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[[The HILLSIDE:Reference desk for COVID-19 Infrastructure/Ventilation for COVID-19]]
 
== Question: ICU Ventilation for COVID-19? ==
 
== Question: ICU Ventilation for COVID-19? ==
 
--Question posted anonymously 11:16, 19 May 2020 (SAST)<br>
 
--Question posted anonymously 11:16, 19 May 2020 (SAST)<br>

Revision as of 13:34, 30 May 2020

The HILLSIDE:Reference desk for COVID-19 Infrastructure/ICU Ventilation for COVID-19 The HILLSIDE:Reference desk for COVID-19 Infrastructure/Ventilation for COVID-19

Question: ICU Ventilation for COVID-19?

--Question posted anonymously 11:16, 19 May 2020 (SAST)

"Assuming the virus is a low risk from an aerosolization point of view is it worth investigating the use of HEPA filters to purify the air in the room where we accommodate the COVID-19 patients? The same question can be asked with regards to the use of UV. Is it not better to try and reduce the virus within the room, rather than filtering the air through a HEPA filter.

  • The existing HVAC places our ICU is under positive pressure. For risk management when housing COVID patients, we wish to convert it to negative pressure. Any advice/ pointers?
  • Please provide advice on recirculating air in an ICU, under COVID-19?

"It became clear to me that the spread of COVId-19 is directly connected to the spread of the active virus. Having been Hospital engineer at a 1200 bed local hospital, I am acutely aware that virus longevity depends on, inter alia.:

  1. actual time that virus is inside its transmission-carrier fluid,
  2. actual temperature during its transmission, and
  3. concentration of the virus in carrying fluid (as fluid may evaporate).

Could you consider providing a guideline on these time/temperature characteristics of the virus?
Only thereafter could architects, engineers etc. identify effective risk-reducing protocols. This could lead to more financially-justifiable 'anti-Corona' measures"

Discussion

These questions are largely unanswerable at the moment but we can try to help by contextualizing what is known, and what a prudent response would be.

SARS-CoV-2 seems to have caused many to rethink their understanding of droplet and airborne transmission. These two transmission mechanisms form a continuum, but the following is is generally accepted:

  • Infectious particles <5μm in size can remain suspended and viable for many hours and these contribute to the airborne spread.
  • Droplet transmission involves larger particles which can also spread through the air for some distance, but the range of transmission is generally considered to be less than 2 meters whereafter particles fall out of the breathing zone. It is important to remember that within this 2 m distance these larger droplets are essentially 'airborne' and diluting ventilation systems have little effect on reducing the risk of droplet transmission.

Droplet precautions, therefore, include standard precautions like PPE, hand washing and distancing while airborne precautions include negative pressure isolation, respiratory protection, special exhaust or filtration regimes, etc.

Diseases seldom obey only one mode of transmission (obligatory routes) but often have preferences (preferential routes) while occasionally exploiting circumstances which provide rare opportunities for transmission (opportunistic routes).

SARS-COV-2 is understood to be preferentially droplet and contact spread (a form of droplet spread) with possible rare opportunistic airborne spread, although an extensive outbreak review revealed no indication of airborne spread[1]. There is still no convincing evidence that it is long-range airborne spread in the sense of droplet nucleation, as with TB[2]. Where evidence of short-range airborne transmission has been reported this can be seen in the context of short-range droplet spread[3].
Somewhat confusingly, an often reported laboratory study has shown that SARS-CoV-2 can remain viable in air for extended periods[4], but no evidence for airborne viability has been found outside of lab settings. Correlations between culture viability, particle size and the real world infectious quantum were not described in this study[5] and I do not think it was the study's intention to claim COVID-19 was airborne. More importantly, similar lab studies have also demonstrated a 3h airborne survival for viral strains not thought to be airborne[6]. This makes the direct application of these lab studies in real-world settings difficult.

The understanding of the mechanisms of COVID-19 transmission is still largely reliant on what is understood of SARS-CoV-1[7]
This similarity is reinforced by van Doremalen's survival study[4]

The CDC's advice regarding SARS-CoV-1 transmission is still as follows:

"The primary way that SARS appears to spread is by close person-to-person contact. SARS-CoV is thought to be transmitted most readily by respiratory droplets (droplet spread) produced when an infected person coughs or sneezes. Droplet spread can happen when droplets from the cough or sneeze of an infected person have propelled a short distance (generally up to 3 feet) through the air and deposited on the mucous membranes of the mouth, nose, or eyes of persons who are nearby. SARS-CoV-2 also can spread when a person touches a surface or object contaminated with infectious droplets and then touches his or her mouth, nose, or eye(s). In addition, it is possible that SARS-CoV might be spread more broadly through the air (airborne spread) or by other ways that are not now known." - US-CDC [8]

Studies which have found real-world SARS-CoV-2 in air, ducting and on extraction fans have so far failed to prove that the virus found was still viable[9][10]. It has been suggested that high temperature and humidity would reduce the spread of the virus. The temperature ranges suggested (>50°C) are beyond what anyone could endure in an ICU but the humidity ranges of between 40-60% are achievable. The high humidity slows the nucleation of the viral droplet and increases its settling speed, thereby reducing its range.

Much of the work being done to understand the transmission mechanism of COVID-19 is focussed on community transmission. It is important to remember that transmission risk in an ICU will not be the same as in homes and workplaces. The conditions and procedures in ICUs could promote transmission<see WHO 2020 below[11]. Firstly, in a COVID ICU unit, the contamination source strength is much higher than other spaces since infected patients are congregated there. These are presumably ill patients with high viral shedding. Secondly, procedures like intubation are understood to release high quantities of aerosolised particles, unlike with general talking or coughing. Additionally, viral shedding through talking and coughing can be more readily mitigated than from intubation.

The WHO's advice regarding SARS-CoV-2 transmission during clinical interventions is as follows:

"In the context of COVID-19, airborne transmission may be possible in specific circumstances and settings in which procedures or support treatments that generate aerosols are performed; i.e., endotracheal intubation, bronchoscopy, open suctioning, administration of nebulized treatment, manual ventilation before intubation, turning the patient to the prone position, disconnecting the patient from the ventilator, non-invasive positive-pressure ventilation, tracheostomy, and cardiopulmonary resuscitation." - WHO 2020[11]

Answer

Without good viability studies of viral particles found in ventilation systems, no firm guidance can be offered regarding the radial rate of viability reduction for SARS-CoV-2 particles. Until that time I think it would be prudent to assume that the virus should be considered as airborne within the confines of an ICU only, based on the guidance of the WHO. This would affect how we treat the filtration and ventilation in a COVID-ICU but I do not believe is sufficient evidence for negative pressurisation of the ICU.

I still believe that air recirculated within an ICU should always be (H13) HEPA filtered for reasons beyond just COVID. Therefore, assuming systems are designed in accordance with the IUSS BES guide, There should be no reason to change their configuration or pressurisation. Risk assessments should be conducted for ICUs immediately adjacent to public waiting areas or other high traffic areas, with corrective actions including reducing occupancy times and rates for these areas.

In all likelihood, we will be able to look back and say we overreacted in the name of patient and worker safety, but we should be wary of being criticised by retrospective experts of not having had the best interests of our staff and patients at heart.

--Tobyvan (talk) 11:16, 19 May 2020 (SAST)


Notes and References

  1. https://www.who.int/news-room/commentaries/detail/modes-of-transmission-of-virus-causing-covid-19-implications-for-ipc-precaution-recommendations
  2. World Health Organization. Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19) 16-24 February 2020 [Internet]. Geneva: World Health Organization; 2020 Available from: source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf https://www.who.int/docs/default- source/coronaviruse/who-china-joint-mission-on-covid-19-final-report.pdf
  3. Wenzhao Chen, Nan Zhang, Jianjian Wei, Hui-LingYen, and Yuguo Li, “Short-range airborne route dominates exposure of respiratory infection during close contact,” medRxiv preprint, https://doi.org/10.1101/2020.03.16.20037291
  4. 4.0 4.1 Neeltje van Doremalen, Trenton Bushmaker, Dylan H. Morris, Myndi G. Holbrook, Amandine Gamble, Brandi N. Williamson, Azaibi Tamin, Jennifer L. Harcourt, Natalie J. Thornburg, Susan I. Gerber, James O. LloydSmith, Emmie de Wit, and Vincent J. Munster, “Aerosol and surface stability of SARS-CoV-2 as compared with SARS-CoV-1,” The New England Journal of Medicine (2020), DOI: 10.1056/NEJMc2004973 [1]
  5. https://www.nejm.org/doi/pdf/10.1056/NEJMc2004973?articleTools=true
  6. Robert Comparison of the Aerosol Stability of 2 Strains of Zaire ebolavirus From the 1976 and 2013 Outbreaks Robert J. Fischer, Trenton Bushmaker, Seth Judson, Vincent J. Munster J Infect Dis. 2016 Oct 15; 214(Suppl 3): S290–S293. Published online 2016 Oct 4. doi: 10.1093/infdis/jiw193 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5050463/
  7. Isao Arita, Kazunobu Kojima, and Miyuki Nakane, “Transmission of severe acute respiratory syndrome,” Emerging. Infectious Diseases 9 No. 9 (2003):1183-84, [2].
  8. https://www.cdc.gov/sars/about/faq.html
  9. Santarpia et al, “Transmission Potential of SARS-CoV-2 in Viral Shedding Observed at the University of Nebraska Medical Center,. medRxiv preprint (2020), [3]
  10. Po Ying Chia et al, 2020 (Preprint) “Detection of Air and Surface Contamination by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) in Hospital Rooms of Infective Patients,” medRxiv preprint (2020), https://doi.org/10.1101/2020.03.29.20046557 [4]
  11. 11.0 11.1 WHO 2020, Modes of transmission of virus causing COVID-19: implications for IPC precaution recommendations https://www.who.int/news-room/commentaries/detail/modes-of-transmission-of-virus-causing-covid-19-implications-for-ipc-precaution-recommendations