Skip to main content
ERJ Open logoLink to ERJ Open
letter
. 2023 Feb 9;61(2):2202287. doi: 10.1183/13993003.02287-2022

Reply: Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery

Piotr Harbut 1, G Kim Prisk 2, Robert Lindwall 1, Sarah Hamzei 1, Jenny Palmgren 1, Catherine E Farrow 3,4,5, Goran Hedenstierna 6,, Terence C Amis 3,4,5, Atul Malhotra 2, Peter D Wagner 2, Kristina Kairaitis 3,4,5,
PMCID: PMC9909203  PMID: 36634927

We thank M. Ackermann and co-workers for their interest in our recent publication [1]. These authors highlight our report of persistent increased alveolar dead space in 30% of 17 patients studied within ∼2 months after an acute episode of mild–moderate COVID-19. After outlining their own work, demonstrating secondary pulmonary lobule pathologies found in the lungs of deceased COVID-19 patients, they then hypothesise that secondary lobular micro-ischaemia may be responsible for the elevated alveolar dead space found in our study.

Short abstract

Increased dead space following COVID-19 may be due to microvascular injury or secondary micro-ischaemia https://bit.ly/3Fypdwz


Reply to M. Ackermann and co-workers:

We thank M. Ackermann and co-workers for their interest in our recent publication [1]. These authors highlight our report of persistent increased alveolar dead space in 30% of 17 patients studied within ∼2 months after an acute episode of mild–moderate COVID-19. After outlining their own work, demonstrating secondary pulmonary lobule pathologies found in the lungs of deceased COVID-19 patients, they then hypothesise that secondary lobular micro-ischaemia may be responsible for the elevated alveolar dead space found in our study.

Our study findings support persistent pulmonary vascular injury in recovered COVID-19 patients, for which M. Ackermann and co-workers provide pathological evidence. However, while we hypothesised that persistent microvascular obstruction was a likely explanation for the elevated alveolar dead space, M. Ackermann and co-workers provide an alternative and possibly complementary hypothesis linking functional and structural abnormalities. Both hypotheses, however, remain unproven, and the question of how the pathological findings from patients with fatal COVID-19 (provided by M. Ackermann and co-workers) relate to the functional physiological findings from patients recovered from an episode of mild–moderate COVID-19 (as in our study) remains unanswered. Resolving these issues will likely require a multidisciplinary approach combining physiological, pathological, radiological and interventional methodologies.

Shareable PDF

This one-page PDF can be shared freely online.

Shareable PDF ERJ-02287-2022.Shareable (231.2KB, pdf)

Footnotes

Conflict of interest: A. Malhotra has received grants from the National Institutes of Health, and consulting fees for medical education from Livanova, Equilium, Corvus and Jazz. P.D. Wagner has received consulting fees from SMS Biotechnology and Third Pole Inc., and has participated on the data safety monitoring board on Dr Levine's (UT Southwestern, Dallas, TX, USA) PPG. No other author has a conflict of interest to declare.

Reference

  • 1.Harbut P, Prisk GK, Lindwall R, et al. . Intrapulmonary shunt and alveolar dead space in a cohort of patients with acute COVID-19 pneumonitis and early recovery. Eur Respir J 2023; 61: 2201117. doi: 10.1183/13993003.01117-2022 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

This one-page PDF can be shared freely online.

Shareable PDF ERJ-02287-2022.Shareable (231.2KB, pdf)


Articles from The European Respiratory Journal are provided here courtesy of European Respiratory Society

RESOURCES