Welcome participants to the 2020 AAPMNR Virtual Annual Assembly. This session is a live session on COVID across the spectrum of rehabilitation. To pose questions to the faculty, please type questions in the Q&A field on the left side of your screen. We will answer questions at the end of the presentations. Hello, and thank you for the introduction. Today's talk is going to be divided into three parts. The first part, I will be reviewing an ICU rehabilitation paradigm for COVID-19 to mitigate the neuromuscular complications, followed by Dr. Franz, who will be going over the electrodiagnostic and neuromuscular ultrasound features of COVID-19 survivors. And lastly, we'll have chronic neuromuscular impairments in COVID-19 long haulers by Dr. Gutierrez. The objectives of my talk today will focus on discussing the benefits and safety of early mobility. I'll discuss each rehab discipline's role during the acute COVID-19 recovery stage starting in the intensive care unit, identifying a paradigm in early mobility to enhance neuromuscular recovery. I have no relevant financial disclosures. I don't really need to introduce this. As you all know, in late 2019, COVID-19 emerged causing a global pandemic with millions of cases worldwide. COVID-19 is known to cause substantial pulmonary disease like pneumonia and acute respiratory distress syndrome. There is emerging literature suggesting there is extra pulmonary dissemination or widespread immunopathological sequelae of the disease. Mechanisms that may play a role in the pathophysiology of multi-organ injury include direct viral toxicity, endothelial cell damage, thromboinflammation, dysregulation of the immune system. Critically, the mechanisms and the pathophysiology of COVID-19 are not fully understood. COVID-19 is a multi-system disease that requires a multidisciplinary rehabilitation team. The complexity and severity of disease in patients recovering from severe COVID-19 necessitates rehabilitation starting early from the ICU to post-ICU recovery. Rehabilitation starting in the ICU should continue through all levels of care. The multidisciplinary rehab team includes physical therapists, occupational therapists, speech language pathologists, physiatrists, rehab psychologists and neuropsychologists, and nurses. Individualized plans of care are developed focusing on aerobic capacity and endurance, pulmonary hygiene, strength, nutrition, dysphagia evaluation, and neurophysiological dysfunction. We are able to bring our experience from prior early mobilization studies conducted on patients with acute respiratory failure receiving mechanical ventilation in the ICU to COVID-19 patients. Benefits of early mobilization of patients with respiratory failure on mechanical ventilation include improved strength, physical function, and quality of life. Minimization of sedation and management of delirium can facilitate patient participation in an early mobility program. Studies by Morris, Needham, Thompson, and others have shown that early mobility programming can reduce length of stay, cost, delirium, sedation, and duration of mechanical ventilation. Pronation has been utilized in the treatment of patients with acute respiratory distress syndrome and is now considered a simple and safe method to improve oxygenation. However, extreme care must be taken when pronating patients as patients can develop joint stiffness, overextension, nerve compression, brachial plexus injuries, contractures, shoulder subluxation, shoulder dislocation, and pressure injuries. Therapists are well equipped to help prevent these complications and advise bedside nurses on proper positioning. Patients that require proning should have their face turned every three to four hours to decrease facial edema and pressure damage to ears and cheeks. Patients should be placed in a swimmer's position alternating every two hours. To reduce risk of overextension of the anterior capsule and injury to the brachial plexus, a pillow should be placed under the chest, allowing shoulders to fall forward slightly. Pillows should also be placed under the anterior lower legs to allow knees to be slightly flexed when ankles are floating for gravity-assisted dorsiflexion at rest. To reduce the severity of facial and periorbital edema, the patient's bed should be placed in reverse Trendelenburg. Splinting can be performed on patients who are supine. Proning teams should be advised to not pull on wrists and or arms when turning and repositioning patients. So why did we start rehab in the ICU? We know that ICU survivors can develop post-intensive care syndrome, or PICS. There are three major domains, which include mental health, cognitive impairment, and physical impairments. In 2018, the American College of Critical Care Medicine and the Society of Critical Care Medicine updated the clinical practice guidelines for management of pain, agitation, and delirium in adults, patients, and the intensive care unit that were aiming to prevent the PICS. The guidelines have been adapted in the ABCDEF bundle, which is an evidence-based guide to direct treatment to prevent the long-term cognitive impairments, delirium, and physical decline that happens in the ICU, or that can happen in the ICU. Clinicians are recommended to assess and manage pain, they're recommended to do breathing trials and spontaneous awakening, they're looking at the choice of sedative, they're looking at daily delirium monitoring, early mobility, and they're engaging families and empowering families. To focus here, early mobilization has been shown to reduce physical decline, loss of muscle mass, and decrease the duration of delirium. As such, ICUs are employing early mobilization integration of physical therapists and occupational therapists in the ICU setting. Rehab care through the continuum really needs to be bridged. Each patient with rehab needs benefits from an individualized plan of care early. Ideally, patients should have early physiatry involvement for coordination of care, mitigating side effects of impairment, and assessing need for post-acute discharge. Rehabilitation care should be implemented early in the ICU and continue in post-ICU. So how did we coordinate rehab care at Johns Hopkins to bridge the continuum? To answer the question, we must first discuss how we identified patients in the ICU who needed early rehab intervention. At Johns Hopkins, the rehab team followed 60 to 70 percent of patients admitted with COVID-19 in the first wave in the acute care hospital. The Johns Hopkins PM&R department instituted a series of changes to provide care for COVID-19 patients. First in the ICU, physiatry developed a rehab intervention severity category, or RISC, that was modeled off of the pre-existing MICU protocol to screen patients daily for readiness for early rehabilitation intervention outside of the MICU as patients were housed in other ICUs. The RISC score included review of multiple factors. We looked at the length of stay, days on a ventilator, level of sedation, which was through the Glasgow Coma Scale or wakefulness. We looked at level of agitation through the Richmond Agitation and Sedation Scale score. We looked at positioning, medical comorbidities, medical stability, and prognosis. RISC scores ranged from zero to four. With a score of two, the screening physiatrist would request the primary ICU team to place referrals for PT and OT for early mobilization. With a score of three, PM&R physician consult was initiated to co-manage rehab medical needs. With a score of four, a patient was moving to the COVID medical floor and physiatry continued to follow, providing improved continuity with post-ICU care. It was important for us to develop a system that efficiently utilizes our rehab resources to provide care for patients with different functional abilities. Rehab categories were divided into three groups based off of a patient's pre-admission functional status and ANPAC, initial evaluation, and their diet consistency. The three categories are standard of care, acute hospital rehabilitation intensive services, or we called it ARISE group, and the enhanced recovery after COVID, our ERAC group. Patients were able to move through all the categories dependent on their functional progression measured through ANPAC score and diet consistency daily. In the standard of care group, ANPAC scores were between six to 12. Importantly, scores less than 12 require total or significant help to perform basic mobility and activity tasks, and they're more likely to be discharged to post-ICU care. They're more likely to be discharged to post-ICU rehab facilities. The goal of the standard of care group was to ensure patients don't experience further deterioration during hospitalization. In the ARISE group, the acute hospital rehabilitation intensive service group, ANPACs were ranging between 13 to 21. For speech therapy, the patients were either NPO on a pureed and thickened diet liquid till they progressed to mince the moist diet and thin liquids, or they had new onset cognitive deficits. Patients in the ARISE group were seen at least a day, seen at least once a day by all relevant disciplines as tolerated until their ANPACs reached a score of 21, or they tolerated a diet progression. A physiatrist was involved for coordination of medical and rehabilitation care and a plan for acute and planning for post-acute care needs. The main focus of the ARISE group is to prevent any further functional deterioration due to their illness and hasten the functional recovery with the goal of returning home with home care services or improving their function to the point that they can transition to inpatient rehab settings. The ERAC group, or enhanced recovery after COVID, had PT and OT ANPAC scores of greater than 21. Previous data has shown that patients of 22, ANPACs of 22 or higher, were good predictors for discharge home. For speech therapists, patients were on a mince the moist diet or on a soft and bite-sized diet. These patients received two to three visits, followed by a maintenance plan for one week for in-person visits to ensure no regression of function. These patients also had the opportunity to receive daily telehealth education on energy conservation techniques and or therapeutic exercises that focused on strengthening endurance training. The main focus of this group was to transition patients home with home care services. In the acute inpatient rehab unit, or we call it here the acute comprehensive inpatient rehab unit, initially in the first wave, the patients required two negative COVID-19 tests 24 hours apart. They needed improvement in respiratory symptoms of shortness of breath or cough, and they needed to be afebrile for 24 hours without use of antipyretics. These patients received traditional level of inpatient rehab care with three hours of therapy a day with physical therapy, occupational therapy, and speech therapy, as well as needed rehab psychology. However, now our hospital epidemiology and infection control team recommends against retesting patients and following time-based guidelines of 20 days from the first day of COVID PCR swab to enter a group setting like inpatient rehab. In collaboration with the internal medicine department, we've developed an extended acute comprehensive inpatient rehab unit on a negative pressure unit for patients who meet inpatient rehab criteria but remain COVID-19 positive on follow-up tests or do not meet the time-based criteria. These patients receive traditional level of inpatient rehab care with three hours a day of physical therapy, occupational therapy, and speech therapy, and rehab psychology involvement while remaining on a negative pressure unit under the care of a physiatrist. We have worked hard here at Johns Hopkins to integrate rehabilitation early in COVID patients ICU course and continue intensive therapy while in medical wards with the goal of discharging patients home safely. Preliminary results suggest that our patients are sicker at the Johns Hopkins downtown campus compared with our other Johns Hopkins affiliates but from our rehab intervention this group has become more ambulatory and have a higher rate of discharge home. For those patients who continue to need ongoing intensive rehab in an inpatient setting, we were able to provide traditional inpatient rehab and inpatient rehab on a negative pressure unit. I just want to give special thanks to the Johns Hopkins team that significantly contributed to designing the COVID rehab programming. I will now hand off to my colleague Dr. Franz. Thank you Dr. Pruski. I'm going to talk now about electrodiagnostic and imaging especially ultrasound features of COVID-19 survivors. I have a lot of people who share credit with the data that I'm going to show you from at least our experience as well as the other projects we're involved with but I particularly will highlight some of the trainees who are involved as we go along. We're going to talk about neuromuscular complications found in post-COVID survivors who require inpatient rehabilitation. We're going to demonstrate their electrophysiological and neuromuscular characteristics and we're going to display the role of advanced imaging especially ultrasound to refine localization and support clinical management. Neuromuscular complications of COVID-19 really boil down to just three major issues so far. Muscle involvement, muscle injury and myopathy have been reported. Neuropathy, polyneuropathy, length-dependent neuropathy as well as Guillain-Barre demyelinating and related neuropathies as well as multiple modern neuropathies be it compression injury, potentially inflammatory nerve injuries. Looking through the timeline as we've learned more about the neuromuscular manifestations of COVID-19, I can tell you that it started off with observations just about elevated creatinine kinase levels, reports of GBS that were anecdotal in case series, larger reports then coming of nerve injuries with more characterization as well as from their both inpatient rehab facility standpoint as well as in acute care. Let's take a closer look at muscle involvement. This to light was a group out of Wuhan, China that had reported on that over 200 patients. Hypercekaemia essentially was the extent of the characterization although the average elevation was mild with a median of 400. There were cases where there clearly was more involvement, I think over 20,000 in some cases and that occurred about 9% of those hospitalized for COVID-19. A subsequent study out of Spain looked also at hypercekaemia levels which reported similar findings of about 9.2% but also did myopathy evaluations and select patients using electrodiagnostic testing and found that 3.1% of the patients had an EMG confirmed myopathy. Even larger study out of Italy that just was published more recently lumped myopathy and critical illness neuropathy together and found an incidence of 6.6% in that cohort. This is not a peer-reviewed study yet but a group out of Sweden looking just at ICU patients, 111 consecutive patients in ICU. What I liked about this study and the preprint that you can access online is that there was an incidence of 9.9% in these critically ill patients with 6.3% of it being neuropathy and 3.6 myopathy. With myopathy, one of the harder things to get at is the involvement of muscles that we can't always test with electrophysiology, for example, the diaphragm muscle. And a lot of the long haulers and also those who are critically ill with COVID are short of breath and some of the assumption is that it may be related to the pneumonia but there may be a neuromuscular underpinning. Being able to evaluate the diaphragm muscle using neuromuscular ultrasound has been all the more important because classic tests like PFTs or EMGs are sometimes not available in acute care and the PFTs can generate aerosols, so this may be a safer method as well. I'll describe it briefly with a big credit to Dr. Farr, who's a senior resident here at Shirley Ryan Ability Lab, as well as of course Dr. Boone from the Mayo Clinic who described this technique. But briefly, you can see a picture of a diaphragm through an intercostal window in between ribs eight and nine. Intercostal muscle is marked and you can see the diaphragm muscle with normal thickness. And as you have someone resting and then if you have to take a breath in, the muscle contracts and thickens. You can see the thickening of the diaphragm on the next image here. And in different conditions, this is an example of someone who had a phrenic mononeuropathy, the diaphragm can become quite atrophic and it can be difficult to identify. Here we're using the lung, the positioned lung, and actually pushing the diaphragm off the chest wall to confirm the anatomy because it's quite atrophic and doesn't contract. And we have recently published an article describing how this could be useful for phrenic mononeuropathies, just simply characterizing by whether or not there's severe atrophy with the paralysis that you see in conditions like neurologic atrophy. But what is known about this technique in myopathy? Not as much is published on myopathy as opposed to other neuromuscular conditions, but Dr. Boone has published a series of 19 patients showing that diaphragm ultrasound is able to pick up abnormalities. She oriented to this graph, the thickness of the diaphragm is plotted on the x-axis, the thickening ratio or the amount that the muscle thickens with an inspiration compared to at rest is plotted on the y-axis. And you can see that the majority of patients will have measurements, this is better outside of one of those two values. So if you're left of that dotted line, you have severe atrophy. If you're below this dotted line, you have impaired contractility. And it turns out about 73% of patients have one or the other abnormality on their ultrasound, which was consistent with the suspicion of diaphragm involvement in their muscle disease. The muscle diseases there were quite varied, but there were three patients at least with critical illness myopathy, for example. In our experience here, we've been measuring patients in the inpatient rehab setting with diaphragm ultrasound. Dr. Farr and Dr. Wolf, a pulmonary fellow who have been working on this quite, this is all unpublished data and they've been working quite hard, so we can have some data to show here. So you are seeing this for the first time. And you can see first, when you take our 26 patients, we plotted each diaphragm as a separate data point, so you see 52 data points, that the red dots are diaphragm readings that are outside of normal limits based on the normative data published by Dr. Boone. And as you can see that if you look at the number that have impaired contractility and or severe atrophy, it works out to roughly 73% of COVID-19 survivors who had severe COVID with ARDS have diaphragm muscle dysfunction once they reach inpatient rehab. In perspective, we've been trying to study non-COVID ARDS patients as well that we get, but they've been a lot less frequent and to extent that we've had six of them so far that only three of them fell outside of normal limits, but this is a work in progress. So getting back to our timeline of discovery, GBS was one of the earliest things that was reported in COVID-19 patients as far as neuromuscular complications. There's now been over 60 cases. This is recently summarized in the Journal of Peripheral Nervous System here in this systematic review. And as you can see, looking at their data that just in keeping with the preponderance of COVID-19 in males with severe disease, that we see a high preponderance of males. You can see that the clinical presentation of a sensory motor ascending weakness is common, roughly 70%. And also the classic demyelinating electrophysiological characteristics are seen in over 70% of these patients with some of the other variants, including the axonal form also appreciated. So one of the big questions that's come up is COVID-19 increasing the rate of GBS worldwide or in different regions? It's hard to give a clear answer on that. One study in Italy reported an unusual cluster, for example, of eight patients with GBS within a short period of time, March and April of 2020, raising the possibility that there could be something about this virus that is more likely to trigger GBS. Keep in mind there's some of the analysis has shown that there's a high co-infection rate with influenza, especially more recently. On the other hand, a large study out of Northwestern that I haven't been a part of, had looked at the first 509 patients in our hospital system here in the Chicagoland area and found no cases of GBS. So the jury is still out, but I will tell you that from what we see in the GBS cases that have been published so far in case series and case reports is that the clinical and electrophysiological patterns are largely comparable to non-COVID GBS cases. Getting into this mononarytis multiplex or multiple peripheral nerve injuries that we've seen, we published a paper, and I really have to credit Dr. Malik as well as also Dr. Wolfe, the pulmonary fellow who was involved in the diaphragm study and Dr. Malik, who's our chief resident for putting together this case series rapidly about patients who developed peripheral nerve injuries. What we noticed was asymmetric weakness on the rehab unit in patients that were coming to our hospital between April and June, essentially, of 2020. They hadn't had EMG testing before. When they arrived, we noted many different sites of compression of what we assumed to be compression. I'll show you why. Nerve injuries, particularly as this heat map shows, the ulnar nerve at the inside of the elbow, which you can see there in substantiating a compression mechanism is this example here of a case with an MRI showing a hyperintensity of the ulnar nerve there at the cubital tunnel, as well as that's highlighted with the long arrow, and then an arrowhead that's pointing to overlying soft tissue edema, implying that there was soft tissue compression and ischemic injury and inflammation at that site. So we've come to calling this swimmer's elbow in light of the swimmer's position. So care is needed, and we've been working on this quality improvement with our colleagues in the critical care unit to prevent some of these complications. Looking at the whole list of 12 patients that we included in this case series, that were 12 out of the first 83 patients admitted to Shirley Ryan's inpatient COVID unit. And they came from 19 different facilities to our hospital, indicating that it wasn't just a one hospital protocol issue. And 11 out of the 12 patients, or 92%, had been prone for their ARDS and acute care, which we think relates to why so many of these injuries from the upper extremity. Injuries were often associated with overlying edema, like the example I showed. And the majority, the vast majority, almost 95% had axonal loss characteristics when we did their EMGs, indicating a more severe type of nerve injury. And I'll show you some examples of how advanced nerve injury was useful for localization and characterization. We have more cases now, over 25 confirmed, and we're looking for cases that anyone else who's seeing a lot of these to feel free to work with us and try to characterize them better. So, Seeing is Believing is the title from Dr. Nussbaum's poster, which was nothing to do with COVID initially, but has, I think, a little bit of content about how ultrasound can help us manage peripheral nerve injuries. And I'll show you some examples of how we use imaging, how we use imaging to refine our localizations. So you can see these two cases here. I just pulled straight out of my table. One patient with multiple mononeuropathies. You might ask, how do you get a median nerve, a radial nerve at two different sites and an ulnar nerve all together? And be sure of that, because that can be certainly a hard thing to pull out electrophysiologically. Well, with imaging, we can clearly see this is an enlarged median nerve at the wrist that was demyelinating in character. One of the few demyelinating injuries we saw. But how do you figure out there's a pin and a radial injury? Well, we were able to see that there was a radial nerve injury in the EMG, but when we couldn't figure out why the distal muscle was so impaired in this patient, we didn't have a distal neuropathy to explain it. And we found enlargement of the pin. So the pin was totally knocked out in this patient at the lateral elbow, which may be the down part of the, you know, when you put the arm up or down in the swimmer's position, we suspected, because we saw a few of these wrist drops that were severe that might be related to that position in critical care. That's not proven, but it's our current hypothesis. And then another patient where we concluded they had a brachial plexus injury. And you can see in this patient, we were able to get MRI neurography of the plexus to show that there was enhancement of the corresponding plexus to sort of substantiate that localization. So two cases that both looked like to me initially as plexopathies, one of them turned out to be multiple modern neuropathies. Severe COVID patients can expect a long haul to recover. This is different than some of the long haulers who never come to the hospital. But one of the ultimate long haulers, you know, given I'm mainly focused on peripheral nerve injury, is the rate of axon regeneration when we have these axonal loss injuries is so slow. Axon regeneration is inefficient and slow, about an inch a month. And you can imagine with these proximal nerve injuries that these patients are going to be recovering for a very long period of time, up to two years for full regeneration. With that being said, the real long haul bit of this presentation will be given by Dr. Rodusco Gutierrez right now. I'm going to hand off to her. And she may go a little bit long, but we'll do questions at the end with any time remaining for all the presenters. Thank you. Hi, so glad to be here today. I'm Monica Rodusco Gutierrez. I'll be talking about the neuromuscular complications that are long after COVID-19. So thanks for being here today. We will get to the questions at the end. And I'm learning a lot. So I'm going to start a little bit with the pathophysiology, just because I think it's important also when our patients understand this, so we know why some of the symptoms are so, are occurring so long-term. Talk about the adverse impact of them, how I'm doing the rehab program, what the rehab program is, and what are some of the long hauler, especially neuromuscular type complications I didn't put here, but I have no disclosures related to this content. I'm not making big money off of COVID or big COVID pharma or anything like that. So still just get paid the same at the end of the day. Regarding pathophysiology, we know this SARS-CoV-2 enters a respiratory system. The spike glycoproteins are what attaches to the ACE receptors, which are in the lung and in the upper airway track. There are also post-inflammatory cytokines that are revved up during this process. So there's kind of three main things that happen. There's the direct effects, which is the direct effects of the virus, and then there's the direct effects, the indirect effects with the post-inflammatory cytokines. And then those macrophages also take the SARS-CoV-2 infection to the rest of the body. And then you have your immunologic response. In regards to where it goes, once it either goes from your lungs or goes into the bloodstream and goes all over the body, it will go into organs that have high expressions of ACE2. Those organs can be the brain. And so that's why people are having issues with brain and with some of their neurologic functions. Of course, the lungs, the GI tract, the pancreas, the bones, the muscles, the heart. Of course, we're seeing some patients getting cardiomyopathies, vasculature as well. So there's increased permeability there. So they're getting coagulation and hypercoagulation, kidney. And with the brain, it also becomes, the blood-brain barrier opens up some more and then it can get into, cross into the blood-brain barrier, cause effects on neurons in the brain that affects neurologic and physiologic symptoms as well. And then, like I talked about the immune system, the immune system has now been shown to be dysregulated. And from the study that came out of science, that showed that there was three types of immune responses. So when they followed the immune response in patients who had had COVID in the past, had active COVID or once then they had a control group, there was three different main type of immunotypes. One was that they had a hyperactive immune response to everything. And when their immune response went, it just went and it continued up, up, up. And this is something different than we see in other diseases, where you just kind of get one little blip up and down. There was one that kind of had just a middle of the road response and made some helper CD4 cells or some memory B cells. And then there was one with very little low immune response. And that one did have a negatively correlated with disease severity. So again, people's immune responses are very different, which I think ties in a little bit, that we don't know completely with some of the patients that are having long haul or symptoms. One thing I do want to bring up is that this disease we've seen has been affecting disproportionately certain groups, including persons who are minoritized groups, Black, Native American, Hispanic groups. And you can see from this, no more cases, more hospitalization, including increased death rates as well. And so that was something that was important to me, especially being in a city that has a large Latinx population, knowing that we would have more patients who may be affected, who may get ill, and who may have more sequela and morbidity, especially if there are higher rate of hospitalization in our area. And so that really kind of moved me to do this kind of work. I also feel that as a specialty, it's so important as physiatrists that we are physicians that can work from the ICU to the football field and outpatient settings. And as you've seen, even in this presentation, we can take care of them in the ICU, in the inpatient rehab unit, and then long-term in the clinic. Our field came out of the polio epidemic. It was one of the ways that our field came out. So we're used to being stars in epidemics, and we really need to start with multidisciplinary rehab for COVID-19 patients at all levels. So what does recovery look like? You heard a little bit about how patients are doing in the ICU and how we're trying to protein them and mobilize them and how important mobilization is. And you heard about the effects that they're still seeing in the acute care setting. And we know that they're thinking of COVID-19 has a wide spectrum of disease. I see people more in the mild or moderate. Some of the more severe ones, they kind of put, gotten their inpatient rehab. They're maybe doing therapy somewhere. They're dealing with their symptoms. They're getting an outpatient or a home health therapy program. And some of the patients that I see never were in the hospital. They maybe just started as having some uncomplicated upper respiratory symptoms or didn't need to go to the hospital, but they still continue to have symptoms. And this disease is different than other types of ARDs. Especially with the immune response and with the cytokine storm and all the pro-inflammatory cytokines that we're seeing. Plus the patients happen to be younger, usually have a good functional baseline status, but as you see, can still do very poorly and hopefully don't have too much comorbid disease. And then we know there's extra challenges due to COVID-19. Other than PICS, you've heard about some of the things that happens, prolonged intubation, proning, sedation, neuralytics, paralytics. They're getting steroids, which is also can cause some steroid myopathy as well. And then there's the psychological sequela that we don't think about or that we haven't talked about. They can't have visitors. Their family members may have been sick. Even if they're not in the hospital, they have to be away from people. And then lots of people losing their jobs, not having a dispo. And it's kind of, it's been the perfect storm. What are the complications we're seeing? This is a paper that I wrote with 11, with other authors from 11 different countries that came out earlier in the year, where we talked a little bit more about what can we do in the pandemic? And we base this a lot on what was seen in SARS and in MERS before we had SARS-CoV-2. And a lot of the complications that we saw then were similar ones to what we're seeing now. So again, just going to prove that physiatrists can play a role, that we've had a role all along in this. What am I seeing? Because going back a little bit to the disparity issues is it's a little of a, we've heard of the tale of two cities, a tale of two patients. So we have these patients with significant risk factors. They're ventilated, they're sedated. There's delirium, prolonged critical care, especially if they get intubated. There's hypoxemia. We're seeing a lot of issues with anoxic brain damage and not even major, just little anoxia. Isolation, very limited post-acute services. At one point, even our inpatient rehab unit had to be shut down to be able to take care of acute patients in the surge. So in some cases, you have patients who get the early mobilization, who do get disposed to an inpatient rehab, even if it was a community one and continue to get aftercare. And that patient did much better than the ones who had COVID, ARDS, vent, isolated. There was no rehab beds for them. Maybe they didn't have insurance, so there was no options because the one in the hospital was closed and then they went home and they didn't get home health or no one came to help them, especially when the surge was very bad. And you know that those two cases, the end is gonna be very significantly different. We have to think about what long COVID and the long effects of COVID-19 are going to cost economically in the future. So again, this was something that I thought was very important to bring to South Texas. I was part of a paper where we talked about when we started seeing the disparities and papers coming out on disparities of COVID-19. And we wrote an article as a call to action for physiatrists to provide rehabilitation care to black survivors who were disproportionately being affected. And so in Texas, I started a Coronavirus Recovery Clinic. We'll tell you a little bit more about that. In our Rehab Medicine Post-Recovery Clinic, first, with everything, I think you have to know your why and find your why. And so we have a mission where we wanna serve our diverse patient population. San Antonio is the largest majority minority city in the United States. And we had a lot of patients affected by COVID-19 and we want to treat their physical, cognitive, and functional difficulties. And we did that for patients. We started a lot. We're doing a lot with telemedicine, especially the assessments from the physicians and then making appropriate referrals depending on what the patient needs and based on our systematic assessment of the patient and making referrals and prescriptions based on what they need. It focuses on everything, on all the things that you've heard about, about the weaknesses. They're getting sent for EMGs. They may have already been diagnosed with critical illness, myopathy. Some of them have had strokes, pressure injuries or wounds, amputations. A patient with limb amputation who's one of our post-COVID patients and also had a stroke. And so we're seeing also patients just with the long haul or symptoms, which I'll get to next. So this is what they're calling long COVID. And it's also a better probably way to say this is post-acute COVID. So once patients get rid of or finish that acute stage, they continue to have symptoms. So this was one of the first papers published on it that came out of Italy that showed that this was 56-year-old patients, not that old. 37% were women. For ones that were hospitalized, there was 72% had interstitial pneumonia. And these were not patients who were super sick. Only 5% had invasive ventilation. So it wasn't even the sickest of the sick. This was a big compilation of patients. And they looked at their symptoms before and then 60 days later, they looked at their symptoms as well. And after 60 days, still 87% of patients had symptoms with, in this study, the most common one was fatigue, then dyspnea, joint pain, chest pain. So again, we're seeing, this was one of the first studies that came out looking at some of the post-acute long hauler patients. This was another study that came out of the University of Indiana, where it talks about the most common long hauler symptoms, where there's a Facebook group, there's different groups. This one's called the Survivor Corps, and they looked at their long haul symptoms in over 1,500 survivors of COVID-19. And of course, these are people in a group that are self-proclaimed, that they continue to have symptoms. And then you can see what the top ones are, fatigue, muscle body aches, shortness of breath, difficulty concentrating, inability to exercise, headache. Another interesting thing to know is in these patients, about 25 or 26% are having painful type symptoms. So again, things that physiatrists can take care of. A lot of, probably in some of those studies, some of the paresthesias and feeling of burning of the skin can occur in two to 5% of patients. I'm sending patients for different EMGs. Some are finding as little as okay, carpal tunnel. Some are, it's a more central type pain. Some are just having aches and they're testing to be normal and they're just having kind of more myofascial pain due to some of the inflammation that they initially had. So this is a slide that I use when I talk, but usually I'm a neuro rehab doctor, which also made it really easy to start taking care of patients with COVID and with prolonged symptoms of COVID. And the more I thought about it, it's like this is very similar to stroke recovery. So this is the slide out of my, what are the major determinants of stroke recovery? And I just put the COVID sticker on it. So it's very similar. What's the initial injury? And then you have to look at, there's something genetic factors that we don't know about. Is it ACE2 receptor expression that someone has? We don't know. We're still looking at that. Is it, again, genetic factors? Is that someone's immune response? We do know immune response does correlate with some of disease severity. And then there's things like age, race, gender, comorbidities. We know that also factors into what their recovery and what they're going to look like, what rehabilitation therapeutics we can give them, which we need to give them, and then depression and in general, just mental health and mental illness. And that is something that we're starting to look at in our assessment of COVID-19 in our clinic. We're looking at PHQ-9, GAD-7, PCL-5. So again, looking at anxiety, depression, PTSD, and a lot of these patients are being positive for all of these things. And then this goes with who does poorly post-stroke? It's almost the same of who does poorly post-COVID. And what's interesting is that when in stroke and in traumatic brain injury, after you have that injury, there is a secondary inflammatory response in the body, including immunological response. You can see changes in the spleen. You can see changes with IL-6 and with the inflammatory markers as well. And this is why we study stem cells in this population, because it actually more than bringing in new cells, it actually regulates the immune system, which helps the outcomes long-term. And so those are also why I think it was easy for a physiatrist to take care of some of these neuromuscular complications. So this is a different study that they looked at prolonged COVID-19 symptoms. So just, again, symptoms are not limited. Recovery is volatile. You're gonna hear patients feel like, I was getting better and then I wasn't, and then I was good for two days and it came back. And so it's gonna be like that. And then there's a lot of stigma and lack of understanding as well. And so this is a tweet that I had written that everyone's different, everyone's symptoms are different and we have to listen to them without stigma and be really willing to treat what they have. What kind of assessments? I talked a little bit about things that we're doing in our clinic. This is also, I've been working with UT Southwestern who are doing similar assessments. And the order depend on the symptoms that the patients have. There are guidelines for return to play, and this is also for active adults. There's also a more recent one that came out in JAMA cardiology for athletes and for the master athletes too. I won't go into those, but just to know that they're there to guide your outpatient rehabilitation. Again, patients that I'm seeing, either they had a really severe COVID pneumonia or they were mild to moderate and they weren't hospitalized and they suffered at home. And both of them can have long hauler symptoms and some neuromuscular complications. So some more serious than others. We have seen stroke and increase in stroke, especially in thrombogenic strokes. Thrombogenic strokes are about twice more common from COVID-19 versus when you look at just regular large vessel occlusion strokes in the usual population. And if an older person has a stroke, especially if they're over seven, there's a higher risk of mortality. And in this study, when they looked at multiple case series of strokes, the younger, less than 50 stroke was often one of their presenting symptoms. So definitely at one point, our stroke neurologists were taking care of all the strokes, even if they had COVID and they were having a lot of, they're almost running a COVID service themselves. Other neurologic sequelae, they've been shown 36% develop neurologic symptoms. I'm seeing a lot of headaches. I'll talk about that in a second. Disturbed consciousness, seizures, and even in patients who weren't hospitalized, of course, the anosmia and aegysia, stroke, the critical illness, myopathies, neuropathies that you've heard about. Myasthenia gravis, Guillain-Barre, functional neurologic symptoms. And then I'm also seeing tremors and Parkinsonism. And I just read another case series that we're talking about some of the Parkinson's presentations and tremors that patients are having as well. The headache is gonna be one of the most common neurologic presentations and different studies so far have shown anywhere from six to 71% of patients having headache. And it's different. Some are saying hemicranial pain, some it's holocranial pain, some it's tension type headaches, others they might get more migrainess headaches. And they just describe it in different ways. The way I say to treat this, there's not good data, of course, we don't know, is I kind of treat it based on the type that it looks like. So if it seems more myofascial or tension, then incense, ibuprofen, acetaminophen, and sending them to therapy, we need to work on some myofascial release and some posture type things. If it is more migrainess, and I also, in some cases I do do MRI, but for migraines and I will treat usually with triptans, I'm using some of the CRGP antagonists, even have used some botulinum toxin for prevention of migraines that have become very chronic. Cognitive sequelae, of course, usually with PICS we see it, but we are seeing it even in some of the long hauler patients, they're just feeling that they're foggy, the brain's fog, they can't think the way they used to. And so there are studies in COVID-19 patients where it looks at MRIs and there is edema in certain areas of the brain, including in the areas that we know is very sensitive to anoxia, like in the hippocampus. And for these patients, if they need it, they'll go to refer to speech therapy, neuropsych medications in some cases. A lot of post-viral fatigue, and then the question is, is it myalgic encephalomyelitis like? We don't know, some of it I'm treating it like that, but at first I make sure they have pulmonary and cardiac screens just to make sure it's not coming from lungs or heart. I have had some patients who do have a lot of dysautonomia type patients, dysautonomia type symptoms, and some of them also I'll send for cardiac screens, like echoes, and have caught some abnormal echoes from even patients who are not hospitalized. Check vital vitamin levels, make sure that they're sleeping. Some are so anxious that they're not therapy, but I do not exercise them to fatigue, and then do just some other kinds of natural things that might help decrease inflammation in their body, melatonin, omega-3, meditation, and then duloxetine I like, especially if there's a pain component to it. We know psychological sequela, we're seeing that very significantly right now, so getting behavioral health counseling for patients, whether they have PICS or were just suffering at home, and using a community-based approach, just finding different resources around town, of course our own institute, but working with other people. And we will spend the rest of the time on questions. Thank you. So, I'll moderate the questions. This has been a great series of talks, particularly the other two. I will say that the secret to any young faculty organizing a session is to get people who are smarter than you, and then they help make you smarter by listening to their talks, but also make you look good. So, thank you to the other presenters. The first question about post-COVID follow-up in the outpatient setting, what is the easiest thing to miss? If you don't ask the patient this question, what would they maybe not tell you that really impacts their quality of life after COVID, or their persistent symptoms? So, right now, what I'm thinking, honestly, is that some of the mental health things. So, really, if you just talk to them, or they come see you, it might be like, I'm really fatigued, I don't want to gab, I don't want to do that much stuff. And then we all, we know that mental health conditions can cause a psychoneuroimmunologic response and inflammation in the body as well, and make everything a little bit worse. So, kind of making sure that you're looking for that, screening for that, and treating any underlying psychological complications. And then listen to the, the other thing is listening to their symptoms. So, if they are like, I'm tachycardic, my heart rate won't go down, and a lot of them, you know, they bought the little ox monitor so they can watch what it is. Then, you know, again, getting them an, it's troponin, EKG, echo for cardiac symptoms. Perfect. Dr. Pruski, we talked a lot about the long haul for people recovering from COVID, but you get a chance to work with them earlier than most physiatrists. Do you think that compared to other people that undergo ICU level rehabilitation, that these patients are recovering slower? It's actually very interesting of a question. Thank you so much for asking it. We actually see in the hospital that a lot of these patients in the beginning are quite sick, but when we give them the appropriate rehab and therapy recovery activities, they are able to get home sooner than people who would be more medically complicated in the same scenario before COVID existed. So, we think that this very structured rehab program can be very beneficial to their overall recovery if started early. Thank you. Regarding my presentation, there were questions about modern neuritis multiplex, like a neurologic amyotrophy or Parsonage-Turner versus other mechanisms, as well as the involvement of a phrenic nerve in addition to the diaphragm dysfunction. I can answer both questions saying that we are working on this project right now. We have seen some, what looks to be phrenic nerve, asymmetric diaphragms with severe atrophy on one side and not the other, as well as qualitatively and in large, they don't have normative data that we use for the phrenic nerve appearance that suggests that these may be compressed in the prone position in some patients versus the possibility that the patients are having a disimmune, autoimmune type of reaction, or there's a lot of possibilities. These patients are at a higher risk when you look at their comorbidities. That answers both of those. There was a very straightforward, simple question here. What vitamin levels would you check in your outpatients with COVID in rehab? What can be done to optimize that aspect? So other than checking labs, then I'm checking also vitamin D, just because vitamin D, and almost everyone's low. No one's going out and getting sun during the pandemic, especially now it gets a little, it's the fall months. No one's going to walk. Everyone's staying indoors or they're socially isolating themselves, especially when they're sick and vitamin D levels are really low. And we know that more normal or higher vitamin D levels are better, especially in painful conditions and in neurologic conditions and in autoimmune conditions. And so, vitamin D is kind of one of the main things, of course, if anything else like magnesium flow, et cetera, then I'll want to check that. And some patients who are feeling, one thing is I am sometimes checking, again, it always depends on the symptoms. I have one lady, it's like, she seemed very much like it was presenting like dermatomyositis afterwards. She just got very weak. It was hard for her to stand up. She couldn't do stairs. She got a rash. And so in that case, I checked CPK and send her for an EMG and also checked all the autoimmune labs where you talked about autoimmune response. We don't know how the body is, again, the immune response is high. We don't know what it's starting to cause. Are we seeing more autoimmune diseases like you talked about? Yes, very possibly so. And there may even be certain autoantibodies that we don't know about. And there's a neurologist out of Austin, Texas who has an NIH grant where she's looking at that. She's almost all the patients she's seeing and I'm sending her all my neurologic patients too with kind of these interesting tremors and different symptoms or neurologic symptoms that aren't even MRIs normal. Then she's just looking at all sorts of antibodies. And then there may be ones that we don't even know of. And I'm getting high CRPs and ESRs as well. Great. I have a question for Dr. Pruski. It's actually from my colleague, Dr. Farrar from Shirley Ryan Ability Lab, who's a current applicant for TBI fellowships. And it's absolute rockstar. She asked Dr. Pruski about extrapolating the data from the ICU to get better patient outcomes for people who have COVID but aren't in the ICU. Sorry, I thought that the- How are you using that? The better outcomes of getting the ICU patients, yeah. Yeah, so we're actually extrapolating a lot of this data and taking it to different patient populations throughout the hospital system. We have various acute rehabilitation intensive service programs here in the hospital and they're very syndromic based. So those programs are ranging from transplant patients that we bring this kind of programming to, to stroke patients. COVID was actually our third population and as well as the traditional MICU rehab patients because we find that if we're able to give early more intensive rehab, we're able to mitigate a lot of the risks of prolonged hospital stay, such as essentially you increase the length of stay, you get more delirium with these patients and the more touches from therapy, the sooner a lot of these patients get to go home or get to go to that next post acute level stage. I have a question. I think I'll wrap this one to Dr. Villescaz-Guerreras because I know she's doing work on telemedicine and getting care to people who have difficult access. So for clinics that including rehab centers that aren't accepting outpatients with COVID or reduced access, how are you getting them the care they need, the rehab care they need? So first it's a lot of education. The CDC has transmission based guidelines. A lot of these patients, it's 20 days. So if they're having symptoms, it's going to be 20 days that they're actually going to be able to, after 20 days, then they're not going to be transmitting any more COVID. So then they are fine to go in and do things. If they have underlying immune deficiency, then it's 28 days. So just to be safe, we don't let anyone in our clinic before 30 days from when they had their symptoms of COVID. And I have the same rules for our outpatient rehab. And then there's some rehabs that are doing telemedicine or tele-rehab. And then there's some home health companies that are willing to go, especially if it's out of that, after a month. And all these, the patients that I see that are kind of the long hauler ones, they're at this point that they're seeing me, it's already been a month, two months, three months. And so they're definitely not able to spread their disease at that time. And then they still, we wear masks, we wear face shields whenever we do see people in person. Ooh, really bad lip reader. Doctor, what was that? Oh, inpatient medication management in the inpatient facility of Tremors post COVID. In inpatient or outpatient? Inpatient. IRF. So I'm not doing inpatient, but I can tell you what I'm doing in outpatient. There's some interest in doing. Okay, so for patients with tremors, I go through the similar things that we would do for Parkinson's patients. Sometimes it's dopaminergic agents that we try. If it's more of a myoclonus type tremor, then we may do something like Keppra or one of the benzodiazepines for that. We try to make sure that there's nothing that we can reverse. I've had some patients try, there was one patient that had a very interesting tremor and she was having pain too, and I sent her to a pain physician. The pain physician actually treated her with a spinal cord stimulator, which helped her tremor tremendously as well. So not that I'm saying send all your patients for spinal cord stimulators, but just try the usual medications that can help with tremor and then doing therapy. And then again, in case there's any psychological undertones and making sure that they have counseling and support. And fortunately, we have lots of questions left that we didn't get to. We have to wrap up. This has been an outstanding session, a very timely session, and I'm so proud to work with you and be able to provide this information to our colleagues here at the AAP Mariano meeting. And with that, feel free to reach out to all of us on Twitter, email, whatever venue for further questions. We're happy to talk to you offline.

COVID-19 pandemic

rehabilitation

ICU rehabilitation paradigm

early mobility

neuromuscular ultrasound

chronic neuromuscular impairments

long-haulers

multidisciplinary approach

early intervention

ongoing research