This webinar was recorded on June 13th, 2023
What is the latest science about long Covid and lung health? Join us as we learn about lasting lung problems.
Speakers:
- Dr. Lekshmi Santhosh
- Dr. Shari Brosnahan
Resource:
Transcript: While this transcript is believed to be accurate, errors sometimes occur. It remains your responsibility to evaluate the accuracy and completeness of the information in this transcript. This transcript is not intended to substitute for professional medical advice.
>> Hello, everyone. Just hang tight for a few more seconds. We are going to allow some of the people that are attending to join. We will just wait for that little wheel to keep spinning. Just hold tight. Thank you in advance. Thank you all in advance for holding. We are just waiting a few more seconds where there are some people that are going to be joining us. We know it takes a while for the connection to go through. Just hang tight for another 10 seconds and we will start the webinar. Hello, everyone. Thank you for joining us today. I am Andrea Jensen. The education specialist and a certified asthma educator for allergy and asthma network. We will be recording today’s webinar and we will post it on our website within a few days. You can find all of our recorded webinars at allergyasthmane twork.org. The webinar will be one hour. That will include time for questions. We will take those questions at the end of the webinar. You can put those in the Q&A TAB at any time. That is on the bottom of your screen. On the left side. Please put them in the Q&A. Sometimes they are missed if they are in the chat because the check can get quite lengthy. We will get to as many questions as we can at the end of the webinar. We do not offer CEU’s for this particular webinar but you can get a certificate of attendance and we will put the link to that in the chat. You will receive an e-mail a few days after the webinar. That will have a link to be able to review the webinar, share it with anyone that you wish. We will also have a link to the certificate and any other resources about long COVID. Long COVID impacts millions of Americans. About 60 million Americans. Are you one of those with long COVID and lung problems? I know that I am. Today we will learn more about research and treatments. Allergy and Asthma network is a grassroots organization started over five years ago. By a mom who knew that other moms like her needed resources and support. Our mission is to end the needless death and suffering to to asthma, allergies and related conditions through outreach, education, advocacy and research. Today is my pleasure to introduce our speakers. Dr. Lekshmi Santhosh and Dr. Shari Brosnahan. Lekshmi Santhosh as an associate professor of medicine and pulmonary and critical care medicine and hospital medicine. Clinically, she attends the medical ICU, the neuro I see you on the internal medicine teaching awards and has a clinic at the UCSF Parnassus outpatient practice. She is the medical director of long COVID at the post I see clinic at UCSF health. She serves as the associate program director for curriculum for the internal medicine residency and the associate program director of pulmonology and critical care medicine Fellowship. She’s also the director of the Department of medicine grand Rounds. She obtained her Master and health professions and education from UC Berkeley. Related to ICU transitions of care, women in leadership, clinical reasoning and subspecialty career choices. Now for Dr. Shari Brosnahan. She has an attending pulmonary and critical care physician at NYU Langone health in New York City. She received her medical degree from the University of Texas health science Center in San Antonio and completed her internal medicine residency at Temple. Completed pulmonary and critical care fellowship at NYU where she was the chief fellow and joined the faculty in 2017. She holds a Masters of science and clinical investigations from NYU and is an assistant program director for the Fellowship program. Her research interests include acute sound chronic pulmonary embolism, COVID , long COVID brain, and ICU outcomes. At this time, please take it away. Thank you so much for taking time out of your busy schedules and the ICU to help people across the U.S. understand more about long COVID.
>> Thank you so much for the kind introduction and invitation to speak. Here are a conflict of interest disclosures and information. Just to set the stage, I remember and I still have this paper copy of the New York Times where it says U.S. deaths near 100,000, an incalculable loss. And here we are after having millions of who have COVID and now a subset of those patients with long COVID. I always tell people that COVID is down but it’s not out. This is particularly relevant when it comes to long COVID. You see the New York Times trucker. They stopped updating regularly in March of 2023. Even our current data has become more difficult to ascertain. There are people still in the news, like my own Department of medicine chair, Dr. walked — Dr. Wachter, still trying to spread the message that we should be trying to avoid COVID and he says in this article “there is still a fair amount of COVID around and I still don’t want to get it. The main reason is the data we see on long COVID is very concerning. Not just the chance you will feel crummy a few months from now but also the chances you are limiting your long-term risk of a heart attack or diabetes were more.” These are serious considerations when talking about public health messaging about COVID and long COVID. How are we going to spend this hour together? First we will talk about defining long COVID with a particular focus on the pulmonary symptoms. We are going to talk about the why. What are the current understandings of biological mechanisms? And we will talk about who is at risk and how so. We will talk about pulmonary conditions that increase long COVID risk or how they intersect with long COVID risk. I think early in the pandemic, back in March 2020, investigators and clinicians all found out that COVID can affect multiple organ systems acutely. Not just the lungs. But also the heart, the brain, the immune system. Even the reproductive system. It is no surprise COVID also affects multiple organ systems long-term. Everything from long-term lung scarring, heart impacts, mental health and brain impacts and neuromuscular impacts. In a subset of the patient’s, we found out fairly early on that they actually have this different kind of condition where there’s kind of a waxing and waning symptomatology. Symptoms kind of come and go. They can flare up. There’s a lot of fatigue particularly post-exertion only. There’s tingling, cognitive impairment, brain fog, shortness of breath and palpitations. The CDC with latest research has found out and estimate that about one in five adults actually have a health condition that might be related to a previous COVID illness across the whole body. We are learning more about this as the research progresses. These are two examples of studies that have come out in the last couple of years, which show that again there’s multiple organ systems with multiple symptoms involved that comprise long COVID. Which is first and foremost an amazing patient community generated term. I just wanted to call that out specifically that this is a patient generated term that we are using to be patient centered in the line of the patient community. The other thing we commonly combat the misinformation about his “it is just like the flu.” The study by colleagues showed even compared by influenza, COVID has much more significant impacts in multiple organ systems. Let’s focus for the rest of the stock on the pulmonary symptoms, which is our charge today. Even before we knew a lot about COVID, when you people were sick and the ICU for a lot of pulmonary problems with acute risk reduce stress syndrome, ARDS, recovering from a daycare plague from my toddler, we know they could have pulmonary function tests that were abnormal for years after initial study. This is a great slide that I love from my counterpart who runs the long COVID clinic at UCLA, Dr. Kristin Schwab. She points out that when patients deal with persistent shortness of breath after COVID, there’s a lot on the differential. Common things being common, one of the things we see is people who didn’t have asthma or COPD might actually have a new unmasking. Whereafter a viral infection like COVID or RSV or influenza, they got sort of a new diagnosis of asthma or COPD or other obstructive lung disease. Sometimes that could be in your diagnosis. Sometimes that could also be a worsening of baseline lung disease. Dr. Brosnahan we’ll talk about that a little bit more. — will talk about that a little bit more. Now they are kind of a severe category. We will talk about that. That’s one of the most common reasons for shortness of breath after COVID. The second one is deconditioning. I don’t mean that to say that all shortness of breath is deconditioning. There’s multiple mechanisms. These are just five of the most common mechanisms at play. Deconditioning is when our muscle strength goes, the breathing muscles get significantly impacted. One of the third things we see is organizing pneumonia which is a very specific subset. It is a special type of interstitial lung disease that is often responsive to steroids that we see with a classic CT scanner finding. That is rare but that is one to 2% — 1% to 2%. Post ARDS or lung fibrosis is another thing wit — another thing that we can say. People can plateau in different levels. Last we are learning a lot more about the role of pulmonary vascular disease. We learned early on many people with Covid have high hyper coagulant ability. We are still learning a lot about, when does that risk go down? What is the risk of blood clots? There’s a lot of intriguing research about micro clots and things like that. But the big acute blood clot, PE after Covid, we know it is highest risk in the early days in learning more about what is the risk after the early days? Other things to consider are also classic causes that are not Covid related, such as reflex often gives a cough, neuromuscular disease, vocal cord issues, tracheal stenosis, malasia, etc. particularly in people with prolonged intubation from Covid. We are not just reaching immediately from our treatment because we are trying to figure out, which of these mechanisms is at play? Could there be multiple mechanisms at play? Speaking of mechanisms, why do people get long COVID? This is a great article led by the patient community. The first author of the article is Hannah Davis. This is a great review article that came out in 2023 with a lot of great graphics. Including this one. This one shows what are the current streams of scientific evidence about why long COVID exist. It is everything from immune dysregulation from persistent infection perhaps, viral replication, dysregulation of the gut, micro bio, difficulties with autoimmunity and immune priming, blood clotting, filial abnormalities — ehi lial abnormalities. One of the challenging things we will talk about throughout is there is no one long COVID. Because different people likely have different mechanisms at play. So not everybody has all of these mechanisms. Some people might have a couple. Which bears challenges for how we treat this complex heterogeneous condition. One of the studies — one of my coinvestigators at UCSF is Dr. Michael Peluso. His study linked with the LIINC study has provided early insight into long COVID. Including this graphic here showing the specific elevated antibody levels is associated with people who have COVID related shortness of breath and chest pain and palpitations. We are learning more slowly but surely. I know progress is painstakingly slow. What we are learning more about, what is the role of antibodies? What is the role of inflammation? How does that actually correlate with the symptoms people are experiencing? We also have this new case definition the WHO came out with last year. The definition is nice because it really encompasses a couple of key variables. Talk about history of probable or confirmed SARS-CoV-2. How you need to exclude an alternative diagnosis. They talk about the common symptoms of fatigue, shortness of breath, that people can have waxing and waning or fluctuating symptoms. We will talk more about the latest definition that came out in the new JumboTron. There is no one long COVID. Each patient is unique. There are some common symptom clusters that we will discuss. But really each patient has really different symptoms. They probably have different underlying scientific mechanisms. The one-size-fits-all treatment is unable to be helpful. What is the underlying signs. — What is the underlying science? Things like that, we have a long way to go before we continue to make progress on this. And clinicians on the call listening and should make short to try to think critically about, how is this patient unique? What are this patient’s primary symptoms? How can I treat these primary symptoms? Let’s dive into the latest trial that came up just this month — came out just this month. From the NIH recover study. This was a really well-done observational cohort study of nearly 10,000 patients that used a very validated questionnaires — very valid questionnaires and they created a series of models that defined PASC or long COVID. What they did was they looked at these specific symptoms based on specific times and came out with this essentially classified list looking at the most common symptoms and essentially assigned a scoring criteria to help capture those altogether. This is just the first phase they point out. They point out this is currently used for research and not clinical practice. This is not a clinical score where you say, you get this score, you definitely have long COVID. But we are getting closer to being able to further define this. As more imaging and pathology and labs from this NIH trial come through, we can probably integrate that information in this model which is great. Here are some pictures showing the methodology of the different PASC symptoms they looked at. You see here some of these symptoms like post exertional malaise, fatigue after exertion are extremely high. Almost 90% of participants in the study experience that. Fatigue was another extremely common symptom. Brain fog. Dizziness. G.I. symptoms. Palpitations. You see how this is a hugely impactful condition that really touches on multiple organ systems and symptoms. Here is where they looked at kind of the score to identify an optimal cut off/threshold using this essentially summary score. This data — These data really track what Dr. Fauci and many other clinicians have said and many other patients have said for many years. Which is many people with long COVID have a post viral syndrome with a lot of overlap with chronic fatigue syndrome or my object encephalomyelitis. — myopic encephalomyelitis. There are patients with different symptom clusters. Some have a couple of symptoms that cluster together. There was one group that seems to be not that symptomatic and had fewer symptoms, there was one group — a very dominant group where they had a lot of chest pain and shortness of breath and palpitations. Other groups have clusters with a lot of joint pain. Headaches and muscle pain. Things like that. There are patients with the prominence of the post exertional malaise and fatigue, cognitive symptoms. Many times, when I talk about these findings, this really resonates with people because they say, that’s exactly me. These other the group of symptoms that I have. We’re are getting closer to kind of teasing apart, one of the symptom clusters? What is the underlying biology? How can we treat that? Now, I’m going to turn it over to Dr. Brosnahan to talk about what comes next when different pulmonary conditions people already have in fact there long COVID risk. Turning it over to you, Dr. Brosnahan.
>> Thank you so much. That was so well done. We will go through the very common pulmonary comorbidities and talk to you guys about how that might affect your long COVID or long COVID brisk. We will talk about OSA. A study that was part of the recover initiative looking at EMRs as well. We took three different cohorts of EMR data and looked at patients who had OSA prior to getting COVID and did not have it prior to getting COVID. What we found was there was a striking increase in the risk of long COVID in patients who had the comorbidity of OSA. Interestingly, that did not happen in children. Only in adults. And as we control for other comorbidities, that went down. If you look at the three cohorts we used, the range of increase OSA contributed was anywhere from 12 to 75% — from 12% to 75%. That is a pronounced difference. But what we found were, inpatients that were sicker, who had more comorbidities, OSA was almost additive to that. Patients who had more OSA, had more comorbidities, had more likelihood of long COVID. We also found OSA was much more likely to be additive in women. This was perhaps possibly — OSA tends to be found later in women and can be more severe because of that. So there’s not — This study is an EMR related study and does not give us basic pathology but it will be the basis looking for various different mechanisms. We know it can be restorative. Next slide. Another common condition is asthma. This is a meta-analysis from JAMA that took all different comorbidities looking at specifically asthma related, there were 13 studies that were included in this meta-analysis of 640,000 patients. If you can see, this is a — I’m not sure if people can’t see my pointer. You can see the total effect size is 1.2. Meaning there is an increasing risk. Underneath that you see a production interval. That tells you how much — how likely the study is to be run again. If the same result will be gotten. This shows there’s a good fidelity between the studies and it appears that asthma is clearly associated with long COVID and these patients. But what happens? We spoke about this a little bit earlier. What happens to asthma control after COVID? This was a study out of the U.K. looking at about 4500 patients in the first wave. Patients have not been vaccinated. That is a caveat to the study. But it showed after someone had a COVID infection, what happened to their asthma control. You can see the top bar, people who identified as not having long COVID. And the bottom bar are people that are identified as having long COVID. You can see they say their asthma control is significantly worse. On the right side, the right graph is talking about how their breathing is in general, not specifically about their asthma type symptoms. So did this impact their lungs or could it be a different mechanism like we are talking about? Causing a second physiology. Not just a reactive airway. And it appears these people felt dysnea was different than simply uncontrolled asthma in themselves which is interesting that we might be at risk for getting another pathophysiology mechanism in this patient population. COPD is an interesting story. It does seem like it is likely associated with long COVID. But the amount that we can predict, whether these results are true or not, is a little bit less. There could be a lot of reasons for that. This is an analysis in that same article looking at 10 studies, slightly fewer. Now we are at 250,000 patients. Still a lot of patients. And it did appear when we did the meta-analysis in the study, that there was a total effect size. You can see 1.38. That does not cross one. But what is interesting is the production interval does cross 1. Meaning there could be variability of we repeat — if we repeat these studies again and there may be a negative study. There are some reasons why there was heterogeneity within the recruitment of the studies. But ultimately one of the feelings of several authors in the study was that unfortunately COPD was tied to death during COVID and that will keep people from getting long COVID because they will have passed away. So they feel like severe COPD patients who might if they were able to survive and would have gotten long COVID were kind of pulled out of this cohort. So I think there are stills — there is still some confusion on whether COPD is truly linked to long COVID. But it seems likely associated. Next slide. Let’s bring this back to a case. There’s a 45-year-old female who has a past medical history of getting COVID in late 2020. Who then developed symptoms of PASC or long COVID. Shortness of breath, faint fog — brain fog, petite, exercise intolerance, and chronic cough. We were talking about the pathophysiology of the different mechanisms. I put shortness of breath and chronic cough together in my mind. Then I put fatigue and exercise intolerance together. That guides kind of the beginning of my work. Next slide. If I think about working up for dyspnea, fatigue, and chronic cough, I often do an exercise evaluation and a pulmonary function test — fatigue, I will do is sleep evaluation, we are not going to touch on sleep immediately in this talk, because it could be a whole hour in itself, but I will say we have seen a lot of strangely related disorders that have been appearing including REM related disorders. People having very vivid dreams and night terrors, acting out, restless leg syndromes. Things like that that can be linked to cognitive dysfunction in the patient’s. Not simply hypoventilation events which we think of from SOA. Really getting someone who was combining a fatigue or complaining of unfulfilling sleep to a sleep specialist will be very important. I also would do an exercise evaluation in this and someone who has a chronic cough, I would do a pulmonary evaluation, looking at the lungs themselves as well as a GERD evaluation and chronic cough as we often do. We will jump into some of the testing. I’m going to focus on what we found in the radiology. Next slide. When I classically think of what we have as access to us, and a normal clinical setting, it is chest x-ray, C.T. scan, and pulmonary function test. In terms of pulmonary. Then cardiac, we will touch on EKG, ECO, six minute walk, and CPET. There are a lot of other mechanisms that are being looked at to evaluate a long COVID patient in terms of dysfunction testing or other things that can be done in the lungs. Like true dual energy CT scans looking for micro clots. These are just — I’m just covering the garden-variety. Of what a patient might com to you with already done. Next slide. I think a chest x-ray is very much a helpful screenings will. And can tell you if there is a big thing there. But it never rolls out if there is any abnormality within the lung. This is a study that looked at basically time discharge from hospitalization three months and six months after patients. What it shows is about 50% of patients even three months after their hospitalization will still have abnormalities seen on their chest x-ray. But it’s hard to get a lot of information just from this. Next slide. When we look at CT scans, this is a study that was done over the course of the year, looking at CT scans over one year. They found nearly 50% of patients had abnormalities on CT scans in the year. Those patients predominantly or ground glass opacity with particular patterns and they were able to find that those radiographic abnormalities actually correlated with PFT abnormalities. Specifically the reticular patterns would characterize with total lung capacity decrease and residual volume abnormalities. Radiographic abnormalities were more common in patients who are older. They had other comorbidities including smoking and hypertensive, had a lower oxygen saturation during their clinical evaluation, and also succumbed to a secondary bacterial infection at the time of hospitalization. Acute phase. Next slide. Here’s some represented of images of patients who have acute COVID over the course of two years actually. D is two years out. A is the acute hospitalization of COVID. B is about six months later. C is 12 months later. D two years later. You can see the fibrosis and cystic changes kind of evolve over time. We see some areas of what we call traction dilation of the airway. The majority of patients that have gradual improvement over these two years. 50% similar to our last study showed abnormalities at six months. 40% of those patients still had abnormalities at two years. The most common abnormality was fibrotic disease. Some people had none fibrotic disease. — non-fibrotic disease. Early in COVID, we saw a lot of patients come six months later with fibrotic disease. Classically we were taught that fibrotic disease does not get better and we felt we were going to see a lot of patients that would just become oxygen dependent overtime. We also saw some improvement of these fibrotic changes over time. And I think that is showing us again that this is a new field that we don’t know what we don’t know to some degree. And we have hope, in that I cannot successfully prognosticate for all these patients yet because I do not know what happens in the disease course. Next slide. If we look at pulmonary function tests, we also see a similar story that pulmonary function tests are persistently worse at six months. They do tend to improve up to two years. But they have retracted abnormalities. I think PFTs are very hard tests in this patient population because I think it shows a lot of different abnormalities. They can be very difficult to make sense of. The one that is very interesting and does correlate with severity of illness tends to be DLCO. The restrictive disease of FVC was significant at six months and slowly improved over time. The says — This is the meta-analysis looking at DLCO. I apologize these are relatively small slides. But you can find this in respiratory research in 2020. What this shows is the DLCO was about 80%. So that one year for these patients. The mean was 80%. This was relatively found in 30% of the population. The FVC and TLC were slightly lower, only 95%, and only happened about in 10% of the population. So less of the time. Next slide. I think this is why it is so difficult to correlate PFTs. We talked about how really bad illness can impact lung disease. This breaks down PFTs by the severity of COVID illness. And hospitalization and non-hospitalized. You can see the patients that required hospitalization had a worsening DLCO, FVC, tec. But it’s not to say that people with mild symptoms and not have these conditions. But only to say that it was variable across the group. I think PFTs can tell us a lot of information but there is no PFT in my mind — of someone who has long COVID. Next slide. I think this is a very difficult study, COVID and the heart. Difficult discussion as well. It was found that SARS-CoV-2 does affect the myositis in general and there can be pericardial information — pericardial inflammation and that can progress to edema and sometimes scarring. Pericardial effusion, they can have these micro clots that can cause endothelial damage in these patients’ cardiovascular system, heart attack even, fibrosis, having a change in the cardiac function of the heart in general. Next slide. When I think about how to work out these patients, what I hear a lot is patients are complaining of palpitations. 10% of patients complain of palpitations. What is remarkable is some patients complain of this tachycardia that happens when they move from even a sitting or standing position. This is postural orthostatic tachycardia syndrome. POTS disease. Having a large overlap with COVID. I’m not sure of the exact mechanism. People are discussing whether they think it is autonomic insufficiency or they is some problem in these patients. If someone does come in complaining of POTS disease or a syndrome, I do think of long COVID often in these patients. I will say that there is evidence of QTC prolongation in these patients. That is also related to the fibrosis or these scarring I was speaking about. Now we are not talking about cardiac MRI in these patients during this talk. But those would be things that would be working up that condition more. Other things, this is just an article that was talking about different cardiac conditions in patients with COVID. There are a lot of things that can be seen on echo. Chest x-ray and CT scan can be a good screening test, but not one thing makes me think of long COVID in these patients. You can see systolic or diastolic dysfunction, thrombus, you can see myocardial infarction, somewhat you can see pulmonary hypertension. These are things that on echocardiograms, it would make me think — it will confirm the diagnosis that I was thinking maybe this patient does have long COVID. But definitely not having these conditions does not make me think that the patient does not have long COVID. Next page. A cheaper test and easy test to do is a six minute walk. I think this is an important test in all pulmonary clinics. Especially around COVID. It can be used over time to see how a patient is improving. This is just an info graphic on how to do a walking test and someone who is on oxygen. Just want to bring up the point, just because someone is on oxygen doesn’t mean they can’t do a six minute walk test. It is important to still do those tests on this patients. I think it is important to also celebrate small wins with your patient in the clinic. If they do improve on their six minute walk test, we can celebrate with anything, even if it is 15 more feet. Next slide. A more advanced test that can be done to figure out the exercise of a patient could be a CPET. A cardiopulmonary exercise test. It basically looks at ventilator — at the ventilation, the cardiac, and the oxygen extraction. It sees what basically fatigues first in a patient. So you can see this is the reason why the person has dyspnea. If I could figure out how — If I could figure out why the patient has dyspnea, we don’t necessarily know why, I could fix that one ideology. They can be helpful. But what I want to point out is a slight on the right. — a slide on the right. A figure on the right. There is very little overlap in findings on patients that have long COVID. We see a lot of exercise intolerance. But we don’t see a prominent physiologic problem in them that says, yes, patients have dyspnea because they have mitochondrial poisoning and problems with oxygen extraction because they have these pulmonary DLCO impairments causing them not to be able to get oxygen out. We don’t have one mechanism. While that might be helpful on a case-by-case basis, it will not seal your diagnosis of long COVID. Next slide. I’m going to talk a little bit about the studies being done and I will give it back and talk about what we should do in our clinics. Next slide. I think what I’ve said is pulmonary trajectories do improve for about a year. May be up to do. This is in some patients. If your patient is not improving, that is not abnormal. We should validate the fact that they might not. But I do see a pronounced improvement that happens between six and nine months after COVID. Fibrosis is the least likely to improve. But it can. And that is something that we did not think possible. And traction Brunk accesses tends to stay. Brunk — traction bronchiestasis tends to stay. The pulmonary treatments that can be focused on these different modalities that you would’ve seen continuing and patients are persistent ground glass abnormalities. We spoke a little bit about organizing pneumonia. This would be on the differential. These patients could be targeted for steroids or other types of immunosuppression. Anti-fibrotic agents. There are clinical trials currently underway to see if those can help regress these fibrotic changes. Pulmonary rehab — I want to put a giant Asterix on this. I know that post exertional malaise Israel. — is real. Telling someone that you need to exercise more is wrong. It’s not just deconditioning. It’s a lot of things. Pulmonary rehab can be done in a very slow model and focused on how to improve patients with post-exertional malaise. This is very important in talking to your patients because that will be a huge turnoff. I would put a giant Asterix next to that. There might be patients with persistent viral infections. Paxlovid. It is being investigated. Microvascular disease, I think this is not necessarily ready for prime time. There are no large clinical trials yet. We need to target patients that do have persistent coagulopathy. Those can be targeted with possible anticoagulation or antiplatelet agents. This should be done in a research setting. I will give it back.
>> Thanks so much, Dr. Brosnahan. Underscoring how every patient with long COVID is different and therefore your exercise advice has to be customized, this is both of us taking the chance to really emphasize that each patient sort of exercise prescription has to be customized taking into account whether they have post exertional malaise or post exertional symptom exacerbation or not. Johns Hopkins has this Free Guy called bouncing back from — free guide called bouncing back from COVID-19. They have easy exercises to go forth and conquer. The Association of physical therapy says specifically that the traditional model of gradually increasing your exercise is not appropriate in most of our patients with long COVID. They say that you really have to make very slow progressions an activity to increase functional capacity. — in activity to increase functional capacity. It will be difference with patients who have chronic fatigue and overlaps and patients who don’t. Is skilled physical therapist — A skilled physical therapist will figure out, are you one of those patients who has post exertional malaise or symptom exacerbation? Then we will give you a totally different physical therapy pathway. The key concept is rest and pacing yourself. It is very gradual. It’s very graded. You have to master your floor. What is the floor level of activity before very gradually moving onto the next? I talked to patients about, the floor is a concept of what is the minimum thing you can do that doesn’t leave you short of breath? For some people that is walking seven minutes. For some that is walking two minutes. Then we talk about how to sort of master that before gradually increasing it. Not going from seven minutes to 20 minutes but really trying with the slow seven to eight minutes. There often resting, — There’s often resting. We recommend recumbent exercise to start. Those patients often have a lot of those POTS syndromes. A lot will start with protocols where you start with recumbent exercise. Can you move your legs while sitting down. Practice setting up. Things like that. There are websites and breathing exercises programs that really try to link the autonomic and respiratory conditioning together. We know clearly there’s a lot of patients where they have a lot of autonomic issues. That impacts your breathing. Mount Sinai actually early in the pandemic created this stasis breeding program — breathing program for lung health where they talk about autonomic trading and respiratory training to basically retrain your body to have less exertion with controlling your autonomic nervous system. Really intriguing kind of line of thought. A lot of people get better with these principles of autonomic rehab. Studied by Dr. David Petrenko and others at Mount Sinai. This is another area to watch. There’s lots of exercises available online to think about. The last key point for clinicians to remember is all that long hauls is not COVID. Avoid anchoring bias and keep your differential broad throughout. I personally in our clinic have diagnosed people who had a label of long COVID by clinicians and diagnosed them with in some cases metastatic prostate cancer, metastatic lung cancer, sarcoidosis, hypersensitivity pneumonitis, allergic reaction, postpartum conditions, pregnancy, new pregnancy — there are so many different conditions that I’ll clinicians have to kind of keep a broad mind and think, what else could it be? What else am I missing? The detailed work Dr. Brosnahan outline helps you go through that systematically. There was just a recent column in diagnosis by Dr. Lisa Sanders talking about exactly this. She talked about how she had this patient who had long COVID who was sent to the long COVID clinic at Yale. After a while, she actually discovered they had a totally this regulated thyroid. Severe hyperthyroidism that was not identified or treated. So just keep your mind brought and your mind open to make sure there are not other things in addition to long COVID that are affecting the patients that should be treated separately. What other treatments are being studied? A lot of these treatments are actively being studied right now. This is a great table from the article from Hannah Davis. Our long COVID patient and committed activists. She wrote this great article. This table is from there. When I think about treatments, patients asked me about different treatments, I think about a lot of scientific evidence, emerging scientific evidence, things that I’m not sure about, and things I’m worried might cause harm. I think this table does a good job of kind of walking through those things. We don’t want to do anyone harm. What we know works well is this concept of pacing and energy conservation with people with myalgia encephalomyelitis, chronic fatigue overlap. There’s a lot of literature in the community about pacing, racing energy conservation — resting energy conservation. How gradual exercise does not work in that patient population. For POTS , there is both pharmacological measures and nonpharmacological measures. We start first with the nonpharmacological measures. A lot of people get better without alone. That is a high salt, high fluid diet, compression stockings and different exercise modalities like the recumbent exercise. There’s also for some patients with severe pots, there could be beta-blockers, etc. They should definitely be done in consultation with ideally a cardiologist and things like that because I’ve definitely seen situations where people had more side effects from the medication then their — than their long COVID. Make sure that the non-pharm stuff has been tried first. There’s not much data in the long COVID population. We talked about pacing. Definitely helpful. Most concussion syndrome protocols. Definitely helpful. In our clinic we have a cognitive therapist. Occupational therapist who does a lot of cognitive therapy and occupational therapy. Strategies that are similar to postconcussion protocols. They find that really helpful. For the chronic fatigue, pain, neurological symptoms, there’s a lot of good emerging data from the chronic fatigue community on [INDISCERNIBLE] in patients with lung COVID. It seems relatively safe. Well-tolerated. That is something you should consider asking your doctor about. There will be large low trials — larger trials coming on that. There’s a benefit of lo low dose antidepressant. Best to start something like that in conjunction with a neurologist ideally. This last couple of things mirrors the earlier slides. These are being actively studied in long COVID. Anticoagulants, Paxlovid, etc. I would not recommend taking those outside of a child because all of these can be high-risk medications. There was even a study on — outside of a trial because all of these can be high-risk medications. There was even a study that helped patients but harmed outpatients. It is complicated. I would not advise taking that outside of a trial or close supervision by a blood specialist. Paxlovid is being studied as we speak. There’s a trial going on in Stanford in my area and centers around the country looking at it. I would not recommend taking Paxlovid long term come off label. We are still studying the effects very closely. Stellate ganglion blocks syndrome. It is a specialized procedure. Only a couple of people can do it. The antihistamine, there’s a lot of overlap with lung COVID, chronic fatigue syndrome. That is an area to watch. I think there will be more evidence on that. And people who have taken antihistamines often find for some people, there can be significant side effects for some. These are all things to discuss with her for — with your clinician before starting on your own. I think one of the key things that emerging literature is focusing on is disentangling the umbrella term of PASC or long COVID and thinking about the recovery trial and other trials are focused on, how can we really customized al — customize the long COVID treatment? How can we take this huge umbrella term and break it up to, one of the symptoms people are experiencing? With the underlying biology? What is the treatment? — What’s the underlying biology? What is the treatment? We are trying to separate that out in a way that makes sense for patients in treatment. Dr. Brosnahan shared how the pulmonary and cardiac imaging can be helpful but often does not tell the whole story. There is no one pattern that is diagnostic or classic for long COVID. But if there are abnormalities seen, or other conditions, we can definitely treat those. We talked about pathways of fibrosis or asthma, COPD, arrhythmias. Things like that. There won’t be one treatment that’s right for everyone. We need to work on researching rapidly these new therapies. When — We need to expedite clinical trials. We need more funding for long COVID. Ourselves and many patient communities are very actively advocating and lobbying at the local, state and national levels for more research funding. More clinical trials. We know that the pace is slow for patients. The last take-home point is listen to everyone in the room. Believe patients. Patients, researchers and clinicians all need to listen to each other. Listen and believe in patients. We are hopeful the next time that we come back and give this talk, we will have more exciting your treatments, updates, insights to share. Thank you so much for listening. Thank you for your time. Here is both of our contact information. We will pause for Q&A. Thank you for the kind invitation.
>> Thank you so much. This has been fantastic information. A lot of thinking, weight, what did they say? When he took a back and listen to that. Have no fear. We will be recording this. You can review it in its entirety and we will have the slide deck there. Let’s go over a few questions. The first one is obesity and comorbidity in patients with OSA that developed long COVID. Was not more of a problem? — Was that more of a problem? That could explain the pediatric versus adult incidents.
>> It was a multivariate analysis that did control for obesity. It still did show that OSA accounted for an increased risk of long COVID. There are a lot of mechanisms. Sleep is very restorative to our brain. It could be part of the reason why patients are more likely to get kind of brain fog after a COVID diagnosis. Definitely obesity was a component to it. When those comorbidities coexisted, there was a higher rate of long COVID.
>> Thank you. Our next question is, what the sleep evaluation, is at best to go to a facility? — with the sleep evaluation, is it best to go to a facility? Or your own bed and actually get some sleep? Which do you feel is best?
>> They test two different things. I am not a sleep doctor. As a pulmonologist, we do a little bit of sleep training. But I would say that there are more tests that can be done in a sleep lab than a home test. It depends on what is right for you based on your symptoms and you need to talk to a sleep doctor to get the right test for you.
>> Perfect. As you’ve mentioned, there’s such a variability with people with their symptoms and some other health issues they have. There is no one-size-fits-all. Thank you. The reminder about that. — Good reminder about that. Thank you, Doctors, for the very informative presentation. I wonder if it is part of standard care to ask patients if they have been diagnosed with COVID during an annual checkup. Can patients be tested to see if they have COVID? They may be referring to antibodies or something with this question.
>> This is a great question. I would definitely encourage patients to view it as a part of your health history. When you see new clinician, to say if you have had COVID, what were the symptoms you experienced, the symptoms you are experiencing now. I encourage you all to carry that as part of your medical history. Because it may be relevant to future things. It may not be relevant to future things. But it never hurts to ask about that and bring it up. Some health symptoms — Some health systems have a flag for COVID status and vaccination status in an easily accessible tap on the left. Quickly whenever I prepare for a patient, I always look at that to look at people’s vaccination status. The antibody testing, it is a great question. A lot of the studies on antibody testing showed different labs have different classes and it can be hard to interpret. The best use case right now is often for people with transplants and things like that, to look at antibody levels and look at has their body responded to vaccination, and that is where the antibody testing is very well studied and useful. In general, we are not using antibody testing for now to see, did I have COVID in the past? Because we know the antibody levels can go down over time. They are impacted by vaccination and things like that. Your doctor might order them if you have severe immunocompromised. But generally not. It is not a test that we say less order for everybody to see if you have had COVID or not. I wish there was a test that said, this person had COVID this many times. But it’s just not quite ready for that kind of use as of now.
>> We know COVID is very complex. Good point on that. Ken fibrosis eventually clear on its own — Can fibrosis eventually clear on its own?
>> Before the pandemic, I would’ve said, this is scar, it’s never getting better. That being said, we have learned some fibrosis does regress. That does not mean that all fibrosis will regress. I would say patients with other types of fibrosis, I don’t think that has changed my opinion on that.
>> Thank you. What was the association of lung COVID for all ages? Just for adults? We know children can get long COVID as well as adults. That might’ve been with her question was. Since 2019, one of the most recent findings regarding long COVID patients who completed COVID vaccine regime and those who did not? That is always a data question that may be hard to answer.
>> We actually have a lot of research data on that now. Multiple trials including this Charlie mentioned showed — trial I mentioned showed the amount of long COVID is less and people that have had vaccinations. I tell folks that is never too late to get your first vaccine if you haven’t gotten one already to decrease your risk of getting long COVID. We see that experientially. Patients who got infected in March of 2020 where there was no vaccine available are often the ones with the most severe lu — severe long COVID symptoms. Vaccination’s been well studied.
>> We need that protection that we can. Is there evidence to promote —
>> I think it is not one-size-fits-all. I think this needs to be done. Some patients can rehab after an acute illness. I don’t think long COBE it is something that can necessarily always be done independently — COVID is something that can necessarily always be done independently. I want to make sure we are giving an individualized care plan on how to get stronger. Depending on symptomatology it depends on how fast we can go with patients and rehab. Our team and colleagues are amazing and they appreciate them everyday. — I appreciate them every day.
>> That is one of those underutilized options people have for that. Some people have not even heard of it.
>> Sarcoidosis is one of those diseases that can do a million things. They can do anything. In general, it is not found with tons glass opacities. We are not sure exactly why patients with lung COVID — some of them have these ground glass opacities. We are hoping to figure out the phenotype looking at different labs and figuring out if they do have an autoimmune process that is underlying it.
>> I’m sorry we are going a little bit over time. We have about four more questions. Have you seen an increase in atypical STREP after COVID?
>> I can’t answer the question about strep directly. We have seen evidence of more atypical infections in general. There have been more fungal elements seen in bloods, in the lungs. This is a part of the area of research looking at the got bio — gut biome. I think it is a big question because we also did a lot of viral infection in the whole world by shutting down for a while. Who is to say what the exact reason is? I will say it appears there are different infections that are happening. I’m not sure if we can say it is exactly because of COVID, global warming, shutting down. But things are different.
>> Someone asked — This is a big question. Do you have any idea how many patients have had to receive transplants due to COVID? I would say that one of those things where people who have persistent — really severe COVID with this fibrosis that doesn’t go away, they are at that stubborn plateau where they didn’t recover. Often people have had other lung conditions before that and got tipped over and now they have never recovered. Lung transplant is so challenging because you have to be quite sick to get a lung transplant but not too sick . The short answer is lung transplants have increased with the COVID pandemic. One of the most common causes worldwide of getting a lung transplant in the COVID arrow was infection due to COVID. That is often for that subset of people. There were severe respiratory failure for people who never quite recovered.
>> More lung transplants on top of our already overworked and burnt out medical staff. Someone else asks, our women more likely to get long COVID?
>> We are having some trouble estimating. There was a question about prevalence. I will direct everyone back to the article again of the recovery initiative that is at least hypothesis generating at this point and does show there is a pre — predilection for women to have long COVID
>> Along with all the other fun things like hot flashes that women get to deal with. We could be here all day. I apologize, we cannot get to all the questions. This is being recorded and will be updated to our website. Please join us for our next webinar which is actually tomorrow. We are doing two back-to-back webinars. Tomorrow is knowing the difference between asthma and COPD. Thank you everyone for joining us. Join us as we work every day to help everyone breathe better together. Thank you again both. You are fantastic and brilliant. Thank you.
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