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Devil is in the airspace: compartmentalisation of inflammation during COVID ARDS
  1. C M Shaver
  1. Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  1. Correspondence to Dr C M Shaver, Vanderbilt University Medical Center, Nashville, Tennessee, USA; ciara.shaver{at}

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Acute respiratory distress syndrome (ARDS) continues to have substantial mortality despite decades of trials of different treatment approaches.1 During the COVID-19 pandemic, there was an unprecedented volume of critically ill patients with ARDS caused by the same virus. While devastating, COVID-19 provided an opportunity to study a more homogeneous group of patients with ARDS and yielded the discovery of several therapeutics, such as dexamethasone,2 Janus kinase (JAK) inhibitors3 and interleukin-6 (IL-6) pathway inhibitors4 5 that improved mortality. These discoveries were somewhat unexpected given the relatively modest systemic inflammation seen with COVID-19 compared with other ARDS cohorts.2 One possible explanation for successful immunomodulation in patients with COVID-19 could be that the degree of inflammation in the plasma may not accurately reflect the burden of inflammation in the airspace. This compartmentalisation between the airspace and circulation has been historically challenging to study given the lack of routine bronchoalveolar lavage (BAL) sampling during ARDS.

In their Thorax paper, de Brabander et al overcome this lack of airspace sampling by employing a protocol to perform BAL of COVID ARDS patients requiring extended mechanical ventilation.6 Patients with COVID-19 requiring mechanical ventilation underwent bronchoscopy after 7 days and then weekly thereafter if not clinically improving. This unique study approach, with simultaneous plasma sampling is a treasure trove for discovery of the relative impact of alveolar versus systemic biomarkers and …

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  • Twitter @C_ShaverMD

  • Contributors CMS generated the article content.

  • Funding This work was supported by NIH HL160551.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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