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The provider should also ask about ADLs, which are the more fundamental self-care tasks such as walking around, feeding oneself, getting dressed, managing continence, and so forth. Functional impairments may correspond with safety issues that need to be addressed; if an older person is having difficulty with finances, it may be a good idea to check for signs of financial exploitation, or otherwise take steps to protect the person financially. Last but not least, impairment in daily functioning is also a criterion that separates mild cognitive impairment MCI from more significant impairment including dementia. In MCI, a person may be experiencing some cognitive impairment, but it should not be bad enough to significantly interfere with performing their usual daily life tasks.
Check for the presence of other behavioral, mood, and thinking symptoms that may be related to certain causes of cognitive impairment. Checking for tremor and stiffness both of which are associated with Parkinsonism is also recommended. Excessive use of alcohol, certain prescription drugs such as tranquilizers , or of illicit drugs can affect cognitive function. Suddenly stopping or reducing the use of alcohol or other substances can also occasionally cause or worsen cognitive function.
Review all medications, with a focus on identifying those known to worsen cognitive function. Certain types of medications tend to dampen brain function, and may cause a noticeable worsening in cognitive abilities. The health provider should especially ask about use of:. The purpose of the physical exam is to look for physical signs that may correspond to causes of cognitive impairment, or that may relate to other symptoms the patient or family brought up.
Probably the shortest well-validated test is the Mini-Cog, which involves a three-item recall and a clock draw. This takes minutes to administer, so it often requires scheduling a separate visit. Louis University Mental Status Examination. In most cases, it will be appropriate for the health provider to order blood tests, to check for common health problems that can cause or worsen cognitive impairment. In most cases, brain imaging reveals non-specific findings such as signs of cerebral small vessel disease and perhaps some mild atrophy of the brain.
These are common findings in many older adults and tend to have a variable correlation with symptoms. Most causes of cognitive impairment cannot be definitely ruled in or ruled out by brain imaging. Generally, it will take at least two primary care visits to complete an evaluation for cognitive impairment. The second visit is often used to do a cognitive test such as the MOCA, and can enable the clinician to follow up on laboratory tests that were initially ordered. Even with an adequate initial evaluation, cognitive impairment may take a few months or even longer to completely evaluate and diagnose.
It may not be realistic to expect definite answers. Of course, you may well be facing the problem of not being able to get your older loved one to go to the doctor. Learn more below. This article was originally published in , and reviewed by Dr. Kernisan in Dec Found this article very helpful. How can I get a copy of the article? It is extremely important. If you view my articles on a computer or laptop, at the end of the article right before the comments section , you should see a little printer icon.
If you click it, there should be an option to print the article easily, or to save it as a PDF. From the past few years, I have issues with thinking abilities. It started from around when I observed these issues and now in I found this to be worsened. There is nothing in mind, no new idea, no visualizations, no attentiveness. Can you suggest to me? Hi Rahul. Thank you for this vital and comprehensive article, yes I will share this as well! I hear from folks just after the MD says yes you have AD, no need to come back to see me okay, what? Capacity assessments around specific decision making is critical and hard to find… decreasing risks physical, financial, emotional can be a tough road for families.
I worry most about folks that live alone with cognitive impairment and ask, who makes decisions when the person lacks insight? In my work as a Geriatrician, I refer many individuals to a Social Worker to help sift through these complex issues. Could you provide a pre-formated print option so we can share easily. To create a print-friendly version, try clicking the little printer article visible at the end of the article. That should help. Hi Sue. I hope that helps! They are free to tell what they have observed.
I do think the ideal is for the older person to be aware of and agreeable to a family member communicating with the doctor. If this seems upsetting to the older person, then family members can consider how to go about being more discreet. Options include contacting the doctor beforehand, or simply discreetly mentioning to the medical assistant in clinic that you have something to mention privately to the doctor.
I do recommend putting concerns in writing, so that they can be added to the chart. Now sometimes older adults will actually forbid their family to contact the doctor. This puts the family in a tough spot. Perhaps the very best would be for every older person to talk to their family well ahead of time, about what to do if the older person ever becomes cognitively impaired and is refusing medical or other assistance. All of these steps require competent physical and mental health professionals; the damage that can be done by the incompetent ones is unbelievable. Everything other than an intermediate-length office-based cognitive test could be done in a single visit. It also helps for the older person to be accompanied by a family member for the visit, if possible.
The risks of self diagnosis are much worse than the risks of being misdiagnosed by incompetent medical professionals…. Both approaches are risky! Good article…I shared with my adult children to help them from jumping to ill-founded conclusions…but also what to be aware of. Yes, as you point out, a diagnosis often is necessary for legal and financial issues. A diagnosis — or even evidence of some cognitive impairment — should also prompt the medical team to reconsider some of what they are doing.
The first step is to get the ball rolling with an initial eval and hopefully to not get too much of a run around. Too often they just refer a patient to a Specialist. Then they refer you to another one. I live by myself, have no living or trusting relatives, and just a few friends. Please consider seniors who are aging alone. This was a very informative article. Thank you. Thank you for sharing these comments. You could see how others are tackling this type of issue.
Good luck! Primary Care Physicians are unsung heroes. God bless them! I agree with you that Primary Care providers are key players in healthcare. As a specialist, I collaborate with family doctors and primary care nurse practitioners daily. Some time ago, I wrote about a relative with memory problems. Twice now I have called and said that there are memory problems prior to scheduling checkup appointments. And twice my relative has proudly outwitted the doctor! Second visit doctor said that I had suggested there was a problem — I took some abuse without knowing the cause until just recently!!
This third visit I said nothing, and my relative breezed through the exam and was declared perfectly healthy!!! I believe it! Thanks so much for the heads up on Smart Patients — their help and support got me through sarcoma cancer. Unfortuantely, this kind of thing does happen. Sometimes the older person really does have minor deficits, but in other cases, the clinician is not being thorough enough or attentive enough. There are also online caregiving forums, such as the one at AgingCare. Good luck and take care! I was noticing severe mood swings in my Mom, and it became more obvious after a fall that resulted in a broken wrist. At first I heard that it was sprained so I went to see her because I also know she has osteoporosis.
Sure enough, it was purple and swollen and I told her it should be x-rayed to determine how extensive the damage was. Although I shared this information in writing to her PCP, he ignored me. I continued to observe problems and reported them to this doctor, thinking he would eventually evaluate her, especially given her treatment of my Dad after he suffered a stroke. He would not address my concerns. My brother, a state licensed teacher enabled Mom and our relationship has been damaged. Ultimately I have had to step back. I have a sense of peace in knowing that I did my best for both parents. I appreciate the recommendations here for support groups and counseling. Even when you do the right thing, it can be painful. My question is related to cognitive testing and the interpretation of results.
At what point, is a senior considered unable to make medical decisions? However, my loved one is testing as severely impaired with a score of 1. They are taking advantage of him by having him attend care meetings without family and signing paperwork without family present too. Interesting issue you are raising! Even if the agent has authority immediately, if the agent and principal disagree, the principal gets to decide, unless the principal is incapacitated. Incapacity does sometimes reverse. Not at all clear it was reasonable for them to do so under the circumstances you describe. It sounds like the nursing home decided that your father currently has the capacity to make his medical decisions, and so they are relying on him to participate in care meetings rather than involving you, his healthcare proxy.
The issue for you will be figuring out an effective way to intervene. If you look like you understand what capacity involves, this might impress them. You can also sometimes hire a clinician to go into the nursing home and see him. There are also some patient advocates who are doctors or other clinicians qualified to render an opinion on capacity. Do you think it makes sense for doctors to conduct routine cognitive function screening of all patients at a certain age, e.
He checked his BP, blood work, an occasional viral illness or infection, and physical aches and pains, but that was it. My mom had been taking him there but was no help, since she was in denial that anything was wrong. When I finally took my dad at age 93 to his doctor and provided a list of behaviors that had changed significantly over recent years, the doctor administered a mini-mental test. My dad scored 16 out of Yes, ideally his impairments would have been detected earlier. Unfortunately quite a lot of research indicates that older adults with impairment and even frank dementia are often not assessed or diagnosed by their usual physicians. This is one of many ongoing quality and safety issues relevant to the healthcare of older adults.
In terms of whether doctors should screen: the US Preventive Services Task Force reviewed this question a few years ago and concluded that the evidence was insufficient to make a recommendation. Cognitive Impairment in Older Adults: Screening. Medicare beneficiaries. If there are problems with IADLs then we are quick to consider cognitive impairment. Generally a medical clinic that is specifically designed to care for older adults will do a better job of detecting these problems, compared to a general primary care office. In short, much work remains to be done.
Until the medical system is better at addressing this, we must keep encouraging family members to speak up and be proactive. Your information is most helpful, clear and caring. As someone who has lost a parent, friends and other family members to various types of dementia, and now my husband has been diagnosed, I know how stressful and exhausting this disease can be for caregivers.
However, they overlook the families and friends who are trying to help the patient. Your recommendation to find a support group is spot on! Talking with others who are going through the same thing, or have been there, will provide you with information you will not get from a doctor. Plus you will make friends who will understand, support and advise you through the various stages, and grieve with you as your loved one declines whether through dementia or a physical condition. What do you suggest when your parent is in denial? My heart is in pain and she lives where Dr.
Pickings are poor. Terrible options available and she just refuses to believe that there is a problem. I do recommend connecting with others facing similar challenges; the online caregiving forum at AgingCare. Am finding your articles very helpfull, thanks. I was using low dose mg of Diazepam per night for several years to help me fall asleep again half way the night.
Was told low dosage like that would be OK, but am now beginning to wonder if there possibly is a relation with my memory loss? Glad you are finding the articles helpful. Diazepam and other benzodiazepines have actually been associated with an increased risk of later dementia, but there has been some debate about whether this is really a causational relationship versus an association. I have suggestions on optimizing brain function in this article: How to Promote Brain Health. When we go to the Dr. This got her in reversible financial trouble twice last summer that would have cost her thousands of dollars had I not caught them. Ideally, the doctors would come to some conclusions and give you more advice.
You may want to get a second opinion, especially from an attorney with particular experience in elderlaw. Hello Dr. Kernisan, My mom is 67, she has been taking mg of wellbutrin and mg of Venlafaxine for maybe 25 years. In , it was common that some politicians and the media called out seemingly dangerous behavior by spotlighting people frolicking on beaches, picnicking in parks, or participating in protests [ 66 , , ].
Also, overcautious people picked some studies and media reports to warn against going outdoors and spark alarm about walkers, runners, and cyclists spreading the virus via a slipstream effect over long distances [ — ]. These claims were mainly based on studies with no virological considerations and limited environmental assumptions [ , ]. All these aspects greatly influence viral transmission addressed in section 4. Since long-term restrictive measures come with enormous collateral damage and real-world conditions lead individuals to take some risks, the way forward is to advocate a harm reduction approach instead of social abstinence-only policy [ 29 , 38 , 77 ].
Applied to COVID, harm reduction entails enhancing awareness about SARS-CoV-2 transmission and infection risk mitigation, self-assessment of risk related to personal activities, and engagement through alternatives of safer socializing. Although finding balance in the response plans is not an easy task, harm reduction is a sustainable and realistic strategy and a way of negotiating a middle ground. Allowing people to make their own compromises and informed judgments make harm reduction an ethically correct approach that enhances community engagement and trust [ 30 , 77 ]. Casting shame and blame on people violating public health measures should be avoided [ 29 , , ].
Effective risk communication and education campaigns are therefore central to harm reduction. Harm reduction strategies may also encourage infected individuals to self-isolate and their contacts to self-quarantine in order to prevent further transmission [ 28 ]. Outdoor activities are arguably one of the mainstays of COVID harm reduction by supporting mental and physical welfare and alleviating the pandemic response fatigue Footnote 11 , while curtailing infection risk [ 29 , 33 , 38 , 39 , , , ]. The costs of not encouraging outdoor activities should not be overlooked. Policies that prohibit outdoor activities Footnote 12 may result in the movement of behaviors that are objectively safe outdoors to less-safe indoor settings [ 29 , ].
Outdoor activities are unlikely to drive SARS-CoV-2 transmission substantially because of the higher viral particle dispersion, reduced person-to-person contact, and external environmental factors [ 40 , , ]. The scarce instances of outdoor SARS-CoV-2 transmission suggest an extremely low risk of transmission [ 40 , , ]. Four studies have found that 0.
One study reported that 3. Other studies reported that 5. In a preprint study, both the odds of overall transmission and the odds of SSEs were much lower outdoors A study among attendees of an overnight camp provided little information about the risk of outdoors vs. In the study by Lan et al. Likewise, in three publications based on a crowdsourced database led by the London School of Hygiene and Tropical Medicine [ 37 , , ], there may be an overestimation since construction workers could have been infected indoors the most updated article is the one published by Lakha et al [ 37 ].
The unreviewed paper by Nishiura et al. Mass gatherings Footnote 13 deserve discussion. The risk in mass gatherings is expected to come from unplanned, informal, unregulated, and unmitigated events or activities that lack consideration of risk mitigation measures [ 40 , ]. Several factors influence transmission in these settings [ 40 , , , ]: 1 the environment i.
In addition, the underlying transmission levels or infection rates in a community are likely to influence the impact of either permitting or prohibiting mass gatherings. As for outdoor gatherings, upon consideration of crowd density, size, duration, circulation, and preventive interventions, public health officials may balance and mitigate risk across different factors mentioned [ 40 , ]. That is, an increase in one risk factor may be offset or mitigated by decreasing other risk factors. Therefore, all mass gatherings will not generate equal risks of SARS-CoV-2 transmission and will not need homogenous mitigations [ ]. Since mass gatherings may have sociocultural, economic, physical, and mental health implications, it is critical to consider the societal needs.
No evidence supported a growth in COVID cases following the protests [ 66 , 68 ], which may have been due to the outdoor environment and compensating behaviors such as the observed increase in stay-at-home and masking compliance during the protests. Successful COVID experiences of some countries have encouraged others to incorporate new elements into their plans and reassess existing elements that may be causing harm or may be ineffective. As this pandemic is not over, it is necessary to constantly revisit policies in the name of safety, so that their benefits always outweigh the harms [ 33 ]. In general, a combination of context-sensitive measures should be favored over blanket measures. One topic that has caused intense debate is the closure of schools.
School closures should be the last resort in the COVID response that countries and states pick and rely on. Evidence has emerged regarding limited SARS-CoV-2 spread within schools when sufficient preventive measures are in place, which has encouraged school reopening initiatives [ — ]. Of note, in-person schooling plans in the setting of high community transmission must include well-implemented alternative school-based mitigation strategies to not risk accelerating the pandemic [ , ].
These considerations may allow schools to safely reopen and stay open. Other interventions that should be de-emphasized given their limited or relatively low utility are excessive surface cleaning and disinfection, temperature checks particularly with inaccurate techniques , and some travel-related measures [ 30 , 33 , ]. Increasing vaccination rollout followed by decreasing local infection rates may allow the progressive easing of restrictions [ 33 ].
Gradual relaxation of interventions is essential to gain and recover trust in public health. This must consider the local impact of guidance and social disparities in addition to metrics of vaccination status and COVID deaths. Recently, in May , these guidelines were updated to reflect the successful vaccination rollout and the subsequent drop in cases and deaths in the USA [ , ].
As of writing, the CDC is supporting that fully vaccinated people no longer wear a mask or physically distance in any setting in the country, except where required by local regulations and workplace guidance, and refrain from quarantine and testing following a known exposure, if asymptomatic, with some exceptions for specific settings. Thus far, the effects of such policy decisions are illustrative of positive reinforcement in the context of efficient vaccine rollout. Publicly available data suggest that lifting mask mandates can allow a continued decrease in cases while leading to an increase in vaccine shots [ ].
Vaccines and the subsequent relaxation of NPIs are contexts where messaging hope since it is grounded in reality has proven its value. Another example that has been overlooked is the possibility of relaxing visitor restrictions in hospitals, provided that visitors assess their own risk and take precautions e. Given the endless benefits of visitors in patient-centered care, some authors have called for more accommodating hospital policies with careful use of PPE and monitoring, even before COVID vaccination was made available [ ].
Currently, in places where vaccination rates are high, COVID cases and deaths are decreasing and non-essential community indoor venues are open. In this context, keeping inflexible no-visitor policies in hospitals makes no sense [ ]. One of the biggest challenges in pandemic response for many countries has been the lack of a clearly articulated goal. In infectious disease response, the potential goals are control at acceptable levels, local elimination Footnote 14 , or global eradication Footnote 15 [ ]. Few countries, including New Zealand, Taiwan, Australia, China, and Vietnam, have articulated a goal of elimination as their official pandemic policy [ ]. This goal has spurred leadership to enact stringent and robust COVID responses including quarantine, contact tracing, and travel restrictions, among other measures, and a clear target goal appears to have aided in buy-in from the public.
As a result, some countries and regions have achieved elimination and resumed pre-pandemic life, with only intermittent response to imported cases needed. Further, critiques of elimination goals point to several shared features of successful countries. In particular, many countries that have achieved elimination of COVID are island nations that deployed early, widespread, and stringent mitigation strategies. Indeed, elimination of COVID appears to require an optimal surveillance system and extreme measures and may not be feasible in countries where border control is more challenging [ ].
Only two infectious diseases have ever been eradicated smallpox and the animal disease rinderpest [ ]. Without wide-scale coordination and consensus for eradication, elimination will continue to require intensive case surveillance, quarantine or testing of travelers, and intermittent reinstatement of control measures. Despite this, local and national governments can engage in dialogue about their COVID goals [ ]. When elimination is not the target, control of infection below acceptable levels is the main alternative. The public must be provided with information about the target levels of infection and allowed to weigh in on whether this level is acceptable to them in order to ensure acceptance of, and cooperation with, required restrictions and interventions.
Vaccination can purposefully lower the threshold to achieve elimination by generating low incidence infection rates and high population immunity [ , ], without the need for stringent NPIs. Unfortunately, even with vaccines, elimination is an unrealistic goal for countries suffering from a lack of resources, political commitment, public engagement, and coordinated response plans. Vaccine inequity further complicates the situation. It is necessary to look beyond readily observable symptomatic individuals and those completely asymptomatic yet presumed to be infected.
Reviewing the terminology needed to differentiate infected individuals and the infection stages is therefore the right first step before diving into the complexities between the poles of this false dichotomy. Asymptomatic individuals experience no symptoms throughout the entire course of infection [ 41 ]. The remaining individuals, referred to as symptomatic in its broad sense , initially demonstrate no symptoms during the incubation period Footnote 16 presymptomatic stage , then develop symptoms symptomatic stage , and later become symptomless again during convalescence postsymptomatic stage. As illustrated in Fig.
While classification into these three categories is only possible through retrospective and prospective symptom assessment, the stage is defined at the time of first positive test or diagnosis i. Among individuals with active symptoms, paucisymptomatic sometimes referred to as oligosymptomatic individuals are regarded as those who experience mild or few symptoms attributable to the infection. A population-based study arbitrarily defined paucisymptomatic individuals as those having one or two COVID symptoms except for anosmia and ageusia [ ].
The former individuals undergo three stages of infection: presymptomatic where viral RNA is detectable but there are no symptoms , symptomatic in a strict sense , and postsymptomatic symptoms are gone but viral RNA is still detectable. They are often referred to as presymptomatic, symptomatic, or postsymptomatic individuals. These stages have distinct implications for transmission. Since all SARS-CoVinfected individuals are initially symptomless, testing, follow-up, and a thorough symptom assessment are required to truly differentiate asymptomatic from presymptomatic, paucisymptomatic individuals experiencing mild or few symptoms , and postsymptomatic infection.
SARS-CoV-2 infection can present with a broad spectrum of clinical manifestations and disease severity. COVID symptoms and signs include fever, cough, fatigue, chemosensory dysfunction i. COVID can be categorized into mild, moderate, severe, and critical [ , ]. COVID is mild in most individuals, with no evidence of viral pneumonia or hypoxia and with symptoms that are not significant enough to seek medical attention [ ].
Patients with moderate COVID have evidence of non-severe pneumonia and therefore may present with dyspnea but not hypoxemia [ ]. Patients with critical COVID are those who progress to complications such as respiratory failure, shock, and multiple organ dysfunction, often accompanied by high mortality [ , ]. Few studies have estimated the proportions of COVID across the entire spectrum of severity using the ordinal classification above. All fatal outcomes were consistently reported among critical cases. The case fatality rate was 2. The most common symptoms of PASC are fatigue, neuropsychiatric symptoms e. There are also rare reports of hyperinflammatory syndromes e. The true occurrence of ASI is difficult to evaluate.
However, several concerns with these studies may result in overestimation or underestimation of the true asymptomatic fraction [ 41 , 42 , ]. Issues related to determining the true fraction of ASI stem from multiple factors. First, many studies reporting on ASI were cross-sectional surveys, often with convenience sampling and different testing eligibility criteria and settings, and were not designed to estimate the prevalence of ASI.
Therefore, they are prone to significant selection biases. Second, the paucity of adequate follow-up hampers distinguishing between presymptomatic and asymptomatic individuals in many of these studies [ 41 ]. It is crucial to account for the development of symptoms not only at the time of virological testing since it is well established that symptoms can occur days after testing positive [ 43 , 44 , ]. Based on the incubation period of SARS-CoV-2 [ , ], a follow-up of 14 days from the last possible exposure to an index case or first positive test if exposure is unknown is recommended to exclude most presymptomatic cases [ 41 ].
Also, if the timing of SARS-CoV-2 exposure is unknown, assessment of prior symptoms is recommended to identify postsymptomatic cases, given the potential for long-lasting positivity of quantitative reverse transcriptase-polymerase chain reaction qRT-PCR testing in upper respiratory tract specimens following symptom onset for weeks or even months [ 43 , 44 , — ]. Due to the cross-sectional nature of these studies, it is not clear what proportion of these individuals were presymptomatic or postsymptomatic.
Third, some studies reporting a high prevalence of ASI only evaluated a narrow range of symptoms [ 41 ], leading to information biases. This usually happened in early when smell and taste disturbances and gastrointestinal symptoms were not widely documented. Not only are symptoms subjective and variably ascertained by screening questionnaires or self-reported symptom tracking, but patients may also be unaware of atypical, mild, and prodromal symptoms, may not recall symptoms upon retrospective assessment recall bias , or may recount symptoms caused by other conditions.
Both an inadequate follow-up and information biases in estimating exposure and symptom onset times lead to misclassification of some presymptomatic, paucisymptomatic, and postsymptomatic individuals as asymptomatic, likely resulting in an overestimation of the ASI prevalence. Fourth, ASI estimates from serosurveys with uncertain timing of suspected exposure and antibody testing, and coupled with insufficient retrospective symptom assessment deserve caution given concerns with recall bias and the duration of detectable antibodies [ 41 , ]. Recall bias in serological studies may occur due to interviews or questionnaires gathering symptom information during a prior period, which might be particularly problematic with long or unspecified time windows.
Antibodies are detectable in most individuals two to four weeks following symptom onset [ — ], hence positive IgG titers are out of the presymptomatic period and seropositivity results exclude recent infection. ASI percentages from serological studies have been variably reported. Although two nationwide serosurveys on antibody testing [ , ] were designed to achieve representative samples of community-dwelling individuals [ ], their accuracy heavily relies on measurement-related factors e. Nevertheless, when better understood [ ] and planned, seroprevalence studies may assist in identifying previously unrecognized infections and, alongside virological tests, allow more accurate estimates of the population-wide ASI prevalence rather than of the qRT-PCR-positive population [ ].
Also, serial serological testing may help define antibody decay trends, which is useful to estimate ASI proportion in serological studies [ 41 ]. Fifth, confusing methodological definitions, different settings, and language barriers during international clinical assessment affect the generalizability of ASI estimates. Lastly, studies testing at a single time point or disregarding the time-changing sensitivity of qRT-PCR assays will rule out individuals with initial false-negative qRT-PCR results [ — ], thereby likely underestimating the ASI prevalence.
Five of the eight infected individuals were qRT-PCR negative at enrollment but positive during follow-up testing. Given the inclusion criteria used clinical follow-up, quality of included studies, case definitions , these systematic reviews are more reliable and accurate figures than those from highly publicized narrative reviews [ ] and opinion pieces [ , , — ]. Despite the scientific rigor of the articles cited above, generalizability is unclear and the wide prediction intervals of their pooled estimates reflect the considerable methodological and clinical heterogeneity among the studies included. Other systematic reviews with problematic inclusion criteria and definitions published much lower or higher estimates e.
This raises several concerns. While pooled ASI proportions may be valid and useful when a systematic review meta-analyzes high-quality evidence, the case of presymptomatic infection is a different one. Meta-analyzing proportions of the stages of infection of the symptomatic individuals makes little sense not only because of the variable testing times, definitions, and follow-up in individual studies, but also because the presence of symptoms is not a fixed feature of infection. The pooled proportion of presymptomatic infection of an individual study usually reflects the specific moment of testing or study assessment i.
As a result, the pooled proportion of presymptomatic infection might, at best, give an idea about how often infected individuals that will develop symptoms are symptomless by the date of testing across heterogeneous studies. Therefore, systematic reviews should instead analyze the methodological aspects of original studies and epidemiological parameters and timelines that influence both clinical presentation and transmission. Aggregate analyses of timelines detailing key events e. These features include secondary attack rates Footnote 17 higher for symptomatic and presymptomatic individuals [ 42 , 45 , , — ], viral RNA shedding dynamics longer viral RNA shedding and occasionally higher viral loads in symptomatic and presymptomatic individuals [ 43 , 44 , ], and modeling estimates of the contribution to transmission higher proportions of SARS-CoV-2 infections are estimated to originate from presymptomatic and symptomatic individuals [ , — ].
While these findings support a higher transmission risk for symptomatic and presymptomatic individuals compared with asymptomatic individuals, the latter cannot be dismissed as inconsequential to SARS-CoV-2 transmission [ , ]. Symptom-based strategies e. While vaccination rates progressively increase worldwide, multipronged preventive measures that do not depend on identifying symptoms e. In acknowledging the definitions reviewed in this section and the existing evidence on the proportions of infected individuals and their differential transmission risk, some claims in scientific articles and opinion pieces are misleading e.
Further research that incorporates nuanced definitions and systematic methods will enable a wider understanding of factors potentially influencing SARS-CoV-2 transmission such as viral load and the presence and onset of symptoms. Despite important advances toward understanding SARS-CoV-2 transmission dynamics, estimating the contribution of transmission is tricky and specific scenarios of transmission are extremely complex. Many aspects remain uncertain including the dual role of social behavior and biological features on transmission, evidence of presymptomatic viral load peak from empiric studies, and viral RNA shedding dynamics and infectious timeline of individuals with ASI. New studies will have to conduct rigorous analyses considering the influence of increasing vaccination rates on the clinical presentation of COVID Also, there is a need for carefully designed studies that document persistent symptoms after acute illness, help understand COVID aftermath, and improve care interventions, quality of life, and return to usual health of COVID survivors with lingering symptoms.
The COVID pandemic has reawakened the long-standing dichotomy of respiratory droplets and aerosols in terms of their size and transmission distance [ 47 , ]. Droplets and aerosols are erroneously seen as categorical transmission modes instead of a continuum of respiratory particles influenced by particle size and density, emission composition, turbulence and direction of the exhaled jet plume, and interacting environmental conditions [ 48 , ]. Transmission patterns are on a continuum rather than dichotomous [ 48 ]. Although several issues need clarification and discussion to achieve scientific understanding and effective public communication, no debate exists as to whether respiratory particles of varying sizes can be generated from an individual.
Both aerosol-generating behaviors e. Transmission risk in specific settings is further influenced by existing infection prevention and control IPC practices and public health interventions [ , ]. As acknowledged by the CDC, SARS-CoV-2 transmission occurs through three non-exclusive modes of exposure to infectious respiratory fluids: 1 inhalation of infectious small fine droplets and aerosol particles, 2 deposition of these particles onto mucous membranes nose, mouth, or eyes , and 3 by touching mucous membranes with hands contaminated by respiratory fluids or indirectly by touching inanimate surfaces with virus on them [ 50 ]. As transmission of infectious agents is complex and dependent on several factors, awareness of such distinctions is important for NPIs and public communication.
Although the relative contribution of all transmission modes remains unquantified [ 49 ], substantial evidence exists in support of specific transmission modes. Close-contact respiratory transmission, via short-range inhalable aerosols and droplets, is the primary mode of SARS-CoV-2 transmission [ 48 , 49 ]. Direct contact physical transmission and indirect contact transmission or fomite transmission play a minor role in propagating SARS-CoV-2 [ 46 , 51 , , ]. Long-range aerosol transmission traditionally known as airborne transmission occurs situationally, under certain conditions such as prolonged exposure in enclosed spaces with inadequate ventilation [ 47 , 50 ].
SARS-CoV-2 infections through inhalation at distances greater than 6 ft are less likely to occur than at close distances. The CDC has also emphasized that transmission due to inhalation and mucosal deposition of virus is effectively mitigated by existing intervention recommendations [ 50 ], such as well-fitted masks, adequate ventilation, physical distancing, and avoidance of crowded indoor spaces. Other transmission routes e. Airborne transmission—taken in its traditional definition of long-distance and respirable aerosols—is not the dominant or exclusive route for SARS-CoV-2 transmission [ 48 , 49 ]. Conflicting and polarizing messages pertaining to SARS-CoV-2 transmission modes jeopardize pandemic response plans, resulting in public unwillingness to adhere to risk reduction practices.
Exaggerating the frequency of a transmission route [ ] prioritizes unnecessary IPC measures and social behaviors in hospital and community settings at the expense of effective interventions in place and undercuts public trust. Infectious disease transmission has important implications for deploying cost-effective IPC protocols and allocating resources to achieve the largest impact possible. Overstated evidence can lead to harmful policies. By amplifying findings from studies with methodological concerns and limited transferability of results [ , ], some academics and laypeople have advocated the use of filtering facepiece respirators FFRs in routine healthcare or even in community scenarios [ — ], despite evidence showing that FFRs may not be necessary in some settings to reduce transmission risk [ ].
This has led to risk perception disparities and public confusion. Epidemiological data outbreak, cohort, and case-control studies help determine SARS-CoV-2 transmission mechanisms in real-world conditions. Theoretical modeling, laboratory-based, and in silico studies are useful as complementary sources of knowledge but are not necessarily reflective of the frequency of a transmission mode and the real-life situations, especially if they do not consider SARS-CoV-2 infectivity or are simulated in vastly different scenarios.
Several arguments support transmission through close contact with the infectious source [ 48 , 50 , 52 ]. Second, several observational reports of COVID hospital cases and outbreaks have indicated that transmission-based precautions TBPs for routine care of patients generally work if instituted timely and consistently [ 48 , , — ]. Medical masks have been demonstrated to reduce infectious titers of other respiratory viruses with similar transmission patterns [ ]. The problem is that the evidence is heterogeneous and hindered by suboptimal PPE adherence and underpowered study designs. The need for higher-rated PPE should be calibrated to the degree of risk [ ]. As many HCWs in clinical care and potentially other essential workers are at the highest risk for exposure due to proximity, duration, and infectiousness of patients [ ], access to fit-tested FFRs is indicated for their safety.
The value of FFRs outside of these circumstances is likely marginal but more research is needed [ ]. Third, community-based reports generally support the effectiveness of the existing TBPs if consistently and adequately instituted [ — ]. Accordingly, both the World Health Organization WHO and the CDC have reiterated that current recommendations are in general effective against both inhalation and mucosal deposition of respiratory particles [ 50 , 52 ].
Several SARS-CoV-2 outbreak studies have been published in different settings, including restaurants [ , ], call centers [ ], choir rehearsals [ , ], indoor fitness and sports facilities [ — ], long-term care facilities [ , — ], correctional facilities [ ], malls [ ], churches [ , ], flights [ , ], social gatherings [ , ], camps [ ], ships [ , , ], bus transportation [ ], and acute care hospital settings [ , ].
Many of these outbreak studies have been often cited by other reviews as evidence of airborne transmission. However, long-range aerosol transmission is a plausible explanation in only some of these settings [ 48 ]. Other modes of transmission cannot be ruled out and may fit the particular transmission conditions. In general, published clusters associated with long-range aerosol transmission are singular events with preventable circumstances, such as prolonged duration of exposure, lapses in the use of PPE, increased exhalation, indoor settings, and poor ventilation.
Some laboratory studies e. Unfortunately, such studies under controlled laboratory conditions do not reflect physiological host processes and real-world environmental conditions related to viral transmission [ , ]. Aerosol transmission, direct contact transmission, and fomite transmission have been experimentally demonstrated in multiple animal models [ 49 , — ]. Furthermore, studies in non-human primates, and confirmed in humans, demonstrate that infected individuals exhale infectious aerosols, but this is highly variable across individuals and activities [ , ]. However, this does not mean predominant long-range aerosol transmission of infectious viral particles.
While respiratory particles have a great capacity to travel long distances or linger in the air for some time, transmission risk hinges greatly on how much infectious virus those particles contain and the conditions of the environment. These particles will diffuse and dilute in the surrounding air leading to progressively lower virus concentrations. Droplet dispersion experiments e. However, these studies did not quantify infectious SARS-CoV-2 concentrations, which are likely substantially lower over long distances and under dynamic environmental conditions.
Findings from Stadnytskyi et al. This hypothesis remains scarcely tested and is unknown to be valid for humans and their infecting viruses including SARS-CoV-2 [ , ]. Many studies have looked for evidence of viral RNA in ambient air samples and ventilation systems of hospitals [ — ]. The study by Santarpia et al. In another study, Lednicky et al. It is yet unclear the extent to which these findings represent an unmitigated risk in healthcare settings where PPE and other TBPs are properly applied. Nor is a hospital setting, with robust ventilation, air filtration, and PPE, comparable to risk or frequency in the community [ ].
This similarly applies to fomite transmission, which is not considered a major transmission mode despite numerous laboratory-based studies conducting environmental sampling and reporting SARS-CoV-2 surface contamination and stability [ ]. Some studies conducting community-based SARS-CoV-2 RNA detection in air samples have reported negative findings, including those from cruise ship cabins [ ], quarantined households [ ], residential areas [ , ], open public areas [ , ], and transportation [ , ].
In contrast, other studies have reported positive qRT-PCR-positive air samples from a variety of indoor or crowded public spaces [ , ] and transportation [ , ], with SARS-CoV-2 viability not assessed. Although the implications of atmospheric pollutants on transmission remain elusive [ 53 , ], several studies mostly ecological and commentaries arguing about an association between air pollution and SARS-CoV-2 airborne transmission and mortality [ , — ] have sparked concern about PM acting as a carrier of SARS-CoV-2 and diffusing the virus in open environments.
Available air pollution studies point to correlation rather than causation i. Furthermore, upon theoretical examination, the probability that atmospheric pre-existing PM scavenges virus aerosols is low [ ]. Some scientists have also speculated that airborne pollen [ ] and sea spray [ , ] may act as a modulating factor of SARS-2 infection and transmission, with only ecological data supporting an association for the former [ ]. However, there is enormous potential for confounding due to several factors implicated in transmission of respiratory viruses, including well-known environmental factors such as ambient temperature. In addition, no evidence supports that pollen grains are carriers of SARS-CoV-2, much less does it provide information on their frequency and risk of transmission.
A study of air samples collected in Germany and experiments to examine potential complexes between purified pollen of various taxa and SARS-CoV-2 reported negative findings—in terms of both viral RNA and virus-induced cytopathic effects [ ]. While environmental exposome deserves further examination, evidence must be accurately communicated to avoid panic and misunderstandings. In summary, a low level of air contamination has been demonstrated in both healthcare and non-healthcare settings thus far. The findings of the air sampling studies are related to the sampling methods and duration, storage and transferring conditions, the environmental setting, low viral concentrations, dilution effects, and ongoing IPC measures [ , ].
Further, pressing issues concerning virological testing warrant discussion. However, viral nucleic acid detection by qRT-PCR-based assays does not equate to shedding of infectious, viable, culturable, or replication-competent virions [ , ]. Viral load and Ct values have limitations [ , , ]; their correlation depends on the gene targets used, the nucleic acid extraction system, among other factors. Detectable viral RNA exceeds infectious viral clearance [ 43 , 44 , — ] likely because genomic and subgenomic RNA persists as residual viral fragments or is protected by cellular membranes, and degrades slowly after the immune system has neutralized or lysed virions [ , ]. Demonstrating virus amplification or cytopathic effect in cell culture, or virus quantification by plaque assays or TCID 50 endpoint dilution assays are needed to infer viral replication and infectious virus [ ].
Therefore, these are better surrogates for assessing transmission competency, although the sensitivity of viral culture may be a concern as well [ ]. Unfortunately, infectious titer assays must be conducted in biosafety level 3 BSL-3 containment, so routine measurement of infectious SARS-CoV-2 in clinical settings cannot be done. Further methods to quantify infectiousness [ ] and reproducible research with emerging technologies to sample air particles are needed. There are virological and aerobiological unknowns of SARS-CoV-2 that are germane to elucidating transmission modes, including the minimum infectious dose, the size of particles with major relevance for transmission, and virus concentrations and viability in respiratory particles.
In addition, several factors that influence transmission warrant study: particle emission and composition, particle size transformation and distribution over time, and environmental parameters e. High-quality research is needed to better understand these aspects and attempt to estimate the relative contribution and importance of the transmission routes of SARS-CoV However, this is challenging because of the complexities in transmission [ 49 ], including the fact that respiratory particles containing infectious SARS-CoV-2 are highly variable in different individuals and with different activities [ , ].
It has become clear that aerosol transmission is an important transmission mode. For example, if the public wrongly believes that transmission occurs overwhelmingly from aerosols over an extended distance and time, they may reject guidance to wear medical masks or cloth face coverings given their limited aerosol filtering efficiency in comparison with other facepieces , hoard FFRs, or feel that distancing precautions are futile.
Likewise, if the public believes that the virus spreads extensively in the outdoor air and travels down blocks or across buildings, this may lead to potentially dangerous practices such as closing all windows in residential areas. This has been exacerbated by scientific commentaries claiming with selective citations that airborne transmission is the predominant mode of SARS-CoV-2 transmission, without addressing terminology, practical implications, and critical aspects in public health risk communication and community engagement [ , ]. Miscommunication of transmission modes precludes harm reduction approaches e. Inaccurate analogies have also been increasingly used. While this may meet the physical properties for aerosol scientists, analogies that intertwine sensory reception, such as smelling volatile organic compounds in smoke, can be misleading in terms of respiratory protection efficacy.
Given the societal challenges of COVID, never has there been greater need for meaningful interdisciplinary dialogue. Agreement on actionable terminology that respects different fields is long overdue. The pandemic has underscored the continuum and spectrum that is viral transmission. Such complexities should be addressed with collaborative efforts to communicate in a way that meets the needs of all parties. Nuance and complexity can be understood by the public if communicated clearly and transparently. Public health messaging and risk communication should mention that respiratory pathogens may transmit over long distances via the air under specific conditions, while making clear recommendations about effective mitigation measures.
Central to the use of accurate terminology is the risk assessment of indoor vs. Rather than droplet vs. Furthermore, discussing enhanced respiratory precautions and differences between long- and short-range, as well as risk in terms of types of exposure and activities can effectively inform subsequent public health interventions. Both the WHO and the CDC have utilized this approach with communicating risk, with an emphasis on proximity, activity, environment, ventilation, NPIs, and vaccination status [ 32 , 50 , 52 , 55 , ].
Bridging the interdisciplinary communication barriers and disagreements between the medical and engineering fields has proven complicated. Although academic disagreements may be valid and should not be met with hostility, narratives of misinformation and false dichotomies cause harm or do little to address the global needs for COVID mitigation. There have been large-scale, continued attacks on those working in public health, which undermines public trust and is counterproductive to the pandemic response. Different disciplines should work together [ ], instead of taking an adversarial position against public health agencies like the WHO and the CDC [ , ], which is decidedly not constructive.
In the end, the unresolved semantic dilemma warrants interdisciplinary efforts from the full range of experts, including medicine, epidemiology, occupational hygiene, engineering, and fluid physics, seeking a classification framework that recognizes both technical knowledge and practical implications in the context of public health and reconciles with real-life evidence without drawing inaccurate or unduly alarmist conclusions from available studies.
Nuanced and transparent communication efforts, coming from those actively working to advance health and research amid the pandemic and facing the challenges of media representation of terminology, are valuable endeavors. Preponderantly framed as a medical intervention in the past, face masks have become embedded as a social practice informed by expectations and norms amid the COVID pandemic [ 56 , ]. Masks have provoked a culture war and vigorous debates in many regions, with a volte-face in attitudes from mocking mask wearers earlier in the pandemic to shaming mask abstainers later [ 19 , 54 , — ].
With well-meaning but incendiary rhetoric [ ], some mask proponents overstated the benefit of masks in preventing SARS-CoV-2 transmission and downplayed many considerations needed for community masking uptake and public trust. Likewise, existing evidence was misinterpreted to advocate further benefits of mask wearing related to reduced COVID severity or increased ASI rates , and protective immunity via reducing the viral inoculum one of these papers was a preprint withdrawn by the authors [ — , — ]. Unsurprisingly, deep-seated conspiracy theories, scientific illiteracy, strong political views, and counter-visualizations Footnote 20 have stoked the anti-mask sentiment of the latter group, aiming to overturn mask recommendations and mandates [ 19 , ].
Claims from eminent individuals polarized at either side of this false dichotomy i. Masks—with their benefits and caveats [ 57 ]—are not a panacea or a hoax, nor are they mere symbols and commonsense interventions of the pandemic response [ 54 ]. There is merit in appraising different types of evidence on respiratory viruses and masks, particularly as this is the case of a complex public health intervention. Evidence on masks varies across study designs, settings, and populations; mask types and designs; mask-wearing purposes; and clinical and microbiological outcomes assessed.
Medical masks and FFRs have been shown to prevent respiratory viral infections in healthcare settings [ , , , — ]. In general, clinical studies comparing medical masks also known as surgical or procedure masks with FFRs have reported no statistically significant difference in preventing respiratory viral infections in HCWs [ — ]. As for community scenarios, before COVID, there had been evidence with mixed results for medical masks used by healthy and sick people in households, university residences, schools, and mass gatherings the Hajj pilgrimage but much less research on cloth face coverings also known as cloth or fabric masks to prevent onward transmission source control from an infected person and contracting infection personal protection of an uninfected wearer [ , — ].
Researchers of the only existing RCT on cloth face coverings, carried out in 14 hospitals in Hanoi, Vietnam, initially cautioned against the use of cloth face coverings to protect against clinical respiratory illness, influenza-like illness, and laboratory-confirmed respiratory virus infection, compared with medical masks [ ]. A post hoc analysis found that the risk of infection was doubled if cloth face coverings were self-washed by hand by the wearers rather than laundered in the hospital [ ]. Face coverings laundered in the hospital were as protective as medical masks.
The majority of existing healthcare and community studies have focused on medical masks and FFRs, and have examined clinical endpoints and influenza-related outcomes. Direct evidence of mask use related to infections caused by coronaviruses not SARS-CoV-2 is relatively sparse [ ]. Mask filters collect particles through a combination of mechanisms including inertial impaction, interception, diffusion, and electrostatic attraction [ ].
Several filtration studies of cloth face coverings have reported widely variable filtration efficiency and breathing resistance breathability estimates depending on the mask design and textile features i. Among cloth face coverings, multilayer non-valved masks made of hybrid, closely-woven fabrics show the best filtration efficiency and overall acceptable wearing comfort [ 55 , 58 , — ]. Facial fit, an aspect critical to minimize both outward and inward leakage around the facepiece edges and to improve filtration performance, has been increasingly studied. Several techniques have been suggested e. However, gaps in consistent communication with the public remain. Likewise, fluid dynamics simulation and experimental studies support the role of masks in limiting the spread of respiratory emissions [ , — ].
However, since variations in mask efficacy can be largely explained by the context of SARS-CoV-2 transmission level of infection probability and virus abundance , medical masks and well-designed face coverings should be effective under virus-limited situations [ ]. On the other hand, there are the RCTs, which are presumed to provide the highest quality data. However, RCTs can hardly capture the complexities related to viral transmission and public health interventions [ ]. This study found a non-statistically significant reduction in infection in the mask group vs.
Because of methodological limitations of this study in addition to being underpowered e. The results of this study, however, may reflect the personal protective effect not source control of a mask recommendation in Denmark at the time when the community incidence of infection was modest. Although the science is not definitive, it appears that influenza is transmitted by both large and small droplets ie, transmission occurs through both droplet and airborne routes.
Judson However, although airborne transmission is possible, large droplet or contact transmission is probably responsible for the vast majority of disease transmission. Although some experts seem to doubt that influenza can be spread through small droplets or airborne droplet nuclei, Brankston there are multiple lines of evidence that support this hypothesis. Shulman There are numerous other animal studies demonstrating the spread of influenza uphill against gravity over distances longer than droplets are supposed to travel, strongly supporting the conclusion of airborne spread. Tellier Influenza RNA has been detected in aerosol particles from infected patients while just breathing comfortably. Fabian Influenza has been found in aerosols in random samples of air around an emergency department during flu season.
The total amount of virus found on samplers worn by healthcare providers was about twice that in the air, suggesting that the risk is still highest from close contact with patients, but that airborne spread is clearly possible. Cummings On the other hand, Bischoff did find higher viral loads closer to the patient, but virus was still detected 6 feet or 2 meters away. It has also been proven that humans can develop influenza after breathing air artificially contaminated by the virus.
Francis And I just have to point out that Jonas Salk is one of the authors on this paper! The question is how often this occurs in a real world setting. Therefore, in a 10 minute visit, the health care provider would have inhaled , viral particles, which is clearly above the TCID Thompson Even studies that find lower viral counts in the air approx in Rule will still be well above this threshold. There is indirect evidence that airborne transmission occurs, as good ventilation and UV irradiation limits influenza transmission. McLean ; Shulman ; Drink ; Fiegel ; Tellier There are also multiple influenza outbreaks where airborne spread is hypothesized as the best explanation, however it is impossible to know retrospectively.
Moser ; Klontz ; Davis There is the interesting case report of an outbreak on a plane in Alaska in Because of a mechanical failure, there was a 4. The size of the plane seems to make airborne transmission much more likely than large droplets, which we are told should not spread beyond meters. That being said, if the index patient was the first person to use the washroom, the outbreak could easily be explained by droplet spread. Moser I think the data is pretty clear that influenza can spread through airborne aerosols, and I find that fact reassuring in the era of COVID Although the analogy fails because vaccination and prior exposure to influenza provide a level of immunity that does not exist with COVID Even when a virus can be spread through airborne transmission, you are still much more likely to become ill as the result of close contact.
If COVID is transmitted similarly to influenza, we can be somewhat reassured by our current practices. They suggest that airborne must equate to long distance transmission. They suggest that a low R0 and the lack of large scale outbreaks proves that airborne spread is impossible. I think that is a mistake. I think the animal studies above make it pretty clear that influenza can spread by the airborne route.
This would provide direct evidence against those epidemiologic arguments. Influenza has a low R0. It occasionally causes large scale outbreaks some of which have been blamed on airborne transmission , but those outbreaks are rare. Any infection that behaves like influenza could easily be spread through aerosols. Aerosols are tiny and their concentration drops off exponentially as you get farther from the source especially with good ventilation. The chances of encountering viable virus across the room are just too lw. However, that line of reasoning completely discounts close range aerosol spread. Aerosols will be most concentrated within a few meters of the patient.
At that distance, aerosol spread is almost indistinguishable from droplet spread. In fact, it is generally completely ignored, because many people just assume that short range spread is due to droplets. However, short range aerosol spread would have significant implications for our PPE choices. This short range aerosol spread is exactly what we are talking about when we discuss aerosol generating procedures. It is the people in the room that are exposed to aerosols. However, as we discussed above, normal human activities like talking and coughing produce just as many aerosols as most of our aerosol generating procedures. Therefore, it is important to consider short range aerosol spread in order to appropriate protect ourselves.
Scales In a retrospective analysis out of Singapore, insufficient ventilation on hospital wards was one of 5 major factors that increased the risk of transmission of SARS. An outbreak of SARS that affected more than people across apartments in the Amoy Garden apartment complex in Hong Kong is thought to have resulted from airborne spread of aerosols through the sewer system. It is also pretty clear that these viruses have been spread as the result of aerosol generating procedures. There was a strong association between multiple aerosol generating procedures and transmission of SARS to healthcare workers. Tran That being said, if COVID is aerosolized in large volumes, it is likely that the virus remains viable for at least hours, and maybe much longer.
Van Doremalen ; Fears There is definitely debate on this point. However, others say the opposite. For example, the CDC guidance for coronaviruses has always been to treat them as airborne, although that is based more on the precautionary principle than hard science see here and here. At this point, I think the only safe conclusion is that airborne transmission is possible. Because of their larger size, large droplets contain as much as Although aerosols may carry small amounts of virus, they become very diffuse the further you are from the patient and are effectively managed by modern ventilation systems. We need to consider the potential for aerosol spread, and how that might impact our PPE practices, while simultaneously recognizing that droplets and close contact with patients represent a far greater risk.
One of the most important aspects of managing bioaerosols is good ventilation. Fiegel In medicine, we are used to thinking in half lives. Each air exchange might take away half of the aerosols in a room, and therefore, if you can determine the air exchange rate for your facility, you can estimate the half life of aerosols, and use that to make PPE and clinical decisions. And of course, the most important mechanism for managing aerosols is almost certainly PPE, with a properly fit N95 mask being the medical standard, which I will discuss further below. There is a widely spread infection control concept that as long as you are 2 meters away from the patient, you are safe from droplets. This claim is usually made without citation, and there is plenty of data to say that it is wrong, at least as a definitive cut off.
The idea that all large droplets will fall to the floor within 2 meters seems to have been initially proposed by Wells, based on a very simplistic calculation, with assumptions that have since been questioned, and limited empirical data. Xie Unfortunately, as is reviewed above, most of the existing data seems to refute that hypothesis. For example, one recent study had 5 volunteers cough after gargling with food colouring, and there was visible macroscopic contamination beyond 2 meters with 4 of 5 participants. Loh Simple pictures of sneezes show a droplet cloud out to 8 meters. Cummings We should not rely on the 2 meter rule to keep us perfectly safe. That being said, because droplets spread through 3 dimensional space, the concentration of droplets decreases exponentially as you get further from the patient, and there is data that the majority of droplets created from normal breathing fall within 1 meter, although coughing and sneezing increase that distribution significantly.
Overall, the further you are from the patient the safer you are. You are more likely to become contaminated at 50 cm than you are at 1 meter. You are even safer 4 or 8 meters away from the patient or even better, behind a closed door. Practically speaking, this means that you should take off your PPE as far from the patient as possible. In an ideal world, you would always take your PPE off behind a screen or door to completely limit droplet contamination. However, although increasing the distance will decrease your risk from droplets, it actually increases the risk of contact spread. The risk of spread through contact with fomites is almost certainly higher than the risk from droplets once you are further than 2 meters away from the patient, which is why the 2 meter rule often works practically, even though it is not scientifically accurate.
What this means clinically will depend a great deal on the layout of your own space. If there is an empty anteroom to doff in, that makes the most sense. If you can doff behind a curtain, that would be great. Otherwise, realize that your risk is very small beyond that 2 meter mark as long as the patient is wearing a mask, not actively coughing or sneezing, and there is not an ongoing aerosol generating procedure. Update: A new systematic review examined this topic, and 8 of the 10 studies included demonstrated droplet spread beyond 2 meters.
We actually use masks for 2 different purposes and it results in a common misunderstanding among the lay public. We can use masks to keep droplets out of the respiratory tract to keep ourselves safe , but we can also use masks to keep droplets in to keep others safe. The surgical mask is significantly less effective than the N95 at keeping particles out, but it is very good at keeping particles in. With coughing and sneezing patients in the hospital, one of the most important infection control strategies is placing surgical masks on the patients to limit the number of droplets then make it to the environment.
Similarly, when hospitals are asking employees to wear surgical masks at all times right now, it is not a strategy designed primarily to protect employees, but to limit unintentional spread from asymptomatic or minimally symptomatic individuals. There are a few studies that compare N95 and surgical masks in healthcare workers. Loeb ; MacIntyre ; Smith ; Radonovich All were looking at influenza, so will only extrapolate to COVID if the mechanism of spread is the same, which might not be a good assumption. Similarly, all studies will be impacted by the rate of compliance with the mask as well as things like hand hygiene.
In general, compliance is lower with the less comfortable N95 masks, so the studies may be biased to show no difference, even if there is a difference with perfect mask use. Studies done in an outpatient setting may not extrapolate well to critical care. Finally, although the studies contain what look like large numbers of people, the power of the studies comes from the event rate or the number of people who get sick despite wearing a mask , which is much lower, and so the confidence intervals are very large.
A systematic review and meta-analysis on this topic found no statistical differences, but the point estimates are all on the side of N95s being better, and the confidence intervals are huge. It is hard to know what to do with that information. In an ideal world, I think using N95s as the standard until surgical masks were proven to be non-inferior makes the most sense, but that only works if we have an adequate supply of N95s to use for all COVID encounters. This is a lot of information, and unfortunately it does not allow for any black and white conclusions. There is pretty wide consensus that the science surrounding aerosol transmission of disease is severely lacking.
Morawska ; Chen ; Judson There are more questions than there are answers. We should avoid making definitive statements, and instead discuss the uncertainties and the trade-offs between alternating risks. Judson In other words, we should not be looking for evidence that a practice is harmful before avoiding it, but should instead be looking for evidence that a practice is safe before adopting it. It is clearly far more complicated than that, with larger droplets becoming smaller as they evaporate, and plenty of evidence that virus can be found further from patients than our current models predict.
This literature also makes it clear that almost every activity, including normal breathing, can create aerosols. However, the risk from those aerosols is far lower than the risk of droplets and close contact with the patient. Perhaps most importantly, we need to move beyond black and white statements and think in terms of probabilities. Instead, it tells us that the chance of infection is much higher when close to the patient and much lower as we get further away. We need to distinguish between possible and likely.
Airborne transmission of influenza and COVID is clearly possible, and probably does occur occasionally, but we also have to acknowledge that it is very rare. How can we know that it is rare? If airborne transmission was highly likely, we would see much bigger outbreaks. There have been thousands of COVID patients managed in normal hospital rooms, or behind curtains, and not every person in that department gets sick. Similarly, there have been many sick COVID patients on planes, and although there is some transmission, most people are fine. I think that message is key. You are much more likely to catch it from droplets or close contact, which is why infection control practices are so focused on those activities. If you are a numbers person, people have done some calculations.
There are a lot of assumptions, but the best estimates are that if you spend 15 minutes in a room with a coughing patient, your chance of catching influenza from large droplets and self inoculation contact is about the same and not very high. Transmission through airborne aerosols is about to times less likely than the other two routes Telllier That is reassuring. However, it is a mistake to take that line of reasoning too far. The focus should be on droplet and contact spread. At the same time, we should not ignore the airborne route. The above science review gives hints at activities that could increase airborne transmission: sicker patients with higher viral loads, more coughing and sneezing, higher respiratory rates, longer times spent with the patient, and of course aerosol generating procedures.
In these cases, the risk of airborne transmission increases, and we should consider adding airborne precautions to our standard of contact and droplet PPE. It is clear they exist. I think the above review explains their existence: some people produce far more aerosols than others, and if those same patients have high viral loads, you have an infection control problem.
In my mind, their existence is probably the best argument for universal mask use during an outbreak. I have said many times that the goal of every hospital during COVID should be to ensure that ZERO healthcare workers become infected in the course of their normal duties, while still providing exemplary care to all of our patients. However, that goal may not be perfectly attainable. There are always tradeoffs between risks.
Removing your PPE further from the patient may limit your exposure to droplets, but increases potential exposure to fomites as we carry dirty PPE further from the source. The small risk of airborne transmission might suggest increased use of N95 masks, but if we use our equipment in low risk scenarios it might not be available for us in higher risk encounters.
You might suggest wearing an N95 at all times, but we have already seen providers suffering from skin breakdown and other complications. There are no easy answers. However, that is not the world we live in, and although airborne spread is technically possible, it is incredibly unlikely. I am happy to wear a surgical mask when assessing the average patient with respiratory complaints. But as the patient gets sicker and the risk of aerosols increases either through procedures or natural activities like coughing , I will switch to an N I recorded a podcast that covers this material with Dr. David Hao on the Depth of Anesthesia podcast. Is the coronavirus airborne? Spread of Infection from the Respiratory Tract of the Ferret.
Transmission of Influenza A Virus. Br J Exp Pathol. Aerosol emission and superemission during human speech increase with voice loudness. Sci Rep. Published Feb J Infect Dis. Exposure to influenza virus aerosols during routine patient care. Measurement of airborne influenza virus in a hospital emergency department. Clin Infect Dis. Bourouiba L. Transmission of influenza A in human beings. Lancet Infect Dis. Which preventive measures might protect health care workers from SARS?. BMC Public Health. Published MarThey tried to take him out, but they noticed the fire was choking, so they couldn't Informative Speech On Smoke Inhalation out of the Informative Speech On Smoke Inhalation. Fiegel This could be an important consideration, Plot Summary Of Lord Of The Flies some people are Informative Speech On Smoke Inhalation the use of surfactant to manage Informative Speech On Smoke Inhalation lung disease. The Informative Speech On Smoke Inhalation were freed when they used the water heater to cause Persuasive Essay On Barrel Racing explosion and compromise Informative Speech On Smoke Inhalation door just enough Informative Speech On Smoke Inhalation give them access. Can Informative Speech On Smoke Inhalation ask, were the 8 of you getting Angel Fish Research Paper for a special occassion somewhere, or do you Informative Speech On Smoke Inhalation normally hang out together? Scales In a retrospective analysis out of Singapore, insufficient ventilation on hospital wards was one Informative Speech On Smoke Inhalation 5 major factors Informative Speech On Smoke Inhalation increased the Informative Speech On Smoke Inhalation of transmission of SARS. It Informative Speech On Smoke Inhalation like we are using Botany to fix a car battery issue, and being told its relevant Love In Pope Benedict Xvis Deus Caritas Est both things run on Informative Speech On Smoke Inhalation.