tetano
Editor, Senior Moderator
Anaesthesia. 2020 Apr 20. doi: 10.1111/anae.15093. [Epub ahead of print]
Airborne transmission of severe acute respiratory syndrome coronavirus-2 to healthcare workers: a narrative review.
Wilson NM[SUP]1[/SUP], Norton A[SUP]2[/SUP], Young FP[SUP]3[/SUP], Collins DW[SUP]4[/SUP].
Author information
Abstract
Healthcare workers are at risk of infection during the severe acute respiratory syndrome (SARS) coronavirus-2 (SARS-CoV-2) pandemic. International guidance suggests direct droplet transmission is likely and airborne transmission occurs only with aerosol generating procedures. Recommendations determining infection control measures to ensure healthcare worker safety follow these presumptions. Three mechanisms have been described for the production of smaller sized respiratory particles ('aerosols') that, if inhaled, can deposit in the distal airways. All require the surface tension of the respiratory tract lining fluid to be overcome by shear forces. These include: laryngeal activity such as talking and coughing; high velocity gas flow; and cyclical opening and closure of terminal airways. Sneezing and coughing are effective aerosol generators, but all forms of expiration produce particles across a range of sizes. The 5 μm diameter threshold used to differentiate droplet from airborne is an over-simplification of multiple complex, poorly understood biological and physical variables. The evidence defining aerosol-generating procedures comes largely from low-quality case and cohort studies where the exact mode of transmission is unknown as aerosol production was never quantified. We propose that transmission is associated with time in proximity to SARS-CoV-1 patients with respiratory symptoms, rather than the procedures per-se. There is no proven relation between any aerosol-generating procedure with airborne viral content with the exception of bronchoscopy and suctioning. The mechanism for SARS-CoV-2 transmission is unknown but the evidence suggestive of airborne spread is growing. We speculate that infected patients who cough, have high work of breathing, increased closing capacity and altered respiratory tract lining fluid will be significant producers of pathogenic aerosols. We suggest several 'aerosol-generating procedures' may in fact result in less pathogen aerosolisation than a dyspnoeic and coughing patient. Healthcare workers should appraise the current evidence regarding transmission and apply this to the local infection prevalence. Measures to mitigate airborne transmission should be employed at times of risk. However, the mechanisms and risk factors for transmission are largely unconfirmed. Whilst awaiting robust evidence, a precautionary approach should be considered to assure healthcare worker safety.
This article is protected by copyright. All rights reserved.
KEYWORDS:
COVID-19; SARS-CoV-2; aerosol; airborne; transmission
PMID:32311771DOI:10.1111/anae.15093
Airborne transmission of severe acute respiratory syndrome coronavirus-2 to healthcare workers: a narrative review.
Wilson NM[SUP]1[/SUP], Norton A[SUP]2[/SUP], Young FP[SUP]3[/SUP], Collins DW[SUP]4[/SUP].
Author information
Abstract
Healthcare workers are at risk of infection during the severe acute respiratory syndrome (SARS) coronavirus-2 (SARS-CoV-2) pandemic. International guidance suggests direct droplet transmission is likely and airborne transmission occurs only with aerosol generating procedures. Recommendations determining infection control measures to ensure healthcare worker safety follow these presumptions. Three mechanisms have been described for the production of smaller sized respiratory particles ('aerosols') that, if inhaled, can deposit in the distal airways. All require the surface tension of the respiratory tract lining fluid to be overcome by shear forces. These include: laryngeal activity such as talking and coughing; high velocity gas flow; and cyclical opening and closure of terminal airways. Sneezing and coughing are effective aerosol generators, but all forms of expiration produce particles across a range of sizes. The 5 μm diameter threshold used to differentiate droplet from airborne is an over-simplification of multiple complex, poorly understood biological and physical variables. The evidence defining aerosol-generating procedures comes largely from low-quality case and cohort studies where the exact mode of transmission is unknown as aerosol production was never quantified. We propose that transmission is associated with time in proximity to SARS-CoV-1 patients with respiratory symptoms, rather than the procedures per-se. There is no proven relation between any aerosol-generating procedure with airborne viral content with the exception of bronchoscopy and suctioning. The mechanism for SARS-CoV-2 transmission is unknown but the evidence suggestive of airborne spread is growing. We speculate that infected patients who cough, have high work of breathing, increased closing capacity and altered respiratory tract lining fluid will be significant producers of pathogenic aerosols. We suggest several 'aerosol-generating procedures' may in fact result in less pathogen aerosolisation than a dyspnoeic and coughing patient. Healthcare workers should appraise the current evidence regarding transmission and apply this to the local infection prevalence. Measures to mitigate airborne transmission should be employed at times of risk. However, the mechanisms and risk factors for transmission are largely unconfirmed. Whilst awaiting robust evidence, a precautionary approach should be considered to assure healthcare worker safety.
This article is protected by copyright. All rights reserved.
KEYWORDS:
COVID-19; SARS-CoV-2; aerosol; airborne; transmission
PMID:32311771DOI:10.1111/anae.15093