Good morning and welcome. It's 9.15. We're going to perform a mini miracle today. We're going to get through five topics, each of them 15 minutes or less. We don't want to keep you from the next program that you want to get to. We have, as I said, a lot to get through. Just some general announcements. Number one, welcome. Hopefully you're having a great time at the assembly. Cell phones, please put them on quiet. Don't forget to fill out your evaluation forms and claim your CME credits, and don't forget to visit the pavilion. The work you're going to hear today is the work of hundreds of physicians, you know, based on thousands of patient hours of experience. The PASS Collaborative is a collaborative of many specialists and specialties run by the American Academy of Physical Medicine Rehabilitation, with many publications, eight to date. You can find them online. They're open access. The work we're going to present today is really an update from the work that we did over the past several years. We presented last year and these are updates. It's going to be bullet. It's going to be fast. Hopefully some very powerful information for you. We're going to start with talking about physiatrists and physical medicine rehabilitation and PASC management and key partnerships. Ben Abramoff and Eric Herrmann will be presenting. Dr. Ben Abramoff is an assistant professor of physical medicine and rehabilitation at the University of Pennsylvania Perelman School of Medicine, and Eric Herrmann is a family medicine practitioner who currently practices at the OHSU Gabriel Park Family Medicine Clinic. And with that, we'll get going with Ben. Thank you. So as AAPMNR and this group kind of came together, we really wanted to be conscious of doing it in a very interdisciplinary, multidisciplinary form. And in the true spirit of that, Dr. Herrmann and I are going to be kind of handing off throughout this presentation, demonstrating some of those interdisciplinary collaboration. So I showed this before, but the government, national health organizations, they really feel that finding places that patients can come and getting multidisciplinary care for complex conditions like long COVID is really important. They think, go to one stop shop, don't be going from specialty to specialty to specialty. Unfortunately, there's a lot of hurdles to do that. So when we, you know, if you're creating a long COVID clinic, if you have a long COVID clinic, what are the things you want to consider about your clinic? How do you develop a clinic that's effective? You think about the setting, inpatient versus outpatient, one location, multiple locations. How do you, how do patients get access to it? I think this is a struggle for many of our overburdened clinics. Only people who have resources or they know connections can get in, in a reasonable timeframe. And those who have low health literacy may be left behind. Who's on the team? Physiatrists obviously is, in my opinion, a key component, but how do we work with the primary care specialists? How do we work with other specialists like pulmonologists, cardiologists? The therapists are a really important part of the team. Staffing. So beyond just the medical providers, who's going to be answering the phone? Even in our clinic, which has been there for, you know, two and a half years, three years now, sometimes the schedulers, when they call the main PIN number, don't know about the clinic, don't know who to call, don't know how to schedule, don't know the criteria to be seen in clinic. So this can be challenging. How do you collaborate again with other providers? What do you offer? Are you just doing triage? Are you offering therapy as directly part of the program? Methods? Are you doing virtual visits? Are you doing in-person visits? I think all those are important as you think about how do you collaborate? How do you make a clinic? How do you work with other clinics? I've shown this slide before as well. This is some models that are out there of long COVID clinics, and there's since then even more of these, but they take many different formats, and we'll go into those in a little bit more detail. So this was a study of Canadian long COVID clinics, and they found about four major types of programs. There's units, so multidisciplinary care at one location, programs, a set of services across multiple centers or locations, so all integrated but not at one physical location. Coordinated efforts, so this is not necessarily working together, but everybody kind of focused on the long COVID problem, maybe having specialists that are referred to because they have an interest in long COVID, and then just general chronic care support. So there are all reasonable, but we don't know which of those models is the most effective, and I think that's one of the lessons is that we're still learning about how do we give effective care to these patients. The treatment team, many specialists are involved in caring for patients with long COVID. Therapists, obviously a key part of the team, but neurology, cardiology, psychology, those percentages are from an old survey looking at which specialties are involved in different long COVID programs, and you can see many of the programs had over 10 specialists as part of that team. So, and I'll tell you, having done this and talking to other clinics around the country, specialists and other programs are pulling back. People are like, I don't really feel comfortable taking care of these patients anymore, or I don't have the bandwidth to take care of these patients, or I see so many long COVID clinic patients that I don't have time for my COPD patients or my cardiomyopathy patients. So this was from a technical brief, which we'll be going into in a little bit more detail, but one thing that we really want to focus on in this presentation is how do you work with your primary care providers? So they asked specialty clinics who are long COVID clinics that have pulmonologists and cardiologists, how do you, how do you work with their primary care providers? And these are some of the example responses, which, you know, I think we feel may not be quite adequate. Patients may initiate follow-up care at any time, you know, kind of logical. Transition back following symptom resolution, again, very nebulous. Physiatrists can provide recommendations to the PCP to carry out. Again, not really true teamwork and working together. So, so what do we, what do we think PCPs can offer? And obviously Eric will have more to add on this, but insight into patients pre-COVID status. Do they have issues like chronic pain, chronic fatigue? How do they engage with their patients? Support for other conditions that either come up acutely or new chronic problems? And how did you co-manage? And with that, we'll go back into a little bit more detail about the technical brief. Thanks. So just recently the Agency for Healthcare Research and Quality published a technical brief on the long COVID models of care. And this was really intended to be a state of the union. And they did a literature search and we interviewed about 20 or so key informants. And this gave us the opportunity to kind of understand what's really out there around the country and something internationally. Kind of what is a cogent framework that we can start to think about with these models of care and how can they apply to others that are currently seeing patients or make that more extensible to new sites. And so after we did all the interviews and the dust settled, we came up with about 10 models that seemed to be representative of what we're seeing out there. And to just kind of walk through this quickly, I think the two main core components of this is one, who is the core team managing the patient? Who's responsible for that care? And the other is where is it housed? Where is it located? How are you organizing that system of care to meet the needs of the community? So the first couple you'll see are really truly dedicated sites just for long COVID care. The main difference, who is the principally responsible for the management? The first example, it's physiatrists or pulmonologists, it's specialty practice. They're evaluating the patient, making the plan of care, making referrals, ordering the studies, etc. The next one is a multi, sorry, the next one is sort of primary care led where it's a dedicated site just for long COVID but primary care docs are the one managing it. Others have taken a more multidisciplinary approach. Same thing, there's one core team that's principally responsible but it's a multidisciplinary team. Physiatry, physical therapy, cardiology, psychiatry, psychology. You can see there's some benefits to that but there's some challenges in terms of organizing all the resources. And then the others are sort of moving into some interesting models and there's a scarcity of resources that we all have. And as you can imagine, one clever way of trying to organize all those resources is sort of moving to some virtual pieces. So there's some virtual models. But another one that was coming from the VA that was interesting is a long COVID and sort of a clinic board model. So there'd be a practitioner seeing the patients dedicated to long COVID and then each patient would systematically be reviewed by a governing board of experts, clinicians, telehealth remotely. And so you can see again, there's power and there's possibility there to meet the needs of the community where we can't meet the demand alone in these specialty practices. And there's some others. There's mobile sites that go to rural communities and there's some other practices that are just not long COVID specific, but long COVID, chronic conditions, MECFS. And there's even some that are strictly embedded within the fabric of a busy primary care practice, spending additional time and energy to increase the fluency of those practitioners managing these. So those are all available. And so when you looked at the key principles for managing these patients well at all of these sites, five things still stilled. The first is there really needs to be that nucleus of knowledge. Who are the folks that have the iterative experience, the shared learning, the pearls that they know best about patients of long COVID and keeping that tight. And so who is the core team? That team needs to have access to what's essential for patient care. They need to be able to make referrals to the specialists, particularly physical therapy, occupational therapy, and they need to have access to some of the testing that you might not get otherwise. Autonomic reflex testing, cardiopulmonary exercise testing, those things. It's a complex condition. Every patient has its unique fingerprints of how this condition affects them, particularly if we start to think about things like dysautonomia and such. So really having patient-centered equitable care is essential and meeting the demand. Here are 10 key components, sort of the ingredients of these sites. I'm not going to go over them in details because of the time. The only ones I'll really bring your attention to, I don't know if the clicker works here, let me see. Nope, it doesn't. Five, six, and seven. How are you managing the populations? And I want to put a special call out here for health equity. It's often the last thing mentioned, but never really the first thing done. I can tell you that urgency breeds inequity. And most of our practices, we just did our best to get things up and running, but there are so many people from marginalized communities, non-English speakers, who aren't getting to us. We really need to think about how we arrange our systems of care to do that. And then if you're thinking about your outcomes, that intake becomes important. What are you doing right up front to make sure that you're going to be able to track the outcomes that you want later? And do you really have the system of care to help patients across a challenging health care system? This is it. This is what you want. So, barriers. Obviously, physiatry, this is a new condition. We're still learning. We didn't, many of us, myself included, did not get much education on ME-CFS in medical school or residency. It's a diagnosis of exclusion. So, I know personally, you know, I was going out, I had to learn to go outside my comfort zone a little bit in terms of, you know, these patients have undergone cardiac workups, you know, pulmonary workups oftentimes, but do they need more? You know, they haven't had PFTs. They haven't had a CT scan. Is that something that we want to order, or do we defer back to their referring providers or their PCP? Resource-intensive, needing appropriate staff, time. It's very time-consuming to manage one of these clinics. Coordination, record review. Oftentimes, patients come with stacks of prior records, communicating with these other specialties. Paperwork and disability form. Again, lack of clear evidence. Delays in accessing services. So, you can have a long COVID clinic. It's up, it's running, it's great, and then you say, well, you definitely need to see a pulmonologist, and it's a six-month wait. You know, I think that can be very challenging, not only for us, but for our patients, particularly in mental health support. So, I put long COVID is ideally managed by a PM&R, by, with a star and an asterisk, as part of an interdisciplinary team, and this may not be fully endorsed by all presenting members today, because why? It's a multidisciplinary team. It's a multi-system disorder, just like spinal cord injury, just like traumatic brain injury. It focuses on palliative care, making people feel better. There's no cure yet. Tailoring the treatment to the individual. Oftentimes, you need creativity, continuity of care, and how do we provide adaptations to get patients back to that function, to get them back to work and school? And as you can see from this old survey, PM&R was where many of these clinics are housed. All right, so yeah, I'm the cute and fuzzy family doc here telling you about this stuff, but a couple things. We have very little time left, so I'm going to make a couple points here. One is, you're probably asking the question, what are PCPs looking for? And what I can tell you is, in a word, well two, thoughtful co-management. They want a partner, and particularly when things are rough, they want to be able to go, who can I talk to to make sure that I can get my difficult questions asked? It's co-management. It really needs to be done in a way where people understand what's the role of the physiatrist? What's the role of the primary care doctor? Make sure patients understand that, because otherwise they're going to be calling you and me with lots of questions. Really important to convey that, and then some of the medications for managing POTS and things like that are unique, so really do a careful job of outlining what those medications are. Here is what I think would be the David Letterman top 10 toolkit of the things that you should probably have in your practice as you're managing. The best practices, a lot of the folks in this room have developed some guidelines here around how to manage it. CDC has some. What are the survey instruments you want? MOCA, COMPASS 31 for dysautonomia. Make your documentation template quick and clean, and I'm going to show that just at the end here very briefly. How do you want to get that done? Make your patient instructions concise. They have brain fog. It's hard to manage. Make sure your protocols for PT are shared with your community teams. A lot of PTs aren't familiar with managing post-exertional malaise. Have to try to get that in place, and really think about health equity and making sure that your teams have the ability to help patients with disability applications and FMLA. It could be one of the most important things you do. Here is the documentation template very quickly. The APSO notes right up there in the yellow, nothing there, and then left you'll notice two, this is where the meat is, there's two main questions. What are the symptoms that are affecting their quality of life the most? The symptom list is going to be enormous, and so really getting to what affects their quality of life and what are the goals of care are going to matter, and then the left is your, you know, your impairment issues, and then at the end on the left, what is affecting your employment, your financial status, and social support. And then just to finish up within our time, we don't know the ideal model of care. This is something that is very difficult for any one institution, one person to study. It has to be done really at a national level, but no, you know, think about it. Be conscious of your model. What population are you trying to serve? Are you serving that population? What are the costs associated with it? Is it leading to improvement? What are your goals? What are the outcomes you're watching? Because that's really important for health equity. Ensure strong alignment with your PCP, have a referral and follow-up process in place. I think this can be, as we think about this as a new condition and how we approach it, I think it can really be a model for other chronic diseases, other complex issues, and then the AHRQ technical brief is now open for comment. It's a really great document. Check it out, comment if you have any thoughts. Thanks, guys. That was 15 minutes. We did, because of the introduction, go, you know, I ate into your time, so well done, guys. Next up is Joe Herrera and Alba Azzolo. We're going to be talking about the updates in understanding and management of PASC related fatigue. Dr. Herrera is chair and professor in the Department of Rehab Medicine at Mount Sinai, and Alba Azzolo is assistant professor at John Hopkins School of Medicine in the Department of Physical Medicine and Rehab. Thank you. So I'm from New York, and so I'm a fast talker. So I uploaded all my slides for your own edification. I'm going to run through them relatively fast, because there's a ton of information on there, but I'll highlight the key slides here for you to take a look at. So I just want to acknowledge Dr. Tosto and Dr. Petrino for helping me gather the data, helped me with the slides, and put the framework around our approach to fatigue. So today, and we already went over the definitions, and from the data that we collected earlier to now, it seems to be still the same. Fatigue is one of the higher, most reported disease processes and symptoms that we see in long COVID. So these are our steps towards a comprehensive long COVID clinic. So ours is number two on the list that you saw there. We're a multidisciplinary long COVID clinic. We collaborate with primary care, endocrine, cardio, palm, psych, etc., and all of our patients enter through any of those pipelines and PM&R, and then we send them to whatever specialty that we need at that time. So within our group, we decided on a few intakes. So now we have a standard intake for all of our patients, and we divide it into three different days, mostly because, you know, there's such a long wait now for our long COVID patients. And this is our blood work. Again, I won't sit on the slide. You can take a look at it. We're looking for co-infection, looking at hormones, vitamins, and minerals. They go in and get a second round of blood work for coagulopathy and looking for inflammatory markers. You can take a look at this. It's now built into our Epic, so it's easy to click as we go through, and patients go ahead and get that work. Now I think this is a little bit more important here. Before they even see a physician at this point, the patient reported outcomes, all right? I want to stress that because that's the only way that we know whether or not what we're doing actually works, right? So our patient reported outcomes for fatigue for long COVID versus recovered, this is in the Klein paper that just came out this November in Nature. So our group, along with the group up in Yale and with Klein, we gathered our data, and you can see for those who have long COVID versus those recovered, there is an improvement, okay, according to the fatigue outcome. We also did NeuroQOL, and again, you can see that after our interventions, and mind you, rehab is only one intervention. There's a lot more there, and there's still a lot we don't know. I just want to stress that. So there's still a lot that we're learning from our patients and from our other colleagues. And then this is the health-related quality of life. Again, we see an improvement from those who have long COVID and those who have recovered. Once we have the intake completed, then they see a physician, whether it's a physiatrist, a primary care, psychiatry, and that usually takes about an hour. And I'm gonna probably take your template that you put up there, because there's a lot of information that we go through and it's a true hour, sometimes it's an hour and a half for an initial evaluation. After the intake, then we decide, okay, do they need anything more? Whether it's an EKG, pulmonary function test, chest CT. So then they then go through this whole workup, especially for brain fog, fatigue, et cetera. And then we do the prehab. So this is a great resource. So step one, we educate our patients on symptom management. Long COVID Physio outlines this. We send them this link and now they do their homework on this. And it goes over everything from pacing and energy conservation, emotional regulation, hydration plans, environmental management, planning meals and mealtimes, mindfulness, awareness, et cetera. The other thing that we focus on here is breath work. So one of our researchers, Dr. Wood, along with our colleagues up at Yale, used handheld capnography and found that a number of our patients were hypocarbic. So with our breath work protocol, sorry, hypocapnic, with our breath work protocol, we saw that there was an improvement in a hypocapnia. Is this something that helps them? We're not sure, okay. But we know that there is an improvement in one objective measure that we've seen so far. And a lot of our patients have reported that with breath work, especially with fatigue, there is an improvement in energy. And then once we do that, this is our autonomic rehabilitation program. There's actually a detailed instruction there. So you can hand it to your local physical therapist. So we've collaborated in New York with a number of outpatient private practices within our trusted network. And we share this with them, and we then send a pipeline of our patients to those private practices. And I'm just gonna breeze through this. This is, again, take a look at this on your slides. There's three phases, and here we go. After physical therapy, we do see an improvement in the 10-minute walk test, six-minute walk test, and the number of symptoms that have been reported. Although, again, this is not the be-all and end-all, and this is not the cure for long COVID, all right? So therapy is one key component there. And you have to educate your patients that this will take some time, you know? So it's not gonna get better in a week, two weeks. On average, it takes about three months to see some meaningful results, and meaningful results doesn't mean completely normal, okay? And then, as far as, oh, and this is some of the content that we share with our therapists, so that they can log on and take a mini-course for their rehabilitation guide. And now I'm gonna hand it over. So I'm Alba Azola. I work at Johns Hopkins and I'm an assistant professor and I'm going to talk about fatigue in COVID and how our group has utilized insights from the treatment of ME CFS into treating patients with long COVID or a subgroup of patients of long COVID. No disclosures. Some of the key points, how do we identify the subgroup of patients? What are those features that we're looking for to understand that they meet criteria for ME CFS? Also, this group is not a random bunch. They have many comorbidities that are similar to the ME CFS or what we have seen in the history of ME CFS. So what is the clinical diagnostic criteria? One, substantial impairment in activities that were well tolerated before that are affecting the patient for more than six months. Post-exertional malaise is an exaggerated response with a flare of symptoms that comes after minimal activity. That has to be present. On refreshing sleep, cognitive impairment or orthostatic intolerance, they don't have to have both, actually. But we do find that orthostatic intolerance is one of the main components of the fatigue that we can actually intervene and treat them. So we look at the patient through this spokes wheel model where we look at all the potential common comorbidities that this population has and we see which ones are most predominant in each patient and how we can manage that to improve their function. So I'm going to talk briefly about just a few of them since the time is very tight. But our group at Hopkins in the 90s started identifying this relationship between orthostatic intolerance and chronic fatigue syndrome. Also, within that pathophysiology, we see a decrease in cerebral blood flow and an increase in pathogenic response. But it's not only those patients that meet criteria for POTS and have a brisk elevation in heart rate. We also have patients that have decreased brain blood flow with normal heart rate and blood pressures without significant changes on those. So we have a collaboration with Linda Van Kampen from the Netherlands. They look at brain blood flow through carotid Doppler and vertebral artery Doppler and measure the amount of blood flow that comes in. And they had been doing this work with the MECFS community and they took a cohort post-pandemic of patients with COVID that met MECFS criteria. They looked at the symptom clusters, extremely similar population. Again, this is part of what their work is doing the Dopplers of the carotid arteries. You can see the long COVID subjects before and at the end of tilt. And you can see that there's a 39% drop of blood flow to the brain in patients that are healthy controls. It's only 8%, about 7 to 8%. And when we look at all the different cohorts and how they compare, we have healthy controls with that minimal reduction, which is normal. We have a group of COVID MECFS patients with a more significant reduction in blood flow. But again, we have those normal blood pressure and heart rate patients who still have a significant drop in brain blood flow. So another area that we concentrate in is identifying patients with hypermobility spectrum disorder. This is extremely common in this population. And typically because of this change in the fibular collagen and the fibular collagen is everywhere in our bodies. These are multisystemic presentations. You can catch them because they have early varicose veins or easy bruising, or they've had dislocations of their shoulders. And then this myofascial pain is pretty prominent in this group of patients as well. And you can screen for this very quickly. You can do a Bayton scores and nine point scale and score higher than four. It's kind of the threshold for their likelihood of having hypermobility. I have a nine, but I didn't get long COVID. So there's definitely a relationship between hypermobility and orthostatic intolerance. This was demonstrated again with earlier work. You can always screen them also by asking them if they can do a party trick. They are very flexible. And also noting their healing for wounds. A lot of them have issues with healing and striae that's darker in color actually than normal. We also see acrosianosis in this patient population. So this is somebody supine and somebody, the same person sitting for 10 minutes. And you can see the discoloration, the blood pooling. You can also see a little bit of delay in their cap refill. And in people that have more melatonin, it's harder to see those changes of the vascular congestion. You can always check the bottom of their feet. You can see a change in color there and you can identify that's low cap refill. Hypermobility in patients compare normals versus ME-CFS patients. There's certainly an increase in baton scores. I'm going to quickly go through mast cell activation and some food allergies. Those are extremely common. Again, there's multitude of documentation of this relationship between mast cell activation and orthostatic intolerance and long COVID. We look for new onset food allergies and milk proteins, lactose intolerance, eggs, urticaria, dermatographia is common. This one I'm going to skip by but it really has a multisystemic impact when we look at these patients with mast cell. This is what we're looking for in clinic. They often have blotchiness. It can kind of come and go. And that's it because I don't have time. But also another thing that we look for is vein issues or blood flow issues. They can have pelvic congestion. Sometimes treating that helps treat their orthostatic intolerance. Sometimes if you have a patient that didn't do well with medications and they're still having issues, look for things like pelvic congestion syndrome because that can also be one of the causes. And also cervical spinal issues and that's it. I just want to thank my team. that this session is being live streamed. People who are on the live stream, thank you very much. You can put questions into the electronic system and we'll get them here on the iPad. We'll take questions at the end and people will use the microphone. We're now gonna talk about long COVID as it relates to the cardiovascular system and updates. I'm Jonathan Whiteson, I'm one of the professors of Rehabilitation Medicine at Rusk Rehab. Carmen Terzic is a professor of PM&R at Mayo Clinic in Rochester. Carmen wrote a fantastic article and this essentially you can see here that there are significant issues with regards to cardiovascular disease, all elements of the heart. So the heart muscle, myocarditis, and also you must have heard that many people have been suffering from after acute COVID. And again, a continued elevated instance of their post COVID. These are some of the symptoms that patients may present. We're looking at the potential mechanisms. And again, I'm gonna focus really more on the myocardial of the hyper inflammatory response and also in type two myocardial infarction. And in the long COVID stage, myocardial infarction. This was a study that was just recently published triggers myocardial to have coronary stenosis at postmortem. And it's already known that myocardial infarction and stroke are complications of COVID-19. This was a preamble to the study. It's known that other viruses as well can cause stroke and myocardial infarction. But patients with COVID are seven times more likely to have a stroke than patients who had influenza. So this is different. This is a super virus, so to speak. And the risk for heart attack and stroke remains high for up to one year following the acute COVID. So this was their premise, the possibility that SARS-CoV-2 affected the coronary vasculature. Certainly there was a significant or there's a known to be a significant inflammation in the lungs. And maybe there's something similar happening in the coronary vessels that's affecting the atherosclerotic plaque. So autopsy specimens show that the macrophages within the atherosclerotic plaque were infected by SARS-CoV-2. And it was felt that these lipid-laden macrophages were more susceptible to SARS-CoV-2. And that's what set off this inflammatory response that led to myocardial infarction. In the discussion, they said that the study provides evidence that SARS-CoV-2 presents in human coronary vasculature and demonstrates viral tropism for vascular lesions. That SARS-CoV-2 is capable of infecting and replicating within the macrophages in the coronary vasculature. And that this persistence, you know, is related to the fact that SARS-CoV-2, the virus lives on in macrophages within the atherosclerotic plaque. So in summary, SARS-CoV-2 infection of macrophages and foam cells promoted a strong inflammatory response. The coronary vasculature is more susceptible than other vascular beds. And it's this hyper inflammatory response that really leads to progression of atherosclerosis and cardiovascular complications associated with COVID-19. These are just for your review when you look through the slides. In summary, certainly we see significant incidents of cardiovascular disorder in the acute phase of COVID. And we also see it in the post-acute phase of COVID, but probably not as much as in the acute phase. Again, a lot of this data is somewhat adulterated depending on where you're taking your sample from, whether it's the ICU, whether it's from the initial phase, whether it's from a later phase, whether people were vaccinated or not. So we still have to let the dust settle with all of this. The types of cardiovascular disorder. Yes, we see cardiomyopathies, arrhythmias and ischemia and the biologic mechanisms, mechanisms, plural, it's not singular. Acute plaque rupture, probably related to inflammation of the cytokine storm. The persistence of SARS-CoV-2 within the plaque causing hyper-inflammation and oxygen supply mismatch, immune dysregulation and autonomic dysfunction, which will be part of a talk later on. I will stop there. Hopefully I kept within my few minutes. Thank you, Jonathan, for this nice presentation about the symptoms and complications. As you can see, many, many of them, and we see this in our daily practice. But even in a patient that they don't have documented cardiovascular issues, you can see that there is a significant impairment of the cardiovascular response to exercise. So this is a study that we published from our group showing that the peak of VO2 when they do cardiopulmonary exercise stress testing is a significant decrease in this patient, even if the pulmonary response is within normal. And this is, again, another study from our group showing the percent of patient that they have a decreased VO2 when they underwent the testing, this cardiopulmonary exercise testing. So we don't know if it's the conditioning, because those are, we see this in, of course, if the patient have cardiovascular issues, it's reasonable, I mean, we understand this finding, but some of these findings we see in patient that they don't have any documented cardiovascular disease. So what is the reason the conditioning, comparing O2 extraction, cardiac output? We don't know. It is a cardiovascular disease with other cardiovascular diseases we have not identified, or heart failure with preserved ejection fraction. So we don't know. So more to come in the years. But the most important, that this individual needs rehabilitation. This individual need interventions to improve their cardiovascular function. And again, as you will see, this is the common thing that we don't know. We don't know. There's not enough data that can guide us, specific scientific data that can guide the prescription. This is more a consensus of expert. But those are the general recommendation that I would like to discuss in the few slide. First of all, exercise program have to be individualized, because people have diverse type of symptoms, and the severity of the virus too. And I think it's important to assess exercise capacity before we review that for the outcome. This is very important. Dr. Herrera gave a nice presentation about that. Important to document outcomes. So you can either do exercise stress test. If the patient is very deconditioned, six-minute walk test will be very good. Then PT and OT, don't forget about that. It's not only cardiorehabilitation run by cardiology, but the physical therapy and occupational therapy intervention are key, especially in frail patient that they cannot tolerate too much exercise. Another important element is start with small dose of exercise and progression. So start slow and progress slow. That's this key. Individualized and slow progression. And if the patient develops symptoms, just stop and observe and reevaluate it. You don't have to rush. And participating in cardiorehabilitation program is ideal, because it's not only the exercise prescription, exercise control, supervised exercise, but also control of all their cardiovascular risk factor and psychosocial aspect of the patient, which are important part of the program. However, reimbursement may be not available if the patient doesn't have the criteria that are covered by CMS. And maybe some of our centers are not, in PM&R centers are not, they don't have staff prepared to deal with this patient. But those, I think, if the patient is a candidate for cardiorehab, it can be covered by third payers, please, I think that this will be the best, best intervention for this patient. Another consideration, if the patient had myocarditis, as Jonathan mentioned, many of these patients develop MI, myocarditis, heart failure, you should not start any cardiorehabilitation or any exercise program for three or six months. This is the general consensus. If the ejection fraction is within normal and there's no arrhythmia, then you can start exercise program very light, at three months. But if the patient have low ejection fractions, you should not exercise, the patient should not exercise for six months and should be reevaluated before any decision. And a cardiologist should be the right person to evaluate this patient. In general, following the POTS principle, you start with no weight-bearing activities like recumbent cycles, stepper, rowing, machines, very slow. Daily frequency, multiple daily session, as tolerated, you don't have to do once, you can divide in many session. Five minutes each session, you can add one or three minutes as tolerated. So the goal is to reach 30 to 45 minutes of continuous exercise. Low intensity, using the Bohr exertion scale, I think will be the best. And again, progresses slowly. Keep repeating that. Individualized and progression should be very slow. And for resistant exercise, the same thing, the same principle. You can start with two or three session a week, start slow, increase the repetition slowly, and eight to 10 as three set, or eight to 10 repetition, one, two, three set. Again, start slowly. And you can use elastic band, hand weight, body weight, and then you can progress to more weight training machine. And again and again, gradual progression. This is very, very key. And I like this figure because this really summarize all the recommendation that we have today for patient with long COVID. And we talk about the aerobic exercise with the frequency to start and how you continue. We did talk about strengthening exercises. Now, one thing that we need also to introduce in this population is the balance exercise. We know that many of these patients have a lot of orthostatic intolerance. So balance exercise, flexibility exercise too. Do not forget that. And Dr. Herrera mentioned about that respiratory rehabilitation training. I think this is very important and we don't do this very often, especially for patients that they are very, very deconditioning patient with heart failure. So that have been shown to be a very good intervention. And also psychological treatment, where we talk about cognitive behavioral therapy, relaxation techniques and muscular relaxation, breath control, so very important. So in summary, there is no any evidence-based guidelines for returning or starting any exercise program for patients with cardiovascular symptoms associated with long COVID. So nothing there, it's a consensus. Exercise training, it has to be carefully prescribed, require individualization and appears to be beneficial. We all agree with that. Cardio rehabilitation program is very well placed to provide the supervised exercise training and is advised for all individual that meet the established criteria for cardiac rehabilitation. And others that they don't meet this criteria, they will benefit of a program similar to cardiac rehab and it's recommended that it's provided by a multidisciplinary panel of experts as you have heard in previous presentation. And thank you, and this is my contact number. You have any question? Hopefully we meet on time. Thank you. Okay, Matt, we're now gonna talk about the management of past related pulmonary disorder. Dr. Bartels is lucky. Jason Maley, who was his partner in crime to present was unable to make it. So Dr. Bartels gets his full 12, 13 minutes, very lucky man. Dr. Bartels is Professor and Chair of Rehabilitation Medicine at Albert Einstein College of Medicine, Chairman of the Department of Rehab Medicine at Montefiore Health System. All right, so we're gonna start and I'm gonna be very blinded on this. I'm not gonna talk about whole programs and things. I'm gonna talk about pulmonary stuff. So disclosures, none that are really pertinent to this. So I'm gonna talk a little bit about what we see with PASC and primary care, or the primary pulmonary conditions, a little bit of the respiratory complications, some of the appropriate precautions, some of the correct prescriptions to write and how to progress these individuals so that they're actually advancing in a way that's actually improving them and not actually causing any further complications. So this is a sample case of somebody that was one of our classic cases that we saw in about 2020. 50 year old nurse working at our institution contracted COVID-19 in the height of the pandemic, was in the ICU with high flow oxygen, eventually had intubation in a tracheostomy place, weaned over several weeks, discharged home on six liters of dazzle O2, lost sense of smell, had cognitive issues with decreased memory, word finding issues, concentration, also a lot of debility. After three months was still on high flow nasal oxygen, PFT showed restrictive effects. They've reduced DLCO and there was also residual ground glass on the CT. Six months down to two liters via nasal cannula and four liters with activity. One year was weaned off of O2 and up to two liters with activity and at two years off of all O2 and finally returned to work part-time, still has the tracheostomy. Why? Because she's a keloid former and we can't get the dang thing out. So every time we try to remove it, we have to reinsert it because she scars. But otherwise is doing quite well. Thanks to the New York Times Journal of Medicine. These are some of the nicest illustrations of what COVID lungs look like. You can see there's extensive diffuse damage and scarring throughout the lungs in people who had severe COVID. And what happens with recovery is that this damage continues to persist. It's mostly alveolar and it looks a lot like an interstitial lung disease. We don't have definitive answers on what happens with this, but the people who have this either progressed about five to 10% with progressive worsening of their lung disease. And we have a lot of patients who now have lung transplants or on transplant lists because of it. Or they had gradual resolution, never 100%, but thank goodness they don't need a transplant, but they still have residual lung damage and deficits. Some patients up to a loss of about 30, 40% of their total lung capacity. So it's like and not unlike other conditions, but I'm going to actually do a quick survey here. How many people in this room have not had COVID? Raise your hand. We've seen these things where we're talking about up to 40% of people with COVID have these diseases. How many of you people have long-term pulmonary sequelae? All right. I don't know whether it's because we treat it better. I don't know whether it's because of the vaccines. PaxLavid has been in there. We use steroids appropriately, which we didn't in March when this poor woman was, my sample case had her disease. It's not the same disease. It may be the virus is smarter and it's become a better virus, which means it's more infectious, but less virulent. So it doesn't actually cause as much damage because it's not good for a virus to kill your host. You want your host to live and spread. You don't want your host to die. Also, we have had a recent surge in New York. We had only maybe five to 10 patients in our hospital at any given time with COVID and most of them were not in the ICU. They were just admitted as if it was a severe flu and they went home. We are not seeing the intubated, damaged lung patients that I'm demonstrating here. That doesn't mean that we don't have a lot of long COVID patients with that. I'm still treating patients from three years ago. But new additions to my population are now becoming far less common from a pulmonary point of view. Not talking about the cognitive, the fatigue, those things are still there, but from a pulmonary point of view, this disease has actually morphed into a less severe thing, fortunately, from the most majority of patients we see. But it's undiscovered territory in that this is an infectious, highly scarring disease, so we didn't really know where it was gonna go. It's overlapped a lot of other areas with pulmonary rehab. So fortunately, we had ways to treat this and we actually adapted those. The other thing that we actually did is we took a lot of these patients who had multiple conditions and enrolled them in our pulmonary programs because that would be paid for. As Dr. Teresica just mentioned, sometimes it wouldn't be paid for, but if they had the pulmonary scarring and damage, we were able to get them into the program. And until the end of the public health emergency in May of this year, we could even get at-home pulmonary rehab, which was a very useful thing for a lot of our patients who had limitations because they had to carry oxygen, transport, other kinds of that thing like that. This is just the multidisciplinary thing. I'm just putting in a plug. Most of the recommendations we have in here are still in effect, and all of the workup and things are in effect. Fortunately, we have less severe patients, but these recommendations pretty much still stand. So what are we doing? You should actually assess the patients. I'm not gonna go in detail through this, but you should get a good history, find out if they had pre-existing lung condition. Our experience has been people with pre-existing emphysema or pre-existing interstitial lung disease did worse than patients who never had. Patients with asthma, interestingly enough, had a lot of symptoms, but most of them resolved. So that was actually a very fortunate thing. You also wanna take a look on a good physical examination, see if you find other secondary symptoms. Pulmonary hypertension, particularly in our hypoxic patients, is not uncommon, and that can be a very large problem with chronic management because it's not necessarily the lung disease, it's the pulmonary hypertension, which leads to pulmonary causing right ventricular failure, which can actually lead to really significant morbidity and mortality. So do assess patients. Listen to see if you hear a split P2. If you're suspicious, get the echo. Respiratory issues, chest imaging. Almost all these patients have it because if they weren't severe enough to be hospitalized and get this, they generally don't present you with a lot of pulmonary symptoms. But those patients would have the chest imaging. Follow-up chest imaging has a little bit of benefit in that it shows you that there may be some resolution, but unfortunately, a lot of these patients, it takes a couple of years to have really good image resolution, and some of these patients, particularly with severe disease initially, will never have full resolution. But it is actually sometimes comforting if you're thinking, well, are things getting better? You can do the imaging. Pulmonary function testing is very helpful, but you usually see restrictive physiology, meaning they cannot take deep breaths. It's not obstructive as you have with pulmonary patients who have COPD. The other thing too is that you may find that they have very low DLCO. This is a population of patients that getting the diffusion of the lung for carbon monoxide is a very important part of the test. So it's not a simple spirometry. Get the DLCO, because that actually lets you know if there's more damage causing hypoxemia, because a lot of these patients will present and look great at rest, but when they exercise, they can't keep up and they desaturate, so they may need oxygen with exercise and activity. Accessing breathing. Take a look at how they breathe. It was discussed that with some of the chronic fatigue patients, there seems to be a lot of hypocarbia that you see with patients who have restrictive lung disease. Why? Because it's hard to take a deep breath, so they breathe like they pant. So that they're actually not oxygenating well, but they might be able to actually drive off their CO2. And especially with the scarring, this may be a situation where they have low CO2 and low O2. Doing the respiratory muscle training is actually a very helpful thing to actually get them to do this and take deeper breaths. Also, diaphragmatic breathing. The diaphragm is the best way to reinflate those scarred lungs. So this is another thing that is very important. So I agree also with Dr. Tercik that this is something that traditionally in pulmonary and cardiac rehab we didn't do, but in pulmonary we did. I think it's something in our patients who have had cardiac symptoms or issues from COVID that we should also probably institute some respiratory muscle training. Pulmonary medicine. When do you call them in? If you're a physiatrist who's seeing one of these patients, if they have severe hypoxemia and it's not resolving, or if it's getting worse. Now, if they come to you and you have been having this person referred to you and they're on oxygen, it may, as long as it's stable or getting slightly better, that's probably the natural course of the disease. The problem is if it's getting worse, it's not that we have any real treatments for long COVID interstitial lung disease, but they may need to then be assessed about whether or not they need to go for transplant. Because that progression can actually, if they then get a subsequent infection or pneumonia, cause a rapid decline and actually lead to death. So you don't want to be the person who said, oh, I wish I had referred them six months ago because now they're so sick that we can't actually do anything. Home oxygen. Quick discussion on this. There's a lot of options now that weren't present before. And because of the fact that there was such a need for oxygen at home, there's a lot of it available. And there's a lot of companies now that have excess equipment because they bought all and they stocked up. During the height of COVID and for the first year or two afterwards, getting a portable system for patients was almost impossible. Especially with the supply line and the supply chain disruptions. I had patients waiting six to 12 months to get a oxygen system. It's better now. So you can get the systems if they need it. These are battery operated. They can be plugged into the wall or into the car. It allows people to have a lot more mobility. It's better than using a tank system. Although, if you live in an environment or have the patient live in an environment where blackouts are common and the electricity is not necessarily reliable, liquid oxygen systems are excellent. If you're gonna get blown in by a blizzard and you have a liquid oxygen system, it's full for a month anyway. The R2D2 unit looks like R2D2. The tank will have oxygen for about a month. So as long as they've been tanked up beforehand. Now, what do you do? This is a very simple thing. If you have a patient who lives in one of those environments, make sure that they notify their local police department and fire department that they are on chronic oxygen, that they need this, and that if there's an emergency, they're gonna need assistance. It's better for the local authorities to come knock on their door and say, are you okay? Than have them desperately trying to call 911 because they're running out of O2. So this is something that the local authorities actually appreciate and our patients have actually appreciated because then sometimes when there's a climate related or other disaster, they get picked up by the police, taken to the local hospital and they don't have to actually worry that they're gonna be running out of oxygen and be stuck. All these different systems, you just titrate what's necessary for the patient. When you have really high flow oxygen, it's sometimes better to make sure that they always have humidification because otherwise you dry out all of the mucous membranes and you get all sorts of other issues with chronic sinusitis and so forth. So hydration of the oxygen is also helpful. Other treatments, mobilization, maintain saturation, give the patients as much oxygen as needed. Even in a person who has a history of something like COPD, while they're exercising, they're not gonna get hypercarbic, but they must turn it back down to their base setting because if you go into recovery and rest and you don't turn the oxygen back down, you can become hypercarbic, but don't worry about using extra oxygen during exercise. Pulmonary therapy, if you look at this complex thing, if you get down to the bottom, it's progressive self-directed exercise using a Borg scale or Borg modified Borg we use usually in pulmonary with zero to 10. That's what you use for exercise for these patients. So all of these pathways will end up coming down to that common pathway of self-directed exercise, whether it goes through pulmonary rehab or if the patient doesn't qualify or you don't have it and you have to go through exercise, guided exercise treatment, it all goes that way. There are companies that are still providing home-based pulmonary rehab because pulmonary gets reimbursed at home a little bit better than cardiac, so you can actually engage with them if you have to do that. I'm not gonna go through a whole lot more about the performance exercise testing. Dr. Terzic mentioned it. If those patients are complex, a CPET is a very good way to go. Six minute walk tests are actually a good way to get a baseline assessment and a follow-up to make sure patients are doing well. Right now, what I would recommend for patients who have a severe ongoing pulmonary disease is to make sure they're involved in a good exercise program, transition to a good at-home exercise program, monitor their oxygen requirements. If they're still needing it now three years later, they're probably gonna continue to need it. If you have somebody who unfortunately has a very severe case of COVID and ends up with the ICU intubation course, they may actually progress into having to either have a transplant or have that long recovery. I am just saying that fortunately, in our COVID clinic, we are now seeing mostly patients that are coming in with fatigue, cognitive issues, and those things. But this severe pulmonary disease that we were initially hit with doesn't seem to be as common anymore. In fact, it's kind of an unusual patient that presents with that. And often it's because of a pre-existing condition that was exacerbated, not that COVID took a normal individual and created them as a very severe pulmonary patient. All right, thank you guys. Thank you. We're doing perfect with timing. We're now going to talk about management of pain-related disorders in PASC. Surendra Bhashakar is an Associate Professor in the Department of Physical Medicine Rehabilitation at University of Texas Southwestern Medical Center and is double-boarded in Physical Medicine, Rehab, and Brain Injury Medicine. And Lynn Weiss will also be speaking. Dr. Lynn Weiss is Chair in the Department of Physical Medicine Rehabilitation at NYU Langone Hospital on Long Island, is a Professor of Rehab Medicine at NYU Grossman Long Island School of Medicine. Thank you. All right. So in the next two presentations, we're going to talk about pain in Long COVID. And we have divided it such that I'm going to talk about musculoskeletal and myalgia muscle and bone pain, while Dr. Weiss is going to talk about nerve pain. So looking at this diagram here, cartoon here, we see there's multiple areas where pain is listed. And this was a meta-analysis that was published earlier in 2021. So looking at this diagram, you see on the top there's pain, there's headache, there's joint pain, there's myalgia, there's chest pain. So pain gets manifested in different systemic issues, and it's basically very common in Long COVID. So what do we know so far, or what has been proposed? So this is a cartoon, and the explanation that's along with it talks about the three mechanisms that this particular study proposed, which potentially explains why these patients have pain. So we know that COVID is really, the main pathologic mechanism of COVID is related to your ACE and the running angiotensin system. So that's the first mechanism. Basically what it does, it creates an imbalance between the angiotensin 2 and angiotensin 1, 7. So 1, 7 is antinosusceptive, so it's protective for pain. And unfortunately in COVID, that goes down while the angiotensin 2 goes up. So that's the one. The second one mechanism is a macrophage activation and the immune cells activation, which eventually releases pro-inflammatory mediators, interleukin, TNF, and bradykinins. And then this can cause chronic pain through sensitization and activation processes. And the third one is an exuberant immune-mediated inflammation. So this causes systemic inflammation, causing widespread myalgia and joint pain. And we think that there's some individuals that are predisposed to this versus others. The same summary quickly, and then some other mechanisms that some other studies proposed is this particular, this one study, they looked at artificially infecting hamsters, and they found that there was viral RNA detected in the dorsal lute ganglion. And they thought that this was causing pain. And this was not a thing that was seen in others. So this was different as compared to influenza model. So they think that COVID specifically is affecting this ganglia causing pain. So what is etiology and what are the different numbers that we have seen so far? Some of these studies mentioned COVID in the beginning, like acute to subacute phase. Some are specific to long COVID, but I've just listed some numbers. So pain is very common. In one study, it was seen in about 27% reported joint pain, 21%, 22% reported chest pain. Another study said that up to 20% of patients in the regular floor reported myalgia, 30% of ICU survivors reported myalgia. And chest pain and headache are very common after 35 days. So again, acute, subacute phase as well. Going a little further, chronic pain may affect 50% general population, but in COVID, it was seen to be affecting 63% of the population. And the reference is down there. What they did was they compared these individuals, and then they saw that the people with chronic pain compared to the others were older and more likely to be the female. Unfortunately, we also know that long COVID is common in females. And from that subset, again, the ones manifesting pain was female. And one in six subjects reported new onset pain while the others reported worsening of their pre-existing pain. Other MSK pain, it's very common. The range is extremely wide, I mean 0.3 to 65.2 and this was an analysis. Female gender again was seen to be a risk factor. Higher BMI was a second risk factor. And here they also just proposed some mechanisms in this study itself and they thought it's again pro-inflammatory, a marker of the cytokines, immune hyperactivation and direct virulence. Very similar on the lines that the prior study mentioned. Going to back pain. Back pain we know is already very common but if you compare COVID, long COVID versus people with long COVID, it's more common. So almost 24.5% versus 15% and statistically significant difference here. If they did the regression analysis and they saw that COVID infection directly correlates with back pain. And then they did this symptom adjustment and the only statistical difference was amongst this. So basically moderate COVID was the only predictor of pain in this population. Headache we know is very common. In the prior slide with the diagram you saw headache was mentioned at the top. Headache manifests in different ways. Some of our patients manifest new onset of headache. Some report worsening of their prior headache which was well controlled. It's seen in one study up to 60% of patients reported headache and eventually it'll be any nonspecific headache or then they eventually go to some form of phenotype. The treatment depends on what type of phenotype you're treating here. Most, we still use the same type of treatment that we use for migraines or any other headache phenotype. Fibrocovid, so just one slide or two slides with this. There's this term called fibrocovid. We know that fibromyalgia has widespread pain and with the onset of COVID there's this population which manifests like COVID. So there was a survey that was conducted and the patients were given American College of Rheumatology criteria and almost 30% of patients screened positive based on that criteria for fibromyalgia. So 30 is, I mean, it's a big number. They also saw that the strongest predictor was basically having post-COVID and this was study of 465 patients. These are the mechanisms they propose. I mean, a lot of these are, I mean, we know it's anxiety related to the symptom, it's a systemic manifestation of inflammation and then it's just the overall acute symptoms that eventually manifest into chronicity. And last thing about treatment. Treatment is again, initially symptomatic. A lot of times we use the same thing that we use for general pain but a small slide on lotus naltrexone. This is one study where they use LDN in 52% patients. Actually, most of them reported improvement in not only pain but other domains as well. And these are the domains that actually improved significantly. The others are they had some improvement while they also reported non-significant but still improvement in the brain fog and sleep disturbance. All right, thank you. Thank you. Thank you. So in six minutes, I'm going to tell you all about nerve pain, really concentrating on the peripheral nervous system. So what are my goals in six minutes? I want to basically tell you that it does occur, that patients who suffer from PASC have nerve pain so you should look for it. What is a suspected mechanism of injury? We don't really know the full mechanism or why it happens but it's up to you as physiatrists and primary care physicians to say what type of neuropathy is it? Because you can't treat it unless you know what type of neuropathy it is. So is it large fiber, small fiber, focal neuropathy, or is it something that happened during the acute phase of COVID neuropathy? Briefly talk about the workup and the treatment. So it does occur. In one study, 60% of patients three to four weeks after infection had tingling and numbness. 18.8% reported numbness and tingling after six months. So again, all of these studies basically show that patients do have reports of symptoms of peripheral neuropathy. Here's, again, it could be nerve root, nerve plexus disorders, neuromuscular junction, muscular disorders, Guillain-Barre. And again, less than the flu, including immunizations. But again, 90 days after testing positive, they compared patients without COVID, and it's a much higher proportion of reported pain and neuropathy symptoms in these patients. So what is the mechanism of injury? Is it something CSF or neuropathological evidence is really missing? But, you know, the question comes up whether, you know, it could be a reservoir similar to shingles that comes out after the COVID. You really have to be a good clinician and really question your patients. When did this pain start? Did it start immediately with the COVID? You know, you got a lot going on, they're intubated and things like that, some of them. Or did it occur later? But like Dr. Whiteson said, you know, every organ needs blood flow. So just like you have a disorder of blood flow to the heart to cause, you know, heart problems, nerves need blood too. And is there a problem with the vasonevorum? Is it a problem with the metabolic, hypoxic? All of these things can contribute to damage to nerve cells. And then it's not only the cytokinins, prostaglandins, histamines, all those things. You know, those can cause damage to nerves, but so can stretching of nerves. So it may be due, iatrogenic. It could be due to, these patients are often hypercoagulable and they may be developing thrombuses, so you could have a space occupying lesion. Again, the vasonevorum could be affected. T-cell abnormality, endothelial disease, endothelial dysfunction, mast cell activation, prothrombotic state, all of these can cause nerve damage. So the neuropathy has been described, you know, it can be spontaneous, it can be allodynia, it could be hypesthesia. And again, it may be a generalized neuropathy, it could be a focal neuropathy. We see these patients are often very disabled, very thin, and so they're susceptible to pressure palsy. Critical illness neuropathy and myopathy is very common in patients who have been hospitalized in the ICU. It could be due to overuse, it could be due to hypercoagulable state and injury to the vasonevorum, bleeding and complications, compressions of the nerve from that, weight loss, as I said, and inflammation. All these other things too, dysautonomia, Guillain-Barre. So there's a lot of areas, and again, it's up to you to figure out what's causing it. And these are just some of the other nerves that can be injured. So it can be burning, tingling, sharp stabbing, vibration. All of these words describe these patients, but bottom line, they're in a lot of pain. So, and this is one of the take-home messages. It can be large fiber neuropathy, it can be small fiber neuropathy. So the large fiber neuropathy, usually loss of vibration and position sense, so the patients have poor balance, they're walking in with a cane or a walker, they have positive Romberg, decreased deep tendon reflexes, or it can be nerve damage to the small fibers, the C fibers, so you see decrease in pinprick, pain, impaired thermoregulation. If it's small fiber, a lot of times you get these autonomic dysfunctions as well, and it's thought to be immune mediated to the endothelial. EMGs, obviously I'm a little biased because that's what I like to do, but it's very good to assess for neuropathy in general. Is it a compression neuropathy? Is it a focal neuropathy? Is it a generalized or peripheral neuropathy? And if so, what type? Is it affecting the myelin? Is it affecting the axon? Is it affecting both? Is it affecting sensory, motor, both? Is it segmental, or is it uniform? So all of these things are important in pinpointing what's causing the neuropathy, and again, you can't treat it if you don't know what's causing it. Critical illness neuropathy, again, that's an axonal sensory motor peripheral polyneuropathy, so you'll see certain findings on EMG. Inflammatory neuropathy, and again, very important, you can't assess for small fiber neuropathy with EMG. So a lot of these patients are really suffering, and the EMG is normal. I usually have a disclaimer on my EMGs that say, please note that EMGs cannot assess for small fiber neuropathy. I'm running out of time here, so basically, skin biopsies can help make the diagnosis. Again, autonomic symptoms that can be treated with immunotherapy. Focal neuropathies we talked about. It could be due to COVID that happened, and now the patient is suffering from these nerve injuries, like iatrogenic, proning, Guillain-Barre, critical illness myopathy. We saw a lot with proning. Again, 13.1% of patients admitted for COVID had critical illness neuropathy. We'll skip over this. The workup, it's in your slides. You can download them. Laboratory testing also to help differentiate. Again, consider a skin biopsy, autonomic testing, and then treatments, you know, medication, pharmacological, symptomatic relief. Don't just hit them with gabapentin. I've seen so many people just hit them with gabapentin. Really think about what's causing it. Exercise really appears to increase axonal sprouting, so really can help with these nerve injuries, and then again, different types of treatments, but the most important is the physiatrist, because you're gonna understand, you're gonna look at the patient, you're gonna do a holistic evaluation, and you're gonna have multidisciplinary treatment, and these are just some of the medications. Don't forget about TENS and behavioral therapy, and you know, also making sure that they don't develop the complications from neuropathies, such as ulcers and things like that. Thank you. Thank you. Well, we did perform a miracle, because we finished on time. Doesn't mean, yeah, I think. Thank you so much to the audience. Thank you so much to the panelists. Thank you so much to the Academy for supporting the work in long COVID. I don't believe that any of you don't see long COVID patients, meaning that in all the work that you do, you see people who were infected by COVID, affected by COVID, have long COVID. We presented according to our specialties, but every patient you see will have multiple of these symptoms and disease complexes. This is not like, oh, I'm coming in just with heart issues or neuropathy issues. They have everything. It's great that as physiatrists, you're interested in understanding that many patients will have long COVID, multitude of symptoms. You need to understand it. Again, you can go to the consensus guidance statements. They are available online and we are all here. We're available for some questions. I know we do need to get to a plenary session very soon, but go ahead. If you want to ask a question, please do use the microphone at the back there or on the side, sorry. And the panelists also need to come up and use the microphones here because it's being recorded. Does anybody have experience using Tadalafil for the chronic fatigue and brain fog symptoms? Sorry, I'll ask the question again. Any experience with using Tadalafil? Tadalafil? Yes. Alba? Cialis. Oh, Cialis. Cialis. Thank you. I have not. I've been asked about it because apparently it's going and making the Twitter rounds in terms of patient population communication, but I have not had any experience. I have one patient who is on it for, you know, autonomic sexual dysfunction and uses it, but I haven't had any use of that other than that indication. I use it quite a bit. The constellation of symptoms that it treats, you know, pulmonary hypertension, Raynaud's phenomenon, and the cerebral circulation, it's actually fairly immediately effective. It's generic and it's less than 20 bucks, so. We find Mestinon used to be really effective with that for fatigue, and it helps with that microvascular issue as well. I initiate 2.5 in men, five in women. But it, they'll come back one month later and they'll say it's night and day. Thank you, that's a great point you're bringing up. Something for us to understand. Two questions. My first is, you spoke of hypocapnia, decreased cerebral blood flow, and also the need to reeducate with breathing. I think Dr. Bartels might partially answer the question. It seems like these patients may be hyperventilating, even though it's small breaths. Are they anxious, or which came first? Or is it both? Joe and Matt can answer that. Answers, yes. There is often a degree of hyperventilation. It can be because of the mechanics of breathing, because they have restricted physiology, so they're panting, or it could be that if you're hypoxic, you're hyperventilating. So from a pulmonary point of view, there's a couple of reasons that there may be. Anxiety, PTSD, all of those things also exist in these patients. And autonomic dysfunction. And the autonomic dysfunction can also lead to it. But I'll let Joe comment on that aspect, because I just talked about the pulmonary mechanics. So with regards to the autonomic dysfunction, we do not see the hyperventilation. So that's, it was actually pretty, that's what we attributed the hypocapnia to, is more the autonomic dysfunction. So when the patients would come into the lab, we would tell them to take their mask off for 30 minutes and breathe normally. And out of the 50 patients that went through our handheld capnography, a number of them tested positive for hypocapnia. None of them were hyperventilating. And interestingly enough, we had a patient, I think it was subject number 37, that showed up and during the 30 minutes was doing breath work and tested negative. So it was an interesting finding. I think it was mentioned in the paper as well, but we did not see hyperventilation with the autonomic dysfunction. So we're not sure about the mechanism, so I'm just putting that out there. So it seems like with the breathing retraining, it's almost like a relaxation technique in terms of holding your breath and then slow exhalation. Agreed, 100%. We know that we've seen some better responses and reports after a period of time with breath work. We just don't know the mechanism. Thank you. My next one is for the hypercoagulable state. Injuries of the vasonevurum. Are these clots from infarct and therefore nerve infarctions or are these cytokines producing vasoconstriction of the vasonevurum? We don't know. I walked all the way from here to here to say we don't know. Both of them are suspected mechanisms of injury. There could be both, there could be none. It's likely that both are contributing. Thank you very much. Thank you, great questions. This is excellent. Thank you all. I'm just having my own moment of PTSD and it's very reminiscent of the AIDS pandemic when it first started. And along with that, some of my early work was about showing the presence of HIV persisting. And I want to first go back to the previous comment about pulmonary and just make a little caveat to please remember that pulse oximeters, which are often used and used as a hallmark in clinical practice can be notoriously erroneous on all patients and that they have definitely been shown to be not consistent for people who are highly melanated. The same way you pointed out checking the vascular, capillary refill on the bottom of the feet. I recently had a person with rapid response because they kept saying, please put oxygen on this man when he goes to therapy and the therapist was like, well, his pulse oximeter, he's at 100%, I said, but his respiratory rate is 30 and he can't climb a flight of stairs. So clearly he needs this oxygen because his heart is fine and when he doesn't have it and you exercise him, his heart rate is over 120 and he was a recent BK, blah, blah, blah, long story. Anyway, he stayed on oxygen after the rapid response. So I wanted to add in terms of psychiatric manifestations, we didn't really talk about that. We speak of it in terms of PTSD or anxiety, et cetera, but I certainly in my own experience, having worked the front lines through in multiple states, there is a psychiatric component to this, the same way there was a psychiatric component with HIV when it first presented that I was often mis- or misconstrued and I'm wondering if anyone has done any work around that or around the treatment of that. It's kind of similar to some of the TBI stuff we see, but I definitely had people who were floridly psychotic as well as having significant depression, anxiety and other things and I'm just wondering if there's any comment on that as well. So I wasn't involved with the latest guidance statement that was put out, which was on, if I'm not mistaken, mental health disorders. Yeah, it's just been published and we don't have any of the team members here. There is a second session this afternoon, by the way, which I did want to tell everyone about at 1.45 to 3 p.m., same room, talking about some of the other conditions we see, but I don't know if anyone here is able, Eric? Yeah, the only thing I'll say is there's lots of work around this and it may be helpful for folks who are isolated by this. Yes. And so one thing we've done in our program is we had to dedicate a time to that. It's harder to necessarily tease all that out. Sleep is huge, so Thank you. Okay, and of course I should have asked you Eric to use the microphone so for the and for the tape He mentioned that neuropsychiatry as an adjunct and validating the patient's complaints can be hugely helpful to the whole world treatment plan I have to use a microphone. Sorry The short answer is we don't know but we have a group of Neuropsychologists and neuroscientists in my institution that is looking at my cohort and Implementing some of those tests that they did for HIV looking at the blood-brain barrier disruption Looking at different possible pathophysiologies for for those neurocognitive symptoms, so I just wanted to Okay, so forgive me just hold on one second because we do have people and I didn't see it who put some questions in Who are live-streaming so I'm going to ask this question is the evidence to support IV NAD and nicotinamide therapy for long COVID patients any of our panelists have any thoughts on IV Nicotinamide NAD treatment for long COVID has anyone seen that heard that participated in that All I can say is that I have seen patients do this treatments these are out-of-pocket treatments, they're very expensive and Definitely, there's no sufficient evidence to support its use I feel like the long COVID population is a vulnerable population that can be affected by predatory Snake oil salesmen that will try to to make money off of it right now. We just don't have the evidence to support it and Hopefully there'll be trials looking at that so that we can get some more clinical data. I Think is when you make a great point in terms of the snake oil category and stem cell therapy and Hyperbaric oxygen a lot of these things are very expensive and are not evidence-based not proven I think this next one is a comment more than the question, but I'm going to read it through I find it interesting That there are still large multidisciplinary programs for long COVID But extremely few for fibromyalgia, which has similar symptoms and can benefit from similar multidisciplinary care Fibro care is now primarily education and symptom management and referrals managed by their PCP Oh, here's the question. Forgive me. Is this where post COVID will end up? Especially since multiple specialists are leaving the post COVID programs to correct to care for other patients that came from Rebecca McDonald That's an excellent question And I think you know in in general, you know My personal perspective is that people with CFS me and fibromyalgia were disenfranchised. They weren't taking care of it They weren't enough to get that sort of recognition the attention not just of clinicians a bit of researchers and government agencies This is a different picture now And I think we can all feel I don't know what the right word is a little ashamed embarrassed that we didn't Pay attention as much and I think that will be redressed. But what's the thought of the panel is long COVID going to go? the same way as Fibromyalgia CFS and me are we gonna forget it in a few years because it's just not such a hot topic You can't speak from there. You have to come up Ben So, I think something we all have to be very vigilant about I think it's can happen I think it might happen but I think the momentum is there that I won't go back to nothing and being pushed to the periphery and hopefully the Research funding that is going into long COVID will be Applicable to other kind of chronic pain and other conditions So I think there's a lot to learn here that can be very beneficial to other populations He said it I think this is a really exciting opportunity to understand these inflammatory processes and see how they come together and Really be able to extend this to a lot of other chronic conditions. So I'm actually hop optimistic I think that this could be a really juggernaut for us to try to understand things better and by virtue of the pandemic Maybe it's a silver lining to have the dollars to be able to research this better and put it together. So it's my opinion Because what is happening is that we There's a movement to make long COVID go away. Just like I mean CFS just like fibromyalgia there was a recent article in the Times magazine that Basically stated that we should give up on long COVID that we should not invest any more money on long COVID This was a very prominent Harvard physician and it's important to make the Clear that we have ignored these disorders and now we have the opportunity to help People that have long COVID as well as people that have ME CFS. This is not going away. These patients are chronic They require years and years and years of treatment and There's not not every single one of them There's a significant subgroup that needs attention and that we need to do better and do better science and elevate that So that's one of my main goals is to get everybody in my institution interested in long COVID patients I'm interested in implementing different techniques that they've used for other infectious diseases, etc into Getting more information on long COVID We as physiatrists and partnering with our primary care family practitioners are the ideal physician and Essential, you know, these are all the key buzzwords But we are and we do need to keep this going on because this is disenfranchising individuals with disabilities as well so this is our responsibility to keep that flame alight and this is not a You know a city issue or a state issue or a national issue This is a global issue and what we learn helps people around the world. So it's a great great question I'm gonna take one more question from the The iPad and then we'll come back to you to forgive me Yeah from the iPad from our virtual audience. This comes from Also from Rebecca forgive me how much weight should be placed on a negative tilt table test in a patient with clinical? Manifestations consistent with POTS and or orthostatic intolerance Are there any other tests or signs you rely on to lay label patients which can further direct therapy effort? So this is somebody who has autonomic dysfunction has a negative tilt table test, you know How do we are there any other tests or signs? There are many other ways to test it. I mean tilt table is a picture in time It's just that moment when you were in the in the clinic You can repeat a 10-minute stand test. That should be sufficient to diagnose POTS or neuromediated Neurally mediated hypotension or other disorders and also like I said We have a subgroup of patients that have orthostatic intolerance Meaning reproduction of symptoms when they stand up, but they do not have variations in their blood pressure and heart rate And we are finding that these patients have decreased blood flow to their brains similarly to those patients that have changes in heart rate and blood pressure, so Definitely, it's not just a tilt table and the access to tilt tables is horrible So we shouldn't rely on the tilt table test. We should rely on the POTS or neuromediated hypotension So we shouldn't rely on that as the main diagnostic for autonomic dysfunction Fully agree the other thing I'd add to is look carefully at the tilt table testing because if you can also see that they will list Subjective symptoms that are occurring during that time and so to the patient that's having a heart rate variation of 28 beats per minute So it's not 30, but they're having all these other subjective symptoms You clearly have orthostatic intolerance and dysautonomia in the components of was talking about Sometimes you really dive into the data and you can see that there's other evidence of clear dysautonomia and dysfunction going on, too And one more thing to add on that note The symptomatic management conservative treatment for dysautonomia is relatively safe. It can be very effective things like compression and fluids and electrolytes So even if they don't have those objective measures, it usually doesn't hurt to try to treat it Thank you for your patience Okay, just quick question, is there any evidence for people who are vaccinated are less likely to get long kovat Yes is the answer to that. Yes vaccination makes a difference And then I had another one. Do you find that the long pulmonary problems if people have been in on ECMO? Are they less likely to have them? Matt from here that And I asked personally because my husband was on it for 15 days with Kovat and he has no pulmonary. Yes Because when you actually intubated the patients and they also we don't see didn't use steroids in the early course There's the barotrauma and there's a lot of other complications that come from being Intubated that you avoid when you're on ECMO and that's one of the reasons also for outside of Kovat for patients with COPD Patients with other pulmonary diseases ECMO is now used a lot more commonly than intubation if it's up It's possible, you know as long as this there's there's the ability to sustain the patient So yeah patients who were on ECMO seem to have less Long Kovat pulmonary symptoms that doesn't necessarily relate to other long Kovat symptoms But but as far as the pulmonary yes, because they don't get the barotrauma and the other things from the intubation Hello your husband the best from us that's great news that he did well, okay Just three kind of fast ones with the foams cells rupturing they release cytokines and produce Clots or if you can go over the pathophysiologic mechanism, please You said that the atherosclerotic plaques rupture They release foam cells and then that produces clots further down the vascular tree. Yeah, I'm not a Biologist to that degree. I was reporting on a study that was done so I'm not going to be able to tell you the details of that forgive me for my Limits of my knowledge in terms of how that cascade Cascade goes for the term orthostatic intolerance. I mean, I'm familiar with it certainly orthostatic hypotension But here you're using it as inability to maintain erect posture like with balance and fatigue, etc You're kind of expanding the definition Orthostatic intolerance who wants to take that question just understanding what you were talking about I Yeah, this is a broader definition Because this is actually talking about people who are unable to or have symptoms that are associated with associated with being in an erect posture And so they don't necessarily have to meet the criteria for orthostatic hypotension as was just described You know, you may not have 30 beats per minute. You're at 29 beats per minute, but you're light-headed You don't have the you know, you get fatigued You may have all sorts of other symptoms that actually come along with that. So yeah orthostatic intolerance means you don't tolerate From a number of symptoms the actual change in posture. Okay. Gotcha last one. All right I'm sorry. I know that there's a plenary session going on. I think some of us need to get there I also Huh started a few And I also want to get the panel up if we can because I'd like to get a photograph of everybody so Thank you everybody

post-acute sequelae

SARS-CoV-2

physical medicine

rehabilitation

multidisciplinary approach

individualized care

fatigue

orthostatic intolerance

cardiovascular issues

exercise

cognitive behavioral therapy

long COVID

nerve pain