Daily Archives: September 22, 2022

Whether a new coronavirus variant takes hold in the coming weeks could determine if Michigan will undergo another seasonal COVID surge or enjoy its first quiet winter in three years.

Modeling from The COVID-19 Scenario Modeling Hub offer projections for the next six months, with a handful of different scenarios based on vaccine uptake and the emergence of hypothetical new variants. Health officials have looked to these models throughout the pandemic to help estimate upcoming trends.

The latest models suggest Michigan could see COVID cases and hospitalizations continue to plateau or even decline this fall if there are no new immune-escaping variants of coronavirus that gain traction through the end of the year.

On the other hand, a new variant with the ability to evade existing immunity could open the door to another rise in infections, hospitalizations and deaths this winter, much like omicron caused in 2021.

Its the kind of situation where I would love it if we got a pleasant surprise and we ended up not having a winter spike, but I think we probably should prepare for one, said Marisa Eisenberg, an associate professor of epidemiology at the University of Michigan who assists the state with infectious disease modeling. History has shown that usually we do get one.

The difference between Scenario Hubs most pessimistic scenario (new variant, low booster uptake), and its most optimistic scenario (no new variant, high booster uptake early on), is about 600,000 hospitalizations and 70,000 deaths nationwide.

The group estimates early booster availability and uptake would avert 6-12% of cases, 10-16% of hospitalizations, and 12-15% of deaths.

Related: COVID questions: Are the new vaccine boosters still free? Whos eligible?

Omicron subvariants BA.4 and BA.5 continue to make up more than 95% of sequenced samples in the U.S. Another omicron subvariant known as BA.2.75, originally identified in India, made up 1.3% of sequenced U.S. cases last week and is being monitored by the World Health Organization.

Predicting what the actual new variant is going to be and when it might emerge is a really tough problem, Eisenberg said. It depends so much on transmission happening not just in Michigan but all around the world, and other variables.

There are a lot of different variants that (the World Health Organization) and others are keeping track of. Whether any one of those is likely to kind of emerge and become the next dominant variant is tough to say.

Michigans COVID-19 trends have been consistent from week to week throughout the summer, with steady increases over the last three months. During the last week, the state reported an average of 1,849 cases and 17 deaths per day -- up from 1,588 cases and eight deaths per day three months ago.

Similarly, hospitals were treating 1,174 COVID patients as of Tuesday, Sept. 20, compared to 777 such patients on June 21.

The latest numbers arent far off from mid-September 2021, when the state was reporting about 2,772 cases and 21 deaths per day. Case counts were likely more accurate then, due to less availability of at-home testing.

In the months that followed, a more infectious variant known as omicron took over delta as the dominant strain in the U.S., resulting in spikes in case, death and hospitalization rates. By mid-January, there were more than 17,500 cases being reported per day in Michigan, and hospitalizations neared 5,000 COVID patients as health systems begged for residents to exercise caution.

The models from Scenario Hub show potential for another spike near the end of the year. They also leave the door open for rates to continue plateauing even despite a hypothetical new variant, as its difficult to predict the infectiousness of a hypothetical new variant.

Another big factor at play will be how much of the population will get the new bivalent vaccines. The updated booster shots, which became available to Michiganders earlier this month, were made to offer protection against the original coronavirus strain from the start of the pandemic, as well as omicron BA.4 and BA.5.

Absent of a new variant, the models project early boosters could prevent 2.4 million cases, 137,000 hospitalizations, and 9,700 deaths from COVID.

The bivalent booster will help fight the omicron subvariants, including BA.4 and 5, said Dr. Natasha Bagdasarian, Michigans chief medical executive, in a prepared statement. COVID-19 vaccines remain our best defense against the virus, and we recommend all Michiganders stay up to date.

About 63% of Michiganders got an initial dose of the original vaccines. Of them, about 59% got an initial booster dose. The state hadnt published any data on bivalent booster uptake as of Wednesday, Sept. 21.

Scenario Hub notes that even the best models of emerging infections struggle to give accurate forecasts greater than a few weeks out due to unpredictable variables like changing policy environment, behavior change, development of new control measures, and random events.

Eisenberg said its getting harder to make these models, because the picture of existing immunity and re-infection is getting increasingly complicated with the evolving coronavirus variants. Still, they remain useful.

Theyre not trying to project whats going to happen, she said. Theyre saying if we get a new variant, heres what it might look like. If we dont, heres what it might look like.

To find a vaccine near you, visit the online vaccine finder tool and enter your ZIP code. If youre looking for a bivalent booster, select one or both of the bivalent shots from Pfizer and Moderna.

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Originally posted here:

Will Michigan see a quiet winter or another COVID-19 surge? - MLive.com

Her gloved fingers working quickly yet carefully, Garima Dwivedi filled row after row of little wells on a plastic laboratory plate, pushing a button to squirt drops of clear fluid she had extracted from the blood of mice.

The mice had been vaccinated against a coronavirus infection. Like so many other scientists throughout the COVID-19 pandemic, Dwivedi wanted to see if the animals had responded by making antibodies.

But not just for this coronavirus. This new vaccine, in the University of Pennsylvania lab of Drew Weissman, is designed to protect the world against multiple coronaviruses including those we dont know about yet.

Weissmans research on messenger RNA helped pave the way for the original COVID vaccines, as well as the new boosters tailored to the omicron variant. Yet even before the FDA cleared the initial shots from Pfizer and Moderna, in late 2020, the Penn scientist was worrying about the next pandemic.

In less than 20 years, at least three dangerous coronaviruses have jumped from animals to humans. Before the COVID virus emerged in late 2019, there were SARS and MERS, each of which sickened thousands of people worldwide. A fourth new coronavirus, little known outside China, has so far been found only in pigs. But its a grim one, having killed thousands of animals since 2016.

More than a dozen teams of scientists worldwide are now racing to stay ahead of the next one by developing whats known as pan-coronavirus vaccines. Weissman, 63, is involved with four of them.

Some are designed to guard against all future variants of the COVID virus, as well as the older SARS and MERS. Others might also protect against less closely related coronaviruses that so far have been found only in bats. Some might even work against ones that cause the common cold.

For years, other scientists have tried to make a similarly broad, one-and-done vaccine against the flu, with limited success. But early evidence from Weissmans lab and others suggests that with coronaviruses, the challenge may be more surmountable. He says we cant afford not to try.

Coronaviruses have caused three epidemics in the past 20 years, he said. We have to assume there will be more.

The first COVID vaccines taught the immune system to recognize, and make antibodies against, the coronavirus spikes the dozens of little proteins that stick out from the surface of each virus particle.

That made sense. The virus uses these spikes like a lock pick, breaking through the membranes of cells in humans and other animals. But in someone whos been vaccinated, antibodies latch onto this lock pick so that it no longer fits a certain receptor on the cells exterior the equivalent of a keyhole.

In the early rush to develop a vaccine, scientists reasoned that was enough. No need to teach the immune system about the rest of the virus if the spike cant get through the front door.

Then came the delta variant, followed by omicron. The spike picked up a series of shape-shifting mutations that somehow allowed it pull off a double stunt: avoiding recognition by the antibodies, yet still fitting the lock well enough to open the door.

Thats where the next-generation vaccines come in.

In Weissmans lab at Penn, Dwivedi was testing mice for their response to one of them: a virus-like particle that contains both the spike and other structural proteins.

The idea is that while the spike can change its shape and retain the ability to penetrate a cell, the other proteins appear to be similar across multiple COVID variants and even across multiple types of coronaviruses. Teach the immune system to recognize these shared proteins, or so the theory goes, and it will be prepared to ward off a variety of threats.

But first, it has to work in mice.

Its important to see the response in the animals before you even think about injecting the vaccine in humans, Dwivedi said.

Nearby, colleague Benjamin Davis was analyzing the virus-like particles to make sure they contained the correct proteins. Magnified many thousands of times on an electron microscope, each particle looked like a childs drawing of the sun a blank circle with little rays all around the edge.

Basically, its a coronavirus with nothing inside festooned with enough different proteins to give the immune system a chance to develop an array of defenses, yet lacking the internal machinery it would need to cause a real infection.

Its like an empty shell, Davis said.

But how real is the threat?

Using a combination of demographic and antibody data, one recent study suggests that coronaviruses are jumping from bats to humans far more often than is commonly appreciated likely thousands of times a year.

In most cases, these spillovers appear to fizzle out, says Ken Field, a Bucknell University biologist who studies the immune system of bats. The virus may have picked up the ability to jump from animal to human, but not the ability to make copies of itself inside the person nor the ability to be transmitted from that person to the next.

Still, if viruses jump from animals to humans thousands of times a year, every so often its going to be a bad one.

Weissman, the Penn scientist, likens it to rolling the dice.

In most cases, they just burn out, he said. But every so often, you get a bad roll.

Not that bats have a lock on transmitting viruses to humans. The flu originally came from birds. Other viruses come from rodents, foxes, or raccoons. The key is to exercise caution when interacting with wild animals of all kinds, Field said.

But with continued clearing of forests, industrial farming, and air and rail service connecting formerly isolated areas, risky exposures may be on the rise.

Were making further and further incursions into what used to be wild areas, he said. The animals leave those areas and come out.

Scientists have tried to make universal vaccines in the past, primarily against the flu. But so far, the goal has been elusive.

Thats partly because the flus genome has eight segments, including those H and N portions that lend their name to such strains as H1N1 or H3N2. If a person is infected by more than one flu virus at once, these segments can be swapped, recombining into new virus varieties against which vaccines are less potent.

Coronaviruses are more stable. Yes, they mutate, as the world was reminded with delta and omicron, but scientists hope to train the immune system to focus on the parts that remain relatively unchanged.

Yet much remains unknown about how well these broad-based vaccines will protect humans. A key concern is that the immune system forms an indelible memory of the first time it encounters a virus or a vaccine based on that virus, said Mohamad-Gabriel Alameh, a biomedical engineer who is overseeing the virus-like particle project in Weissmans lab.

This initial memory is so strong that in future encounters, if a person is vaccinated against a slightly different version of that virus, the immune system may respond with antibodies that are more closely matched to the original exposure.

Are these vaccines broadening the protection? Alameh said. If not, we need to change the strategy.

So far, in tests of the virus-like particles, the mice have generated antibodies that match both the original COVID as well as its omicron variant a good sign. Tests with other virus strains lie ahead.

If all goes well, an early-stage trial in humans could happen by early next year, funded in part by the Coalition for Epidemic Preparedness Innovations (CEPI), a nonprofit foundation based in Oslo.

Weissman is involved in three other broad-spectrum coronavirus vaccines with different strategies, including collaborations with scientists at Duke University, the University of North Carolina, and Los Alamos National Laboratory.

All are showing early signs of promise. All consist of genetic instructions in the form of messenger RNA, the technology he developed with partner Katalin Karik two decades ago. One involves an artificial spike made with pieces from multiple coronaviruses. Another features an array of virus fragments attached to a molecule called ferritin a version of the protein that carries iron in the blood.

Cautious by nature, Weissman is unwilling to say which one he thinks will offer the broadest protection. Perhaps several of the strategies will prove successful, and they could be used in a combination vaccine.

In science, you like to have as many different options as possible, he said. We just have to test them all, and see which works best.

The only thing hes sure about is that more epidemics lie ahead.

See the original post here:

COVID boosters take aim just at omicron. This Penn lab is going after coronaviruses the world hasnt seen yet. - The Philadelphia Inquirer

I am guilty of letting my guard down. Thats partly the result of peer pressure. What do you do when you walk into a room full of people and find that you are the only one with a face mask? This is what I did: I settled down into my station and discreetly removed my mask. That allowed me to blend in: a risky manoeuvre if coronavirus is around.

With cases dwindling worldwide, masks have fallen off most peoples faces. I have been largely wearing one indoors and in closed environments like a plane or a bus. But that diligence slipped somewhere down the line, mostly in places where most people are unmasked. I certainly didnt want to stick out like a sore thumb.

Where did I catch the virus? That was the question from most of my friends. Frankly, theres no way of knowing. The obvious ones are gatherings, but then I could have caught it from an acquaintance I dropped at his hotel; I still dont know whether he had an infection. It didnt matter.

Infection and reinfection: the symptoms

There was a silver lining in the reinfection: the symptoms were mild. So mild that I underwent an RT-PCR test only on the third day; that too only after my wife fell ill. In a way, her illness helped. Or else, I would have returned to work on the fifth day and passed the virus to my colleagues.

How mild were the symptoms? For comparison, let me tell you what happened in April 2020. I had a continuous high-grade fever, which broke only on the tenth day. Pains wracked my body, and there were headaches too. But there wasnt much cough. I suffered, to put it mildly.

This time, body pains were milder, and I initially attributed them to the resumption of my yoga sessions. My nasal infection on the first day was followed by a sore throat the next day. It felt more like the flu or viral fever. Yes, a viral fever. Yet, I wasnt thinking it was coronavirus. My scratchy throat led to full-blown coughing, which lasted two days. But by the fifth day, I was on the mend.

Experts say COVID-19 manifests differently in different people. Two people under the same roof can have varied experiences. While I was largely unscathed, my wife reeled from violent bouts of coughing. So severe that she would end up throwing up food and medicines. Four days later, it began to subside.

My medicines and therapy

The contrast between the infections is stark. In two years, our immune systems have been primed by a previous infection and vaccines: two doses each of Sinopharm and Pfizer-BioNTech. And that really helped because we didnt have a high-grade fever; my temperatures were normal, and my wife had a slight fever for a day. Barring the cough, we were generally fine.

The bigger worry was passing the infections to our children. But we isolated well, and all of us were masked when we occasionally entered the common areas. That seems to have worked.

Over the past few years, most people I know have suffered from a coronavirus infection. And each of them coped differently. So when they wished me a speedy recovery, they also dispensed some medical advice. Mostly home remedies. Drink lots of hot water infused with lemon and ginger, one said. Have ginger and honey, was the advice from another.

Although I acknowledged the care and concern behind those words, I chose to ignore them. More because I had survived a COVID attack, and my children were also sickened by the virus in separate episodes. I now have a fair idea of how to handle the infection.

I spoke to a doctor, and my therapy mainly included paracetamols and plenty of sleep. I slept after breakfast and again after lunch. Of course, I continued the tried, tested and trusted steam inhalation and saline gargle.

My wife required more medications since her chest was congested. Teleconsultations and medicine deliveries helped. We are now limping back to normality. After a COVID negative test, I should be back in the office soon.

One question crops up: Do I mask up? I guess you know the answer.

Shyam A. Krishna

@ShyamKris_

Shyam A. Krishna is Senior Associate Editor at Gulf News. He writes on health and sport.

Here is the original post:

COVID-19: How I battled a second coronavirus infection in two years - Gulf News

Our understanding of how to treat COVID-19 has come a very long way since the start of the pandemic. Although many of these treatments are still new and need to be studied further, initial results have been extremely promising.

Monoclonal antibody treatments are a great example of this.

Monoclonal antibodies work like the bodys own immune system to help fight COVID-19. Since they were first approved for emergency use in November 2020, monoclonal antibodies have been successfully used to help reduce hospitalization and emergency room visits.

In this article, we take a look at what monoclonal antibodies are and how they can be harnessed to treat COVID-19.

Monoclonal antibodies act like your bodys own antibodies to help stop the symptoms of COVID-19. They can prevent hospitalization and reduce the severity of your illness.

An antibody is a protein your immune system makes in response to a specific infection. Antibodies are what help your body fight off those infections.

Monoclonal antibodies for COVID-19 can fight COVID-19 because they act like antibodies produced by your immune system.

However, its important to note that monoclonal antibodies do not replace a COVID-19 vaccine. They are intended as a treatment for COVID-19, not as a preventive measure.

Monoclonal antibodies enter the body and attach to the spike proteins that stick out of the coronavirus that causes COVID-19.

The coronavirus cannot enter cells with a monoclonal antibody on its protein spikes. This slows down the infection. It can help other treatments work more effectively and reduce the total time someone is sick with COVID-19.

Monoclonal antibodies are a newer treatment for COVID-19. Its not yet known how long these treatments will last or whether they will protect against future coronavirus infections. But initial research has shown that monoclonal antibodies can reduce hospitalizations and visits to the emergency room.

The Food and Drug Administration (FDA) has authorized a monoclonal antibody called remdesivir as a treatment for COVID-19. The agency also authorized clinical trials of additional monoclonal antibody treatments. These include:

These treatments are only authorized for investigational, or trial, use. They have not been fully approved as COVID-19 treatments.

However, they are available as emergency treatments during the COVID-19 pandemic. The exact monoclonal antibody treatment available can vary depending on your location.

The FDA recommends monoclonal antibody treatment for people who have tested positive for COVID-19 and who have a high risk of severe illness. Its also best to get monoclonal antibody therapy as early in the course of COVID-19 as possible.

Complete qualifications for monoclonal antibody treatment generally include:

Specific healthcare facilities might have additional requirements, such as age, for administering monoclonal antibody therapy.

Monoclonal antibody treatments are given intravenously. Youll receive treatment at an outpatient clinic.

The infusion itself will only take about 30 seconds, but youll stay in the outpatient clinic for about an hour. This allows medical staff to observe you for any side effects or reactions.

Before you leave, medical staff will give you information on what to do if you experience any side effects at home.

Once you return home, its still important to follow quarantine guidelines and any instructions youve received from a doctor. The monoclonal antibodies can help your body fight COVID-19, but they wont be an instant cure.

There are a few possible side effects of monoclonal antibody therapy. Most side effects are mild and will resolve on their own after a few hours. Rarely, more serious side effects have been reported.

Side effects of monoclonal therapy might include:

Yes. You can receive monoclonal therapy if youve been vaccinated against COVID-19.

It doesnt matter how recent your COVID-19 vaccine was, or whether youve had boosters. Youre still eligible to receive monoclonal antibodies as long as you meet the other eligibility criteria.

Yes. Its extremely important to continue isolating according to current local and federal guidelines after receiving monoclonal antibody therapy.

Monoclonal antibodies can help your body fight COVID-19 faster and more effectively, but you will still have COVID-19 after your treatment is complete. Isolating can help prevent getting other people sick.

Its best to continue following all instructions from your doctor and attend any follow-up appointments.

Monoclonal antibody treatment can help your body fight COVID-19.

Monoclonal antibodies work like antibodies made by your own immune system. They attach to the spike proteins on the coronavirus and prevent it from entering your cells. This slows the spread of the virus and can make your case less severe.

Currently, monoclonal antibodies are being used to treat COVID-19 in people who test positive for COVID-19 and have a high risk of severe illness. Monoclonal antibody therapy has been shown to help reduce symptoms and hospitalizations.

Originally posted here:

What Is Monoclonal Antibody Treatment and How Is It Used for COVID-19? - Healthline

Independent Newsmedia

The Arizona Department of Health Services on Sept. 21 reported the number of coronavirus cases in Apache Junction, east Mesa, Gold Canyon and Queen Valley is 20,043 in ZIP codes 85118, 85119 and 85120.

That is an increase of 40 from a week ago when cases stood at 20,003.

More than 90% of cases were mapped to the address of the patients residence. If the patients address was unknown the case was mapped to the address of the provider followed by the address of the reporting facility, according to the ADHS.

85118 ZIP code:

85119 ZIP code:

85120 ZIP code:

Common symptoms of COVID-19 include fever, cough, breathing trouble, sore throat, muscle pain and loss of taste or smell. Most people develop only mild symptoms. But some people, usually those with other medical complications, develop more severe symptoms, including pneumonia.

Medicare Part B (Medical Insurance) covers FDA-authorized COVID-19 diagnostic tests. Go to medicare.gov/coverage/coronavirus-disease-2019-covid-19-diagnostic-tests.

To see full numbers across the state, click here.

See more stories at yourvalley.net/covid-19.

More:

40 coronavirus cases reported in a week in Apache Junction, Gold Canyon area - Daily Independent

Under a tentative deal Washington state employees would get $1,000 bonuses for receiving a COVID-19 booster shot.

The agreement between the state and the Washington Federation of State Employees also includes 4% pay raises in 2023, 3% pay raises in 2024 and a $1,000 retention bonus, The Seattle Times reported.

Gov. Jay Inslee announced this month that all pandemic emergency orders will end by Oct. 31, including state vaccine mandates for health care and education workers. But he has said a vaccine mandate will continue to be in effect for workers at most state agencies.

Most employees were required to have their initial series of vaccination by October of last year or be fired. New state employees have had to be vaccinated before their official start date.

We want to have healthy people so people dont miss work, Inslee said earlier this month. The vaccine still remains a very important thing.

The Washington Federation of State Employees represents nearly 47,000 workers with roughly 35,000 state employees impacted by the tentative deal. The union said it would help address widespread staffing shortages and workplace safety issues.

The union called the deal, which still must be approved by both sides, the highest compensation package in the unions history.

Inslees office declined to speak to the specifics of the tentative agreement announced by the union.

Offering incentives for boosters reflects the feedback and recommendations we heard from employees and labor partners, Jaime Smith, an Inslee spokesperson, said.

See the article here:

$1k bonus for getting COVID-19 booster? Thats the proposed deal - OregonLive

Introduction

Coronavirus Disease 2019 (COVID-19) is a contagious disease that first appeared in Wuhan, China in late December 2019. It is caused by the virus called severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a highly transmissible virus.1,2 The disease has spread all over the world, considered a pandemic by the WHO since March 11, 2020.3 As of August 30, 2022, the world has 599,071,265 confirmed cases and 6,467,023 deaths.4 The clinical forms can be asymptomatic, mild, moderate, severe, and critical.5 Although pulmonary manifestations are common, the disease can affect several organs of the body.6

The main symptoms of Coronavirus disease 2019 (COVID-19) are fever, cough, and dyspnea.7 Some patients present with dyspnea in the setting of severe respiratory distress with a drop in oxygen saturation or oxygen partial pressure.8 Despite the absence of dyspnea, some patients with COVID-19 may have a markedly reduced oxygen saturation as measured by pulse oximetry. This phenomenon is referred to as silent hypoxia or happy hypoxia.9 Each time there has been a major wave of COVID-19, medical facilities have been overwhelmed, resulting in a rapid increase in the number of patients receiving home treatment. As a result, several deaths were recorded among patients treated at home, which became a social problem. Happy hypoxia has been one of the causes of death in COVID-19 patients receiving home care, as the absence of respiratory difficulty despite the presence of hypoxemia delays the seeking of medical care.10

The prevalence of COVID-19 patients with happy hypoxia was variable depending on the definitions of happy hypoxia used, the age of the patients, comorbidities, and the regions where the studies were conducted.11 The prevalence ranged from 31.9 to 65% in Europe11,12 and from 4.8 to 21. 5% in Asia.10,13,14 The prevalence was 4.8 in one American country15 and 6% in one African country.16 A systematic review would be beneficial in aggregating these disparities in prevalence. In addition, some studies have shown that patients with both COVID-19 and happy hypoxia are known to have poor outcomes.11,16 Therefore, hypoxemia in patients with COVID-19 without dyspnea should be identified and monitored carefully.

It is important to identify risk factors for hypoxemia in patients with COVID-19 without dyspnea. No worldwide prevalence survey of this phenomenon has been conducted. This review aimed to summarize information on the prevalence, risk factors, and outcomes of patients with happy hypoxia in order to improve their management.

Relevant studies will be identified through a search of MEDLINE, Europe PMC, and the Cochrane Library. The following will be the primary search terms in MEDLINE: ((COVID-19 [Title/Abstract]) OR (SARS-CoV-2 [Title/Abstract]) OR (coronavirus [Title/Abstract]), which will be cross-referenced to the terms (happy hypoxia [Title/Abstract]) OR (silent hypoxia [Title/Abstract]) The search will be in the English language. The search period runs from December 1st, 2019 to April 1st, 2022. The site preprints.org will search for preprints using the terms COVID-19 or Coronavirus. Official reports from medical societies, governmental institutes, and registries will also be manually searched and included if they match the inclusion criteria. The protocol was recorded on PROSPERO CRD42022293727.

Design

All observational studies report the prevalence, risk factors, and outcomes of happy hypoxia in COVID-19.

Study setting

Worldwide.

Population

All hospitalized patients infected with COVID-19

Publication status

All published and unpublished articles.

Language

Only studies reported using the English language.

Publication date

Published from the December 1st, 2019 to April 30, 2022

Patients who had received oxygen prior to hospitalization.

Two independent investigators assessed the results of the initial search for the title and abstract relevancy. The whole text was checked to see if it met the eligibility criteria. Duplicate articles, reviews, editorials, case reports, family studies, and publications that exclusively report on pediatric cases will be eliminated. Clinical studies that did not explicitly state death as a possible outcome will be ruled out. Furthermore, if a single author published two or more studies on the same patient sample, only the highest-quality publication was considered. Authors, year of publication, nation, study design, study location (number of study sites), sample size, age, sex, outcome, the definition of happy hypoxia, and proportion of happy hypoxia will be all included on data extraction forms. Two investigators (researchers with a masters degree in medicine or the humanities and clinical research experience) independently obtained this information. A third investigator double-checked the list of papers and data to make sure there were no duplicates and to rule out any inconsistencies.

The NewcastleOttawa Scale (NOS) was used to evaluate the quality of the included retrospective cohort studies based on three primary components: study patient selection which is worth up to 4 points, and adjustment for potential confounding variables which are worth up to 2 points, and outcome measurement which is worth up to 3 points.17 Each study can receive a maximum of nine points based on this scale. Articles with a NOS score of 5 were deemed high-quality publications in this study. The quality assessment was conducted by two reviewers. Disagreements were handled by discussion among reviewers, with the assistance of a third party if necessary to reach a consensus.

We will extract the authors, year of publication, nation, study design, study location (number of study sites), sample size, age, sex, the definition of happy hypoxia and proportion of happy hypoxia, gender (male/female), patient comorbidities, and outcome. We performed a meta-analysis of proportions (and 95% CI) for the prevalence of COVID-19 patients with happy hypoxia. The statistical heterogeneity among the included studies will be measured by the Cochrans Q with the p-value, and the extent of heterogeneity attributable to heterogeneity will be measured by the I2 statistic. The descriptive analyses will be performed using Stata version 14.

Through electronic database searches and registries, a total of 70 records were collected, with 25 records being eliminated before screening owing to duplication. Then, out of the 45 articles found, 20 were eliminated due to irrelevant titles, abstracts, or texts. A total of 25 papers were chosen for the full-text review, with 18 being deleted due to the lack of a result of interest, repeat data, or insufficient sample size. Finally, the research looked at seven studies (Figure 1).

Figure 1 Prisma Flow chart of study selection.

The methodological quality was high and the risk of bias was low, with a median Newcastle-Ottawa scale score of 77% (extreme values 7788%). The detailed quality assessment of all included studies can be found in Appendix A.

In total, 7 studies1016 were included in the review. The time period for the studies was 20202021. All studies were published between 2020 and 2021. The studies had sample sizes ranging from 141 to 21,544. One study was conducted in Africa (DRC);16 two studies in Europe, France, and Italy,11,12 three studies in Asia (Japan, India, and Saudi Arabia);10,13,14 and one study in the Americas (Mexico).15 In addition, only one study was prospective,15 and the rest were retrospective cohorts. Six studies took place in a single hospital, while one study in Japan involved Japanese national registries.10 Two studies defined happy hypoxia with an oxygen saturation threshold < 90%, two studies with a threshold < 94%, one study with a threshold< 95% also combining Pa O2 and PCO2, one study used the saturation threshold < 80%, one used the PaO2/Fi02 ratio < 300 mm Hg (Table 1)

Table 1 Study Characteristics of COVID-19 Patients with Happy Hypoxia

All studies reported the prevalence of happy hypoxia (Table 2). The prevalence varied from 4.8 to 65% for all definitions. In a 2020 study, Brouqui et al used an oxygen saturation of 93% as a definition. et al reported in the 2nd largest cohort a very high prevalence of 65% of happy hypoxia situations (Table 2). The pooled prevalence of the 7 studies is 6% (Figure 2).

Table 2 Prevalence of Happy Hypoxia in COVID-19

Figure 2 Pooled Prevalence of happy hypoxia in COVID-19 patients.

Brouqui et al11 discovered risk factors for poor clinical outcomes during follow-up (death/transfer to ICU) in patients without dyspnea. Hypoxemia/hypocapnia syndrome (yellow dots) was clustered with death/ICU, elevated NEWS score, age, male, and elevated D-dimers. Hypoxia/hypocapnia was linked to aging, maleness, and chronic heart disease but not to type 2 diabetes. Death/ICU was strongly associated with hypoxemia/hypocapnia syndrome (OR 95% CI: 4.37; 2.129.03) (p= 0.0001), as were elevated D-dimers > 2.5 mg/l (OR 95% CI: 6.26; 1.9919.75) (p = 0.002). Sirohiya et al14 found that multivariable logistic regression models were fitted to calculate the odds of death with silent hypoxia as the explanatory variable and other clinical, laboratory, and treatment parameters as covariates. We found that though these models showed a higher odds of death among patients with silent hypoxia, none of them were statistically significant. Akiyama et al10 found that hypoxemia without dyspnea was associated with age > 65 years (95% CI: 2.9204.350, p < 0.001), male sex (95% CI: 1.0701.600, p = 0.0087), BMI > 25 kg/m2 (95% CI: 1.1601.500, p = 0.036), chronic obstructive pulmonary disease (COPD) (95% CI: 1.3003.100, p = 0.002), other chronic lung disease (95% CI: 1.0603.400, p = 0.031), and diabetes mellitus (CI: 1.2401.850, p < 0.001). The hypoxemia without dyspnea group had a greater median respiratory rate (RR) than the control group (31/min vs 18/min, p=0.001).

All studies revealed mortality rates among patients with happy hypoxia. Mortality ranged from 1 to 45.4%. The study with a mortality of 45.4% used SpO2 < 94% as a criterion (Table 3). The pooled mortality rate of the studies was 2% (Figure 3).

Table 3 Mortality of Patients with Happy Hypoxia

Figure 3 Pooled mortality rate of patients with happy hypoxia.

Five studies reported other outcomes.1013,15 Four studies reported admission to ICU.11-13,15 According to studies by Alhusain et al, patients with dyspnea were admitted to ICU more frequently than those with happy hypoxia (107 (64%) versus 9 (36%), p = 0.007); and Brouqui et al (31(5.1%) versus 16 (1.4%), p=0.001). For the other 3 studies, the difference was not significant.5,8 Alhusain et al13 reported that the length of stay in the ICU did not differ between dyspnea and happy hypoxia on admission. Patients with dyspnea had a longer length of stay, though the difference was not statistically significant (2 (22%) vs 37 (35%), p=0.783). One study reported the need for ECMO.10 ECMO was used more frequently in patients with happy hypoxia in Japan, 57 (5.1%) vs 221 (1%) (Akiyama et al). (Table 4).

Table 4 Other Outcomes of Patients with Happy Hypoxia

To our knowledge, this was the first large-scale systematic review on the prevalence and outcome of COVID-19 patients with happy hypoxia. This is an understudied topic, with only eight studies specifically reporting the prevalence, risk factors, and outcome of COVID-19 patients with happy hypoxia. Of these, by far the largest cohort was from Japan.

The prevalence of happy hypoxia depends on the definition of happy hypoxia used. Considering all the definitions used, the prevalence of happy hypoxia ranged from 4.8% to 65%. The pooled prevalence was 6%. The highest prevalence of 65% was reported in the study in France, where oxygen saturation of less than 95% was considered in the definition of happy hypoxia. In the same study, in the subset of patients with at least one blood gas analysis (n = 161) who did not have dyspnea on admission, 28.1% had hypoxemia/hypocapnia syndrome, defining asymptomatic hypoxia.11 This value is still higher than the pooled prevalence in this systematic review. There were 2 studies reporting a low prevalence of 4.8%.10,15 One of these studies from Japan had happy definitions of hypoxia with a value of less than 94% while the other study from Mexico had a threshold of less than 80%, which could also explain the low prevalence. Compared with the results of a recent systematic review and meta-analysis on hypoxia in children infected with COVID-19 in low and moderate resource settings, considering the definition of hypoxia with saturation below 90%, the pooled prevalence was 31%.18 When compared to patients with hypoxia and dyspnea who were intubated, the prevalence of patients with hypoxia who were intubated was 28% (95% CI 20%-38%, I 2 = 63%). with a mortality rate of 14% (95% CI 7.424.4%) among these patients.19

Early intubation in COVID-19 has not shown many benefits. The literature does not find significant differences in mortality between the early intubation group and never intubated patients.20

Akiyama et al found that hypoxemia without dyspnea was associated with age > 65 years, male sex, BMI > 25 kg/m2, smoking history, chronic obstructive pulmonary disease (COPD), another chronic lung disease, and diabetes mellitus.10 These same factors are associated with severe forms and mortality related to COVID-19. Patients with COVID-19 with any of these characteristics may have hypoxemia and remain non-dyspneic. Thus, close monitoring of these patients is necessary. Specifically, they should be provided with transcutaneous oximeters so that they can monitor their own SpO2 regularly. Brouqui et al also found that patients with happy hypoxemia were elderly and chronically ill. Diabetic patients were 1.8 times more likely to have poor respiratory perception than non-diabetic controls and therefore had the lowest scores.11 It is well recognized that chronic conditions like diabetes and aging can desensitize the respiratory center, which can lead to happy hypoxia.21

The hypoxemia without dyspnea group had a greater median respiratory rate (RR) than the control group (31/min vs 18/min, p= 0.001). This finding implies that tachypnoea is an important indicator of hypoxemia, even in the absence of dyspnea. Furthermore, RR is an indicator of severe dysfunction in many-body systems, not just the respiratory system.22 It is therefore important that COVID-19 patients and their families know how to predict hypoxemia, even without transcutaneous oximetry, to ensure prompt medical management before the disease becomes severe.10 Brouqui et al found that factors associated with poor clinical outcomes during follow-up (death/transfer to ICU) among patients without dyspnea Hypoxemia/hypocapnia syndrome were clustered with death/ICU, elevated NEWS score, age, male, and elevated D-dimers.11 Hypoxemia and elevated D-dimers strongly suggest that the resulting lung damage is due in part to arterial microemboli and might explain the severity of clinical presentation and the subsequent death. These findings reinforce the recommendation to apply thrombosis prophylaxis in these patients.23

Anticoagulants are crucial for treating microvascular and microvascular thrombosis and inflammation in COVID-19 patients.2426 They also prevent the development of DIC,27 and they help to reduce mortality.28,29 The 28-day mortality was consistently lower in those who got anticoagulation compared to those who did not use.30,31

All studies showed mortality rates among patients with happy hypoxia. Mortality ranged from 1 to 45.4%. The study with a mortality of 45.4% used SpO2 < 94% as a criterion. The pooled mortality of the studies was 2%. A high mortality of 45.4% was found in the Sirohoya study in India.14 Similarly, a study in the UK reported room air oxygen saturation as a significant predictor of patient outcome and mortality.32 This is also confirmed by a Peruvian study reporting that oxygen saturation below 90% on admission was a significant predictor of in-hospital mortality in patients with COVID-19.33 Another study concluded that low oxygen levels on admission were strongly associated with more critical illness and mortality.34 The mortality rate for COVID-19 patients with severe disease can reach 61%.35,36 The primary factor is progressive hypoxia, which damages multiple associated organs, including the lungs.7 The use of standard mechanical ventilation in COVID-19 patients can result in mortality of up to 86%, in contrast to usual ARDS.3739 Before the advanced stage of COVID-19, when edema and shunt develop, High flow nasal oxygen (HFNO) should be taken into account as a superior option for early oxygen therapy. Supraglottic jet oxygenation and ventilation (SJOV) is an option, but more research is required to substantiate it.40

Four studies reported admission to the ICU.1113,15 According to studies by Alhusain et al (107 (64%) versus 9 (36%), p = 0.007) and Brouqui et al (31(5.1%) versus 16 (1.4%), p=0.001),11,13 patients with dyspnea were admitted to ICU more frequently than those with happy hypoxia. For the other 3 studies, the difference was not significant. According to Alhusain et al, the length of stay in the intensive care unit did not differ between dyspnea and happy hypoxia on admission. Patients with dyspnea had a longer length of stay, though the difference was not statistically significant (2 (22%) versus 37 (35%), p= 0.783). Two studies reported the need for ECMO.4,7 In Japan, ECMO was used more often in patients with happy hypoxia. 57(5.1) vs 221(1).10 The use of ECMO in severe COVID-19 patients seems to be the same as it is in ARDS patients that are not COVID-19.

The length of ECMO seems to be longer than in non-COVID-19 ARDS, and older age is a determinant in death.41

This lack of breathlessness deserves medical attention and should not be taken as a good sign of well-being. We suggest that for these patients with mild clinical presentation, it is particularly important to routinely achieve oxygen saturation by full pulse oximetry with blood gas analysis, if necessary, to allow early diagnosis of asymptomatic hypoxia and more appropriate management to reduce the poor outcome.11

Our systematic review had several limitations. First, we only included studies written in English. Secondly, another limitation in assessing prevalence is that the definition of happy hypoxia was inconsistent as there is not yet a standardized and validated definition. Some studies used different values of saturation, others used either PaO2 or the PaO2/FiO2 ratio. Finally, because the articles included are limited to a few nations, the global figure may not be accurate.

The pooled prevalence and mortality of patients with happy hypoxia were not very high. Happy hypoxia was associated with advanced age and comorbidities. Some patients were admitted to the intensive care unit, although fewer than dyspneic patients. Its early detection and management should improve the prognosis.

COVID-19, Coronavirus Disease 1; ECMO, extracorporeal membrane oxygenation; ICU, intensive care unit; COPD, chronic obstructive pulmonary disease; NEWS, National Early Warning Score; BMI, body mass index; NOS, NewcastleOttawa Scale; CI, confidence interval; OR, odds ratio.

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis, and interpretation; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted, and agree to be accountable for all aspects of the work.

The authors report no competing interests in this work.

1. Livingston E, Bucher K. Coronavirus disease 2019 (COVID-19) in Italy. JAMA. 2020;323(14):1335. doi:10.1001/jama.2020.4344

2. Gable L, Courtney B, Gatter R, et al. Global public health legal responses to H1N1. J Law Med Ethics. 2011;39(Suppl1):4650. doi:10.1111/j.1748-720X.2011.00565.x

3. Ucinotta D, Vanelli M. WHO declares COVID19 a pandemic. Acta Bio Med Atenei Parmensis. 2020;91(1):157160.

4. World Health Organization. Coronavirus (COVID-19) Dashboard. Available from: https://covid19.who.int/. Accessed August 30, 2022.

5. Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med. 2020;382(18):17081720. PMID: 32109013; PMCID: PMC7092819. doi:10.1056/NEJMoa2002032

6. Johnson KD, Harris C, Cain JK, Hummer C, Goyal H, Perisetti A. Pulmonary and extra-pulmonary clinical manifestations of COVID-19. Front Med. 2020;7:526. PMID: 32903492; PMCID: PMC7438449. doi:10.3389/fmed.2020.00526

7. Goyal P, Choi JJ, Pinheiro LC, et al. Clinical characteristics of Covid-19 in New York City. N Engl J Med. 2020;382(24):23722374. doi:10.1056/NEJMc2010419

8. Gallo Marin B, Aghagoli G, Lavine K, et al. Predictors of COVID-19 severity: a literature review. Rev Med Virol. 2021;31(1):110. doi:10.1002/rmv.2146

9. Levitan R. The infection Thats silently killing coronavirus patients; 2010. Available from: https://www.nytimes.com/2020/04/20/opinion/sunday/coronavirus-testing-pneumonia.html/. Accessed April 12, 2022.

10. Akiyama Y, Morioka S, Asai Y, et al. Risk factors associated with asymptomatic hypoxemia among COVID-19 patients: a retrospective study using the nationwide Japanese registry, COVIREGI-JP. J Infect Public Health. 2022;15(3):312314. doi:10.1016/j.jiph.2022.01.014

11. Brouqui P, Amrane S, Million M, et al. Asymptomatic hypoxia in COVID-19 is associated with poor outcome. Int J Infect Dis. 2021;102:233238. doi:10.1016/j.ijid.2020.10.067

12. Busana M, Gasperetti A, Giosa L, et al. Prevalence and outcome of silent hypoxemia in COVID-19. Minerva Anestesiol. 2021;87(3):325333. doi:10.23736/S0375-9393.21.15245-9

13. Alhusain F, Alromaih A, Alhajress G, et al. Predictors and clinical outcomes of silent hypoxia in COVID-19 patients, a single-center retrospective cohort study. J Infect Public Health. 2021;14(11):15951599. doi:10.1016/j.jiph.2021.09.007

14. Sirohiya P, Elavarasi A, Sagiraju HKR, et al. Silent Hypoxia in Coronavirus disease-2019: is it more dangerous? -A retrospective cohort study. medRxiv preprint. 2021. doi:10.1101/2021.08.26.21262668

15. Garca-Grimshaw M, Flores-Silva FD, Chiquete E, et al. Characteristics and predictors for silent hypoxemia in a cohort of hospitalized COVID-19 patients. Auton Neurosci. 2021;235:102855. doi:10.1016/j.autneu.2021.102855

16. Bepouka B, Situakibanza H, Odio O, et al. Happy Hypoxia in COVID-19 patients at Kinshasa University Hospital (the Democratic Republic of the Congo): frequency and vital outcome. J Biosci Med. 2021;9:1220. doi:10.4236/jbm.2021.92002

17. Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol. 2010;25:603605. doi:10.1007/s10654-010-9491-z

18. Rahman AE, Hossain AT, Nair H, et al. Prevalence of hypoxemia in children with pneumonia in low-income and middle-income countries: a systematic review and meta-analysis. Lancet Glob Health. 2022;10(3):e348e359. doi:10.1016/S2214-109X(21)00586-6

19. Cardona S, Downing J, Alfalasi R, et al. Intubation rate of patients with hypoxia due to COVID-19 treated with awake proning: a meta-analysis. Am J Emerg Med. 2021;43:8896. doi:10.1016/j.ajem.2021.01.058

20. Mohammadi M, Khafaee Pour Khamseh A, Varpaei HA. Invasive Airway Intubation in COVID-19 patients; statistics, causes, and recommendations: a review article. Anesth Pain Med. 2021;11(3):e115868. PMID: 34540642; PMCID: PMC8438719. doi:10.5812/aapm.115868

21. ODonnell CR, Friedman LS, Russomanno JH, Rose RM. Diminished perception of inspiratory-resistive loads in insulin-dependent diabetics. N Engl J Med. 1988;319(November(21)):13691373. doi:10.1056/NEJM198811243192102

22. Cretikos MA, Bellomo R, Hillman K, Chen J, Finfer S, Flabouris A. Respiratory rate: the neglected vital sign. Med J Aust. 2008;188(11):657659. doi:10.5694/j.1326-5377.2008.tb01825.x

23. Klok FA, Kruip MJHA, van der Meer NJM, et al. Confirmation of the high cumulative incidence of thrombotic complications in critically ill ICU patients with COVID-19: an updated analysis. Thromb Res. 2020;191:148150. doi:10.1016/j.thromres.2020.04.041

24. Iba T, Gando S, Thachil J. Anticoagulant therapy for sepsis-associated disseminated intravascular coagulation: the view from Japan. J Thromb Haemost. 2014;12:10101019. doi:10.1111/jth.12596

25. Mousavi S, Moradi M, Khorshidahmad T, Motamedi M. Anti-inflammatory effects of heparin and its derivatives: a systematic review. Adv Pharmacol Sci. 2015;2015:507151. doi:10.1155/2015/507151

26. Hoppensteadt D, Fareed J, Klein AL, Jasper SE, Apperson-Hansen C, Lieber EA. Comparison of anticoagulant and anti-inflammatory responses using enoxaparin versus unfractionated heparin for transesophageal echocardiography-guided cardioversion of atrial fibrillation. Am J Cardiol. 2008;102:842846. doi:10.1016/j.amjcard.2008.05.025

27. Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M. The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome. J Thromb Haemost. 2020;18:17471751. doi:10.1111/jth.14854

28. Tang N, Bai H, Chen X, Gong J, Li D, Sun Z. Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy. J Thromb Haemost. 2020;18:10941099. doi:10.1111/jth.14817

29. Iba T, Nisio MD, Levy JH, Kitamura N, Thachil J. New criteria for sepsis-induced coagulopathy (SIC) following the revised sepsis definition: a retrospective analysis of a nationwide survey. BMJ Open. 2017;7:e017046. doi:10.1136/bmjopen-2017-017046

30. Cui S, Chen S, Li X, Liu S, Wang F. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haemost. 2020;18:14211424. doi:10.1111/jth.14830

31. Hadid T, Kafri Z, Al-Katib A. Coagulation and anticoagulation in COVID-19. Blood Rev. 2021;47:100761. PMID: 33067035; PMCID: PMC7543932. doi:10.1016/j.blre.2020.100761

32. Gupta RK, Marks M, Samuels THA, et al. Systematic evaluation and external validation of 22 prognostic models among hospitalised adults with COVID-19: an observational cohort study. Eur Respir J. 2020;56:2003498. doi:10.1183/13993003.03498-2020

33. Meja F, Medina C, Cornejo E, et al. Oxygen saturation as a predictor of mortality in hospitalized adult patients with COVID-19 in a public hospital in Lima, Peru. PLoS One. 2020;15:e0244171. doi:10.1371/journal.pone.0244171

34. Petrilli CM, Jones SA, Yang J, et al. Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ. 2020;369. doi:10.1136/bmj.m1966

35. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult in-patients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395:10541062. doi:10.1016/S0140-6736(20)30566-3

36. Wang D, Hu B, Hu C. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020;323:10611069. doi:10.1001/jama.2020.1585

37. Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46:10991102. doi:10.1007/s00134-020-06033-2

38. Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med. 2020;8:475481. doi:10.1016/S2213-2600(20)30079-5

39. Gattinoni L, Coppola S, Cressoni M, Busana M, Rossi S, Chiumello D. Covid-19 does not lead to a typical acute respiratory distress syndrome. Am J Respir Crit Care Med. 2020;201:12991300. doi:10.1164/rccm.202003-0817LE

40. Jiang B, Wei H. Oxygen therapy strategies and techniques to treat hypoxia in COVID-19 patients. Eur Rev Med Pharmacol Sci. 2020;24(19):1023910246. PMID: 33090435; PMCID: PMC9377789. doi:10.26355/eurrev_202010_23248

41. Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for COVID-19: a systematic review and meta-analysis. Crit Care. 2021;25(1):211. PMID: 34127027; PMCID: PMC8201440. doi:10.1186/s13054-021-03634-1

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Prevalence and Outcomes of COVID 19 Patients with Happy Hypoxia | IDR - Dove Medical Press