ABSTRACT
Objective The novel coronavirus disease 2019 (Covid-19) has infected millions worldwide and impacted the lives of many folds more. Many clinicians share new Covid-19-related resources, research, and ideas within the online Free Open Access to Medical Education (FOAM) community of practice. This study provides a detailed content and contributor analysis of Covid-19-related tweets among the FOAM community during the first months of the pandemic. Design, Setting, and Participants In this social media content analysis study, Twitter was searched from November 1, 2019, to March 21, 2020, for English tweets discussing Covid-19 in the FOAM community. Tweets were classified into one of 13 pre-specified content categories: original research, editorials, FOAM resource, public health, podcast or video, learned experience, refuting false information, policy discussion, emotional impact, blatantly false information, other Covid-19, and non-Covid-19. Further analysis of linked original research and FOAM resources was performed. One-thousand (1000) randomly selected contributor profiles and those deemed to have contributed false information were analyzed. Results The search yielded 8541 original tweets from 4104 contributors. The number of tweets in each content category were: 1557 other Covid-19 (18.2%), 1190 emotional impact (13.9%), 1122 FOAM resources (13.1%), 1111 policy discussion (13.0%), 928 advice (10.9%), 873 learned experience (10.2%), 424 non-Covid-19 (5.0%), 410 podcast or video (4.8%), 304 editorials (3.6%), 275 original research (3.2%), 245 public health (2.9%), 83 refuting false information (1.0%), and 19 blatantly false (0.2%). Conclusions Early in the Covid-19 pandemic, the FOAM community used Twitter to share Covid-19 learned experiences, online resources, crowd-sourced advice, and research and to discuss the emotional impact of Covid-19. Twitter also provided a forum for post-publication peer review of new research. Sharing blatantly false information within this community was infrequent. This study highlights several potential benefits from engaging with the FOAM community on Twitter.
ABSTRACT
OBJECTIVES: The majority of coronavirus disease 2019 mortality and morbidity is attributable to respiratory failure from severe acute respiratory syndrome coronavirus 2 infection. The pathogenesis underpinning coronavirus disease 2019-induced respiratory failure may be attributable to a dysregulated host immune response. Our objective was to investigate the pathophysiological relationship between proinflammatory cytokines and respiratory failure in severe coronavirus disease 2019. DESIGN: Multicenter prospective observational study. SETTING: ICU. PATIENTS: Critically ill patients with coronavirus disease 2019 and noncoronavirus disease 2019 critically ill patients with respiratory failure (ICU control group). INTERVENTIONS: Daily measurement of serum inflammatory cytokines. MEASUREMENTS AND MAIN RESULTS: Demographics, comorbidities, clinical, physiologic, and laboratory data were collected daily. Daily serum samples were drawn for measurements of interleukin-1ß, interleukin-6, interleukin-10, and tumor necrosis factor-α. Pulmonary outcomes were the ratio of Pao2/Fio2 and static lung compliance. Twenty-six patients with coronavirus disease 2019 and 22 ICU controls were enrolled. Of the patients with coronavirus disease 2019, 58% developed acute respiratory distress syndrome, 62% required mechanical ventilation, 12% underwent extracorporeal membrane oxygenation, and 23% died. A negative correlation between interleukin-6 and Pao2/Fio2 (rho, -0.531; p = 0.0052) and static lung compliance (rho, -0.579; p = 0.033) was found selectively in the coronavirus disease 2019 group. Diagnosis of acute respiratory distress syndrome was associated with significantly elevated serum interleukin-6 and interleukin-1ß on the day of diagnosis. CONCLUSIONS: The inverse relationship between serum interleukin-6 and Pao2/Fio2 and static lung compliance is specific to severe acute respiratory syndrome coronavirus 2 infection in critically ill patients with respiratory failure. Similar observations were not found with interleukin-ß or tumor necrosis factor-α.