All right, everyone. Welcome to this week's installment of AMSM's National Fellow Online Lecture Series. My name is Matt Wise. I'm one of the current sports medicine fellows at the University of Utah. I have a background in family medicine, and I'm the outgoing fellow liaison to the education committee. Before we get into our topic for tonight, I want to remind everyone of next week's lecture on lower extremity peripheral neuropathies. Our speaker will be Dr. Ho, and our moderator is Dr. Creech. Same time as always, Wednesday evenings. Moving on to tonight, I'm very excited to welcome Dr. Lauren Borowski to speak to us on rheumatology in sports medicine. Dr. Borowski graduated from Drexel University College of Medicine, and then completed her family medicine residency at Wake Forest University prior to doing her sports medicine fellowship at the University of Utah. She is now an assistant professor at New York University in the Department of Orthopedic Surgery, where she is also associate program director for the primary care sports medicine fellowship there. She functions as medical director for athletics at Convent of the Sacred Heart, Baroque College, and Yeshiva University, and is also head team physician for U.S. ski jumping. Before we get started, we also like to mention the goals of National Fellow Online Lecture Series, which are to serve as an adjunct to your individual program's educational content, to provide fellows with direct access to educational experiences with AMSM members, and at times invited guest experts in a variety of different formats. And lastly, and probably most importantly, to assist in CAQ exam preparation. Now, we're recording this ahead of time, so a lot of these last reminders don't particularly apply. We've prepped some Q&A session at the end, and also have included a CAQ practice question as well. So please tune in. And now, without further ado, welcome Dr. Barofsky. Thank you, Dr. Weiss for having me. I'm really happy to be able to be here with you tonight. I know we're recording this ahead of time, but very happy to be invited to speak with you guys. So I'm going to go ahead and share my screen now. Okay, so tonight I have been asked to speak about some rheumatologic considerations that we see in the sports medicine clinic. And I have no conflicts of interest, no disclosures. My objectives are quite simple. I'm going to review a couple of rheumatologic diagnoses that you are going to encounter in the sports medicine clinic, and to discuss the workup that I do prior to referral to my rheumatology colleagues. So I decided to do this case-based. I think that's a good way to approach it. And these are certainly patients that I have seen in my clinic as either a very specific patient or a compilation of patients that I've seen. So the first case is a 27-year-old man with chronic low back pain. And he reports a three-year history of this back pain. His pain, when you ask him further questions, it's worse in the morning. It does get better as he moves around. Now in the state of New York, we have a direct access to physical therapy. So even though he hasn't really seen a physician for his issue, he has been trying physical therapy in the past. So what that means by direct access is that you can actually go see a physical therapist for 10 visits or 30 days, whichever one comes sooner. And some states have this available to them. New York is certainly one of them. He's tried some over-the-counter anti-inflammatories like ibuprofen and Aleve, as well as acupuncture, which I think acupuncture is definitely one of my go-tos for chronic back pain. So I was happy to hear that he tries that and tried that as an adjunct to his therapy and some anti-inflammatories. But like I mentioned, he hadn't yet been seen by a physician, so had not really had any sort of imaging to date, even though he's had it been going on for three years. So when I saw him on physical exam, he had some tenderness palpation of the bilateral posterior superior iliac spine areas. He had good range of motion with flexion, extension, rotation, and side bending bilaterally, but he did have some pain with extension. He did have a positive favor. So in this case, he was positive for pain in the posterior aspect of the hip, so in the low back area. So you can have a positive favor with either pain anteriorly, which is indicative more of an intra-articular hip pathology, like a hip impingement, or you can have it be positive for pain in the back. So it's really whichever one, I consider it positive if it recreates that person's pain. And so this one was pain in the low back area. He had a negative fadir, so a negative for intra-articular signs there, a negative Gainsland's SI compression and distraction, which are also the Gainsland's compression and distraction are all for SI joint pathology. He also had five out of five strength in his lower extremities. So at this point, I started thinking about a differential and really actually before I go into my office, into the exam room, I started thinking about, okay, they're this old and they have this problem going on. What are the things that could possibly be causing this person's pain? So the first thing would be mechanical back pain. Do they just have pain that has been going on for several years because of their biomechanics? Spondyloarthropathy is actually very, very much on the top of my list for a young person that's had pain going on for this long. Spondylolisis, which I see quite a bit of because I treat a population that does a lot of repeated extension. So I see quite a few dancers in my clinic. I do, I have a special clinic just for dance medicine one half day a week. And so spondylolisis is something that I see quite a bit of, or at least have it on my, very high on my differential. Dysgogenic pain. So either a fissure of the, an annular fissure or a, an actual frank herniated disc can certainly be causing this person's pain that he just has recurrent flares of. And then SI joint dysfunction, which I think can sometimes be a little bit nebulous because it doesn't really show up all that often with issues actually on radiographs. So speaking of radiographs and this person, he's been having pain for three years. I would want to start with some sort of imaging. So he's was having pain kind of in his low back, as well as tenderness, palpation, and SI joint. So I start with an SI, with a SI joint x-ray, a sacrum x-ray. What I'm looking for, and I also get lumbar x-rays as well. And what I'm looking for are anatomical variants. Does they have some sort of transitional anatomy? Do they have, you know, large transverse process that's possibly causing some pseudo articulation? Do they have any sort of signs that would lead me to think they've got more of a congenital stenosis issue? And then also looking for that SI joint sclerosis. Do they have issues or signs that already are pointing to erosions and in the area of the SI joints? With lumbar x-rays, now this is not this particular patient's x-ray because it is much more of a later sign. But what you're looking for would be in a spondyloarthropathy case, would be something like this, where you start to have squaring off of the vertebrae, where you start to have new bone formation kind of in the front interior portion of the vertebra. And then the late stage findings of actual fusion of the facet joints and the vertebrae come much later. So it's unlikely to see this bamboo spine in the clinic very often, but it is something that we get taught about in medical school all the time. So this is why I wanted to talk about this, because that bamboo sign, that bamboo spine is not something you're going to see very commonly. So you want to look for other things that might be pointing you down that spondyloarthropathy pathway. In him, if I'm thinking some sort of sacroiliitis because of the tenderness to that tenderness palpation, that posterior superior iliac spine on this x-ray, it looks like there could be a little bit of signs of sclerosis along those SI joints. It's hard to say, but something I'm highly suspicious of, I would start to get labs and the labs I'd be looking for are inflammatory markers like an ESR and a CRP. I usually get a CBC and a CMP to look for other signs of systemic problems, like white blood cell count is either too high or too low metabolic problems. And then when we're thinking about spondyloarthropathies, which is what ankylosing spondylitis is considered, I do get an HLA B27. So there is a correlation between those with ankylosing spondylitis and HLA B27. However, of those that are HLA B27 positive, only five to 6% of those actually have ankylosing spondylitis. So there are plenty of people out there that do have a positive HLA B27 that don't have ankylosing spondylitis. One of the things I usually end up getting because of the fact that the signs of the bamboo spine comes much later in the disease process of an axial arthropathy like ankylosing spondylitis, if I'm concerned about a sacroiliitis, I will get an MRI because it's that much more sensitive for things like this. So this MRI shows bony edema and erosions of the sacroiliac joint, which you can see on both sides, more erosions on that left SI joint than the right, but certainly bony edema on both. And so this can be really helpful in trying to figure out, are they in an acute process? Is it actually there? Is the, is the slight sclerosis that you might see on x-ray actually for real? So in this case, you know, our 27 year old gentleman that came in with three years of lower back pain that was worse in the morning and gets better with activity. He eventually did go in to go on to get diagnosed with ankylosing spondylitis. And it's like I was mentioning ankylosing spondylitis is an axial arthropathy with radiographic evidence and other spondyloarthropathies include psoriatic arthritis and reactive arthritis, inflammatory bowel disease, associated arthropathy as well. And the prevalence is really is, is small. So it's 0.9 to 1.4% of the adult population. The day the diagnosis is very commonly delayed. So people will go on to have these issues for years before someone actually goes to check their labs and looks at this imaging and, and goes on to refer them to a rheumatologist to, to make this diagnosis as well. And I think that most of, most of the time it's because of this, this dramatic phenotype of the spine, this bamboo spine is not seen until later. So what are the other things we need to keep looking for? And if any of you guys were at AMSSM last week and you heard Dr. DeMarie, who was a rheumatologist that spoke about this, she went on to, to say exactly this, we need to be looking for these other signs that could point us in this axial spondyloarthropathy pathway. So the other things that can commonly be seen with these are emphasitis, so inflammation where the tendons actually insert. So in this picture, you can see with this Achilles tendon, dactylitis, so sausage finger or sausage digit that you can see the swelling of the whole digit, buttock pain, spinal immobility, and then postural changes. So postural changes kind of happen later in the disease course too, but one of the ones that you'll see is, is hyperkyphosis. So in the patient that I saw in this, or in this example, he still had good range of motion. Even though he, he may have already had some subtle sacroiliitis and some, and some spine changes, he still had good range of motion when I saw him. The things to really think about when you're thinking of an inflammatory back pain or inflammatory process underlying this person's long onset or long chronic back pain problem is that you want to think of it when somebody is coming to your office and they've had pain for a long time, greater than three months, and they're under 45 years old, it's an insidious typically, and they will have morning stiffness, usually greater than 30 minutes. That's kind of the key here with a lot of the rheumatologic inflammatory issues, right? Is that they'll have morning stiffness. They will have an improvement with movement and no improvement with rest. Oftentimes these people will be woken up from their sleep with pain. And most of the time it's in the second half of the night because they've been sleeping and sitting still and lying still for hours. And they get this stiffness that does improve as they, um, arise from waking from, from sleeping. And then importantly, also this alternating buttock pain too. So you can have pain on the right side one week and then pain on the left side the next week. And it kind of plays off of each other. And so when somebody, when you ask them, which side hurts more, they'll often tell you it switches off and on. What do we do for treatment? It's really about pain relief and maintaining as much spinal motion as we can. The spine was meant to move. And so we're trying to prevent these, um, complications by continuing to have them be active. So physical therapy, regular exercise, postural training. So certainly we don't want to exacerbate the spinal problems that are happening by having, you know, poor muscular endurance of the paraspinal muscles. So working on that postural training as much as we can. Medications like an anti-inflammatory. Myself and a lot of our rheumatologists at NYU will do like a meloxicam because it is once a day. Um, so it's an easy medication to take so that they can tolerate it and they have a good response. It's a, it's a good one to try. And then if that's not enough, then we certainly start thinking about things like, um, TNF inhibitors or tumor, tumor necrosis factor inhibitors. And, um, some of the studies will, some of the recommendations from the American College of Rheumatology. We'll talk about how oral steroids are not recommended. And part of that is because it is an ongoing long-term problem. And so being on long-term oral steroids is not necessarily the best thing for someone's overall health for many reasons. So going on to case two, so case two is a 68 year old man with a swollen right knee. And he showed up in my office, pain and swelling just started two days prior to when he saw me and he was having a lot of pain. He didn't have any specific injury, just kind of started out of nowhere. Um, his pain worsens with any time he would go through the range of motion of the knee. He'd use some Tylenol, uh, but it hasn't been, hadn't been very effective, really stuck to Tylenol because he had other comorbidities with, um, some GERD and coronary artery disease. So he tries not to take any anti-inflammatories. On his physical exam, he had a large effusion, his range of motion. He had good extension. He was able to get to zero, but really not able to get past 90 degrees. And then he had tenderness palpation over both medial and lateral joint lines, negative McMurray valgus and various stress testing and the negative Lachman. So again, even before I go into the room, I started thinking of a 68 year old man with left knee pain, right? So the first thing on my differential is osteoarthritis, which is probably the, by far and away, the most common thing that you're going to see, um, in this age group. But then in addition, you'll also see, uh, degenerative meniscus tears. You can have an acute meniscus tear, an acute on chronic meniscus issue. He did not have a history of gout, but he certainly is in the age group that could have it as well as pseudo gout and then infection. So taking a good history to find out, you know, does he have a prosthetic? Does he have, um, any sort of hardware anywhere else? Did he have a recent infection, um, with, in some other part of the body that could have, you know, hematologically spread and seeded this joint. So a good history taking is, is very important. So for this gentleman, we got x-rays and the x-rays showed just a mild arthritis. And then, you know, you can see that by some mild narrowing of the joint line, on that medial joint line with the tiniest little osteophyte there marginally. And then if you look laterally, which I'm gonna zoom in here in just a second, you will see that there's this haziness in the area of the lateral meniscus. And so I chose this case in particular because it's subtle, right? It's really, really subtle to see these things sometimes. Sometimes it's a lot more obvious or you can have, you know, significant calcium stippling this joint line, but this is subtle. And so sometimes it may not be as obvious to you that there is some chondrocalcinosis in that lateral meniscus area. So I sent for, I did an aspiration and I sent for fluid analysis and the culture didn't grow anything after five days, but it did, and the cell count, which I didn't have listed here, but it was more of an inflammatory process with less than 50,000 on it. So the thing of note was the calcium pyrophosphate dihydrate crystals that were present. So this gentleman was diagnosed with pseudogout. And so pseudogout is sometimes also called calcium pyrophosphate dihydrate deposition disease, so CPPD. And it's clinically, when you see it in the office is very similar to gout. The episodes like gout are characterized by this acute onset of pretty severe pain without an inciting injury. Sometimes it can be precipitated by an infection. Sometimes it can be precipitated by an injury, but usually not, or usually it's unknown to the patient what precipitated it, but they will have redness, swelling, and warmth. The pain can be very intense. And with pseudogout, it actually can take longer to get to the peak of intensity in pain than gout. And it may last longer than three months, even though you've treated it. The knee is most commonly involved, but you can also see it in the, like gout, you can also see it in other joints. With pseudogout, you then most commonly see it after the knee and the wrist, ankle, elbow, toe, shoulder, hip. It's largely a disease of older people. So people in the later stages of life that you would commonly see osteoarthritis in or degenerative meniscus tears. So this can really be a tricky picture sometimes to discern which of these things is actually causing my patient's pain at this time. We're probably seeing a lot more chondrocalcinosis than a lot more pseudogout and not necessarily calling it that. So how do we diagnose it? So again, clinical history, you'll see this chondrocalcinosis on x-ray, and then you'll also see the calcium pyrophosphate crystals, dihydrate crystals on the fluid analysis. So those three things can kind of help you put this clinical picture together. And how do we treat it? So NSAIDs can be very helpful. So an anti-inflammatory, you can use something like an indomethacin. I usually use something like a diclofenac or a meloxicam at first to see if that's helpful. You can do an intra-articular steroid. It can be for more of a mono-articular, possibly two joints. And then oral steroids, if it seems to be more of a wider spread, more polyarticular issue. Colchicine can be effective in an acute flare, but in terms of the long-term medications that we use for gout, they're not effective right now against CPPD. So we don't use things like buboxystat and allopurinol for pseudogout. So now I'm going to ask a couple, we're going to get into a couple of questions. I've kind of sprinkled them throughout the lecture a little bit. So this is a 55-year-old male golfer who presents with isolated right shoulder pain, swelling, erythema, and warmth. There were no traumatic precipitating events. Radiographs demonstrate chondrocalcinosis and needle aspiration of the joint yield synovial fluid with crystals. These crystals would also demonstrate which of the following characteristics, consist of calcium pyrophosphate, exhibit negative birefringence or needle-shaped, or consist of monosodium urate. So if you were listening at all to the last couple of slides, you would know that with chondrocalcinosis and you're thinking pseudogout, it's going to be the calcium pyrophosphate. So let's go through this summary of the answer a little bit though. So, because it pulls out some good points and I've kind of highlighted a couple of them here. So the presence of chondrocalcinosis with crystals in the synovial fluid aspirate indicates pseudogout. Crystals in pseudogout are calcium pyrophosphate. Under polarizing light, pseudogout crystals are blue. So this, I'm going to skip a little bit here, and blue with a pseudogout crystal shows positive birefringence, whereas monosodium urate crystals in gout have a negative birefringence and are typically yellow. A pseudogout crystal is a rhomboid to rod-shaped with blue ends. Gout crystals, monosodium urate crystals are needle-shaped and often yellow, and are yellow, okay? So those are the key things to take away from that for the CIQ. All right, moving on. So case three, this one's a little, this one is a little tricky and I put it in here because of that, because there's a couple of things to highlight with this case. So 13-year-old girl with a swollen right knee, okay? She comes to you. This is a patient that I've had for several years. I've seen her for a number of other things. She's, you know, not always hurt, but does get a lot of things that have her ending up in my office. She plays soccer regularly and she started having, oh, I'm sorry, I mixed up the sides here. It was right knee pain. That should say right knee pain and swelling about a week ago. Hurts with all movements, but not particularly painful at rest. So anytime she moves it, it's painful. And she says it's because it's so swollen that it hurts. And she denies any specific injury. So even though she was playing soccer, she doesn't really remember any specific moment in a soccer game where she had an injury. On physical exam, she's afebrile. She has a respiratory rate and heart rate that were within normal limits. And her range of motion of this right knee is only five degrees to about 110 degrees. So she really can't get full extension and she definitely doesn't get full flexion because her other contralateral knee, her left knee is zero to 140. So she's got really good flexibility on the other side, but because it's very large effusion. So anytime you're walking, putting her through this range of motion, it's painful and she can't bend it very far. She does have tendons palpation over the lateral joint line. She has a negative McMurray and a Thessaly and no laxity with varus or valgus stress. Now, some of this was also hard to get because she was in a lot of pain, just moving the knee at all. So doing a McMurray didn't elicit a painful positive click, but was uncomfortable for her. So what are you thinking when you think of a 13-year-old girl who plays soccer that has knee pain and now an effusion? So my first thought was, does she have some sort of meniscus tear? Does she have a ligamentous injury? Does she have osteochondritis dissecans? Does she have, it's monoarticular, so she only has this one joint that's really swollen. Is it juvenile idiopathic arthritis that could be presenting in this way? Does she have Lyme disease? So I live in the Northeast, I'm in New York City. And even though you may not think that it's in New York City, they've found deer ticks in Central Park. I actually live in New Jersey and now commute into New York and I actually had to stop on the street today and let a deer cross in front of my car in order to get to the playground for my children, so in the middle of the day. So they're out there. It's very prevalent in the Northeast and the Midwest. So I wanted to see what more was going on with this young woman. So I got an X-ray, which showed no acute bony abnormality, but she did have this very large effusion. So if you look here, you can see this very large area here, that fat pad and that effusion in the suprapatellar region there. And I also aspirated the knee because with that much fluid, I was thinking, this should probably be something we should send for workup, right? On that list of things, I did put, I would have thought of infection, but she didn't have, this particular case did not have a lot of redness or warmth per se. And so infection was certainly much lower on my list. When I sent her fluid for analysis, it did come back positive for Lyme via PCR. While I was waiting for the Lyme, I ordered an MRI on that same day that I first saw her, and her MRI came back as showing a lateral meniscus tear as well with a discoid meniscus. So this is why I think this case is a little bit tricky, right? So which one's causing her the pain? Does she have, is it the Lyme that's acutely causing her this issue or does she get this lateral meniscus tear and in the setting of this discoid meniscus, which we know a discoid meniscus can increase your risk of having tears. So this was her MRI, as you can see, she's got a significant effusion with a lot of synovitis. And I think this is the key to knowing which one you should really gonna go for first, right? So Lyme arthritis is going to give you a very large effusion most of the time. So you'll have this significant amount, and this would be a large amount for a lateral meniscus tear. In my practice, I haven't seen someone that typically has this large of an effusion with a meniscus injury. But in addition to that effusion, you can see the anterior horn, and I only have one slice here, but it did go into the mid portion of the body of this lateral meniscus that was the meniscus tear. And this is another view of it, you can see here more peripheral tear here. So with Lyme arthritis, which I said is very prevalent in the Northeast and Upper Midwest United States, it was first described in 1977 after an outbreak of what seems like juvenile idiopathic arthritis in Lyme, Connecticut. And it wasn't until really the 1982 when Dr. Bergdorfer actually isolated that particular spheriche that we know of as Borrelia burgdorferi that causes this Lyme arthritis most commonly in the United States. It is the most common vector-borne illness in North America and Europe. And the vector is most commonly the Ixodes tick, which is a black-legged deer tick, which you can see here, the CDC has this nice depiction of on their website. And most of the time where they're being, it's the nymph and larva stage that can often get missed, and that's what stages are often the ones that will cause the infection. And it happens to be that the tick has to be attached for about 72 hours for there to really be a transfer of the organism. So, as soon as you find a tick, take it off. It has to do with the fact that things get kind of mixed in the mid gut of the tick, and it takes a while for that transference of the actual bacteria. And so, if you see it, take it off. It's not a problem to go and get a one-time dose prophylactically of doxycycline, or if they're younger, do like an amoxicillin. But even if you have it on for about 72 hours, only about 25% of those people will end up having some sort of Lyme disease too. So, don't freak out, but go see somebody if you find the tick. Before antibiotics, up to 60% of people were actually developing Lyme arthritis after they developed Lyme, but after antibiotics, it's been much lower than that because Lyme arthritis is a late stage manifestation. So, it can occur four days to two years after somebody finds that bullseye rash, that erythema migrans rash. And in some cases, the Lyme arthritis is actually the first presentation of the disease in general. And like I was mentioning earlier, they tend to have these very large effusions on exam. So, I wanted to go over a couple of these guidelines because I think, you know, I went to medical school in Philadelphia, and so being, again, in the Northeast, it was something that was like, put Lyme under differential. Like Lyme was on the differential for almost everything, whether it be encephalitis or arthritis. And so, these are practical guidelines that were put out in 2021 by the Infectious Disease Society of America, as well as the American Academy of Neurology and the American College of Rheumatology. And so, it touches base on all of those things, all the different body systems that are affected by Lyme. And so, I just picked out the ones particularly with Lyme arthritis. So, they recommend that we do serum antibody testing or PCR or culture of blood or synovial fluid. And this was a strong recommendation. And if you are thinking that, if you have a seropositive patient who you think has Lyme arthritis and you're considering treating them, which I would, they also recommended PCR from the synovial fluid if you can get it, as opposed to a Borrelia culture. So, you wanna do PCR whenever you can. In my practice, I will get, if I can aspirate a joint, because I think the effusion is coming from an arthritis or a Lyme arthritis, I will send for PCR. But there are quite a few patients in my population that the arthritis has been there or the joint pain has been there for a while. They may not have much of an effusion. It may be something that they have multiple joints going on that I will test for serology. That's one of the reasons why I end up getting Lyme titers is because the picture's just not matching up and no one's ever tested them for Lyme, which is why it's important to test for both the antibodies as then have a reflex for Western blood to confirm it is the way that it's done. What antibiotics do we actually use? So, for patients with Lyme arthritis, we recommend using an oral antibiotic for 28 days. Typically, it's a doxycycline. And then what happens if it doesn't completely resolve? So, what happens if they take that 28 days? Well, there's not great recommendations as to what we should do next. So, you can do a second course of oral or you can start an IV course of ceftriaxone. And so, not great recommendations either way, but in my practice, what I do is I usually do 28 days. I send them to rheumatology to help them co-manage it. So, if they are not better at 28 days, I will extend it for another two weeks. And then at that point, I'm working with my rheumatology colleagues to decide, okay, do we have to start some sort of IV antibiotics? And then what if they failed antibiotics? If they failed oral antibiotics and a course of IV antibiotics? Well, that's when we start thinking about, okay, do we need to start adding in something like a DMARD? So, a disease-modifying anti-rheumatic drug, you can do an antibiotic agent, you can do a synovectomy if it's really prolonged in their refractory to antibiotics. But there has been not a lot of great evidence for these recommendations. But we all kind of agree that antibiotic therapy beyond eight weeks really isn't gonna give you additional benefits. So, we don't wanna completely destroy your gut for much longer than we need to with an antibiotic. So, coming up with these other things to resolve some of these symptoms might be helpful. And now the last case. So, case four, 70-year-old woman comes to you just complaining about having difficulty getting out of a chair. And I made this one purposely vague because this is what you'll see sometimes. Sometimes people will just come to your clinic and they're like, I can't walk anymore. Like, I have trouble walking. I'm not as fast as I used to be. I can't get out of a chair. It's hard for me to get out of bed. So this woman in particular had symptoms that had only really been going on for about two weeks. The stiffness was worse again in the morning. She feels better when she gets up and moving around and her other symptoms were vague. So she had malaise. She was fatigued. She really didn't have any fevers, but she did have pain and difficulty with moving the shoulders in particular. Um, she was up to date on her cancer screening. So really wasn't dealing with any sort of underlying malignancy that we had known of. And the reason I mentioned that we'll come up in a second, we talked about the differential. So on her physical exam, she had difficulty getting out of the chair with using both hands and certainly was unable to get out of a chair without using either hand. Um, and so that timed up and go test was pretty, was pretty abysmal. Um, she wasn't able to get out without using her hands, her range of motion, the shoulders, it wasn't bad once she got it moving. So for reflection at one 60, it looked pretty, you know, okay. Abduction of one 70 internal rotation to about T-10 and, um, external rotation about 50 bilaterally. She had pain though, with all of the movements of the shoulders. And when I started thinking about this differential, it's very broad. Um, cause she had adhesive capsulitis of her shoulders. Sure. But does that necessarily, uh, explain her hips? She could have adhesive capsulitis of the hips, which I've seen, but it's very rare. It's not common. Um, hypothyroidism. So having this just like sluggish malaise fatigue, uh, issue, does she have fibromyalgia? We certainly all see a lot of fibromyalgia patients in our office. Does she have depression? You know, depression can present in a lot of different ways and having, you know, slowed motor skills can certainly be one way that depression depression presents itself Parkinson's disease. So having again, that, that, um, that slowed gate and that, um, that can be a Parkinsonian type feature. Does she have a perineoplastic syndrome? And that's what I meant when I was alluding to having, uh, being up to date and all of our cancer screenings, right. Does she have other things that are under underlying? Is this a multiple myeloma type picture where she's, she's have, has this metabolic storm and metabolic things that are going on underlying her issues. So I bring this up to talk about polymyalgia rheumatica, which is more common in women than in men. And it usually occurs between the ages of 50 and 80. This is something that you will see. Uh, I know certainly from my family medicine colleagues, you'll see it. I certainly saw it when I was, um, we had to do our nursing home, um, rounds and our nursing home, um, rotations in residency, but you will see it come through your, your office as well. And it's just something to keep in mind. Maybe it actually has seen more of you than you've seen of it. It is associated with giant cell arteritis in about 10 to 20% of cases. And generally it starts with this acute onset of shoulder pain and morning stiffness, and it affects the pelvic girdle as well, which is why they have such difficulty getting up and out of a chair. The pathophysiology is really synovial and periarticular inflammation and this vascular proliferation, which is often mediated by IL-6. And the European league against rheumatism and the American college of, um, rheumatology has this classification criteria for, um, polymyalgia rheumatica. And again, like a lot of other rheumatologic problems, it's morning stiffness, um, hip pain or limited range of motion. And then they start talking about some of the labs with the absence of rheumatoid factor and other, um, yeah, other, uh, labs that we will, that we will check for our rheumatology colleagues, absence of other joint involvement. And then this is one that's interesting too. So at least one shoulder with sub deltoid bursitis or biceps tenosynovitis or glenohumeral synovitis, uh, and, or one hip with, um, synovitis or trochanteric bursitis. So you've got all these points and you add them up and some of them, um, require you to use ultrasound or obviously to see some of that sub deltoid bursitis or the, um, sometimes they're trochanteric bursitis. So you can use this as a kind of way to guide your clinical diagnosis as to whether or not they have polymyalgia rheumatica. And so the diagnosis is clinical based on this criteria and getting some labs, like they mentioned, which I'll go over on the next couple of slides as to which ones I get, but the treatment is glucocorticoid. So typically people will get started on penicillin 12 to 25 milligrams daily and their symptoms go away pretty quickly within a couple of days. Um, they'll feel, start feeling very well. However, people can be on this for a long time. So it sometimes can take a very, take a very long time to taper off of the steroids and they may notice symptoms get re exacerbated. It can recur. So they may end up back on steroids too. And then there is some correlation between some cancers, you know, between cancers and this picture. So that's why it's always good to make sure that they are, are up to date on their cancer screening. Sorry. So when do I refer to rheumatology? So when the picture is not clear, when the patients have been coming to me for a multitude of different issues, this is something that I start to think about, you know, am I missing something else? Right. So do I have a patient with multiple joint complaints, particularly small joints, and they are not responding to the typical treatment that we're trying anti-inflammatories we're trying physical therapy, we're trying, we're trying adjunctive therapies like acupuncture and talking about healthy lifestyles, younger to middle-aged patients with multiple emphysitis or tendonitis issues. So this is something that I do have. I have brought into my practice over the last couple of years to be like, okay, well now you've got tennis elbow and you had Achilles tendon issues, Achilles tendon issues before, and you're only 35 and you seem to have some glute tendinopathy too. So it's, it's something to just put into the back of your mind to think of, okay, maybe there's something underlying here that we're missing. Maybe we need to start thinking about this a little bit more frequently. And those with autoimmune inflammatory issues that are now coming to me with a joint presentation. So people who have psoriasis or those people who have some sort of inflammatory bowel disease, whether it be Crohn's or ulcerative colitis, and now they have a significant joint effusion or significant, you know, limited range of motion in a joint. So those are things that I start to think about and will send to my rheumatology colleagues just to say, hey, is this a, you know, an articular manifestation of their underlying process and kind of co-manage with them. And when it comes to labs that I order, these are, these are ones that actually our rheumatology department here at NYU really likes to see prior to us sending to them. And so this is by no means an extensive list of the labs that rheumatology orders because, but this is the basic ones that, that we will start with. So I always start with a CBC and a CMP to make sure that we're not, you know, to look at those underlying metabolic issues or, you know, anemia, white blood cell count. I will always get an ESR and a CRP to look for that, those inflammatory markers and the higher they may be, they could indicate a more widespread systemic problem. A rheumatoid factor, an anti-CCP. I do get an ANA, although I know that many people will have a positive ANA and up to about 10% of the normal population will have a positive ANA and have no other symptoms. So I am aware of that, but it is something that our rheumatology, our rheumatology colleagues here at least like to see. And then the HLA-B27, I don't routinely order HLA-B27. Again, it's only if I see somebody that I'm thinking has a sacroiliitis or a possible axial spondyloarthropathy. And we'll go to vitamin D. Again, we live in the Northeast, so we're always covered up and sometimes a very low vitamin D can cause a lot of discomfort and fatigue and bone pain in some people. So if you can replace that, sometimes people will have some resolution of their symptoms. And then, like I mentioned, the Lyme titers with that reflex western blot. A couple other questions here. So which of the following describes the characteristic distributions of joints affected by rheumatoid arthritis? Asymmetric involvement of the large joints, involvement primarily of weight-bearing joints, symmetric involvement of large joints, or the symmetric involvement of small joints? I know I didn't cover rheumatoid arthritis in this talk, but I think this is something that we should all know and certainly will be asked on the CAQ. So it's the symmetric involvement of the small joints. And here's the rationale behind it. So it presents with pain and multiple joints that is usually symmetric pain and synovitis involving small joints, such as the hands, wrists, or feet. Osteoarthritis is more commonly monoarticular or asymmetric and often involves weight-bearing joints like the hips or the knees. When osteoarthritis involves the hands, it tends to involve the DIPs while rheumatoid arthritis tends to involve the MCPs and PIPs. And there are some of my references and thank you guys. Appreciate you having me. Awesome. Well, thank you for that great talk, Dr. Braske. I think this is relevant in practice given the overlap in MSK medicine. So thank you. A couple questions, a couple follow-up questions for you. Inclosing spondylitis, given that fusion and bamboo spine, like you mentioned, are typically late stage features, do you typically get MRIs or maybe how common are you getting MRIs in patients in which you suspect like an inflammatory cause of their back pain? Yeah, I think that if I am highly suspicious of a sacred, like certainly if I see some sort of signs of sclerosis or erosions on my x-ray, I go, I get it right away. If I don't, but I'm still suspicious of it, I will get those labs that I mentioned, like the ESR and the CRP and I will, and the HLA-B27. I will often have to go through a course of physical therapy and try a different anti-inflammatory and see if just changing up, you know, physical therapy providers or changing up the anti-inflammatory will be enough to help them with their, with their relief. And then I'll send them back for follow-up. If it hasn't changed a whole lot, then I get the MRI. I think it's, I think it's important to, to not let them linger longer because we want to make that diagnosis, right? The other thing that I find tricky about rheumatologic issues is often that they may not be, you may not see it right away, right? So there are things that actually can still develop too, right? So like patients may have, you know, these things that may not add up to you right away. Like they have, you know, some wrist pain, they've got some finger, like some finger joint pain, and they may show up a year later with knee pain. And I'm like, man, let me check their labs. Let me see if it's something, and they're completely normal. And then, you know, five years from now, you may check them again and something starts brewing, right? Like something's been brewing and now the labs are maybe a little bit more positive. So I just having an under differential and then pulling the trigger with that MRI of the, the MRI of the sacrum, I think is, is not unreasonable. That makes a lot of sense. I'm really glad that you brought up pseudogout. I've actually seen that a couple of times already in the past year, one of which was in, was in ski clinic. So that was an interesting conversation. But I wanted to ask, you know, how definitive is chondrocalcinosis for pseudogout? The reason I ask this is because if you see this on films for a patient who's presenting with a knee infusion, do you still need to do like the full workup, for example, like including for septic arthritis and that type of thing? I think the septic arthritis certainly is something that you definitely should work up. If you have a high clinical suspicion for it, like if they have, you know, certainly if they have some sort of history of like a recent surgery or recent infection elsewhere and keeping that in mind, it's going to be extremely painful for them to move that septic joint. I can't say that I do that, that workup every single time, but I will aspirate them and I'll send, I'll send it, you know, I don't necessarily start antibiotics. Right. So I do aspirated every time that I can and send it for, for fluid analysis. That being said, you know, there are some studies that show up to 50% of people by the time they're in their eighties will have some sort of chondrocalcinosis on x-ray. Right. And so it's a high percentage of people that will have some sort of calcium deposition in the hyaline and fibro cartilage of the, of the joint. And so that's why I think it's hard to differentiate sometimes. Right. So that's why sending that, that fluid is, is important, you know, seeing those crystals can kind of make it maybe a little bit more clear for that period of time, because the people that we're seeing it in, we're seeing pseudogout in those people that have degenerative arthritis as well as degenerative meniscus tear. So like any of those things can be causing their acute pain. But I think that, you know, keeping it in mind and then, and knowing that chondrocalcinosis is really prevalent. So that's why maybe going towards the fluid analysis is a better option for diagnosis. I see what you mean. And I was not expecting the Lyme arthritis to be honest, but I think it's super relevant from where you practice. And, and I think Lyme is also in other places. Like I saw it a couple of times in residency in Seattle and certainly actually a fair bit in Texas as well. I think it's interesting that the IDSA recommends the antibody testing and before the synovial fluid analysis. So I appreciate that you brought, you brought that up. Is, you know, if you're getting positive PCRs on synovial fluid analysis, to me that, that may imply that there's some infection in the joint. Is, is like a joint washout ever involved? Or can you just confidently say, Hey, we'll get, we'll get them 28 days of doxycycline or amoxicillin in theiatric population and see how that does? Should we be thinking about this more as an inflammatory condition than like a truly septic joint? Yeah, it's a, it's a really good question, right? Cause you're like, well, if the PCR is that, then obviously there's some sort of, you know, if that PCR is positive, then there's bacteria there, right? Or so we think. But it really sets off a really strong inflammatory cascade. And so when you look at the joint fluid of people with a Lyme arthritis, it often is more of an inflammatory picture than an infectious picture. So they'll kind of hovering in between like 25 to 25, 30 to 50 of that white blood cell. So it's, it's often a little bit more of an inflammatory type picture when you're looking at the fluid, even though you do have that positive PCR and it generally responds really well to antibiotics. And so I think that's why you see them say, you know, let's go the antibiotic route for 28 days and, and avoid that washout if we can. Because most people respond to the, to the actual antibiotic and you want to kill the whole process, right? Like we have to kill, you know, you have to kill it systemically as well. And so I think that that's why, why we see it cause it does usually respond. But for those that don't, you know, those people do end up going on to get perhaps a casinodectomy because the inflammatory response has been so great at that point. Okay. Okay. Well, that's super helpful. Last question for you has to do with PMR. I appreciate you bringing up the diagnostic criteria and it made me wonder how many trochanteric bursitis patients actually had underlying PMR that I, that I haven't diagnosed. But I guess kind of last question would be, do you have a sense of why those, what would you say, bursitities are part of the diagnosis? Do you think it's like secondary to the weakness in the muscles from, from the PMR, maybe loading those tendons? Just want to kind of get your two cents. Yeah. I mean, it's a good question. I mean, so, so, so the, you know, the pathogenesis of it being more of like a synovial and periarticular inflammation I think probably has a lot to do with along with the neovascularization. So you're just bringing a lot more to that area and it certainly could, you know, compound the problem where these patients are feeling weak and then these tendons are not getting, you know, worked in the way that they should. And so they end up getting weaker, causing more bursitis in the area. So it's kind of, I think, I think it's a little bit of a, a compounding issue. But why exactly we see the bursitis, I'm not, I'm not a hundred percent sure. Yeah. Great. Well, again, thank you for an amazing talk. Thank you for everyone for tuning in and we'll see you next week. Thank you guys. Appreciate it.

3rd Edition, CASE 48

3rd Edition

Rheumatology

sports medicine

ankylosing spondylitis

pseudogout

Lyme arthritis

polymyalgia rheumatica

diagnostic challenges

treatment strategies

Dr. Lauren Borowski