] and 21.9 [14;35.1] p<0.01 in these three classes of COVID-19 severity, respectively. Finally, undiagnosed OSA was a factor of COVID-19 severity. Conclusions: Patients with OSA are highly represented in a population of COVID-19 survivors. About 10% of the patients were diagnosed prior to infection, undiagnosed moderate or severe OSA was diagnosed in 48.9% of the remaining patents. Moreover, OSA is likely to be a factor of acute respiratory failure in patients infected with SARS-CoV-2.
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Context: An in silico modelling suggested that SARS-CoV-2 might bind to haemoglobin (Hb). The authors hypothesised that this phenomenon could lead to a decreased oxygen (02) binding and also haemolytic anemia (Liu & Li, ChemRxiv 2020). Although they were not supported by any experimental validation such as in vitro biochemical interaction, or any clinical observation, these conclusions were largely relayed in the media and social networks. The aim of this study was to investigate if Hb affinity for 02 was altered in the course of Covid-19. Methods: In this retrospective, observational, single-center study, we compared the blood gas analyses of 100 Covid-19 patients (from March-April 2020) to those of 100 non Covid-19 patients (from March-April 2019). We also included in a third group 55 patients with carboxyhaemoglobin (HbCO) > 8% (positive controls with altered Hb affinity). P50 was corrected for body temperature, pH and PC02. Results: Patients were not statistically different for age or sex ratio in the Covid-19 and non Covid-19 groups. Median P50 at baseline was 26 [25.2-26.8] versus 25.9 [24-27.3], respectively (p=0.42). As expected, it was lower in the high HbCO group: 22.5 [21.6-23.8] (p<0.0001). When considering the time course of P50, no significant difference was observed between Covid-19 and non Covid-19 groups, from day 1 to day 18. Median Hb concentration at beselinewas 14 g.dl'1 [12.6-15.2] in the Covid-19 group versus 13.2 [11.4-14.7] in the non Covid-19 group (p=0.006). On the 24 Covid-19 patients displaying anemia, none of them exhibited obvious biological haemolysis. Conclusion: There was no biological argument to support the hypothesis that SARS-CoV-2 could alter 02 binding to Hb.