Good evening and welcome to Utilizing Ultrasound in Your PMR Practice. This session will focus on how ultrasound can be utilized to enhance any MSK and neuromuscular physiatry practice. We're going to be going through interactive cases from our own practice with the goal of improving your diagnostic ultrasound skills and procedural ultrasound skills. And we've developed a session to complement the robust step ultrasound certificate program. I'm just going to share my screen. All right. So, again, this is Utilizing Ultrasound in Your PMR Practice. The learning objectives for today are to better understand when ultrasound can be successfully incorporated into a physiatry practice, to understand advantages of ultrasound compared to other imaging modalities, and to understand the role of ultrasound guidance during chemo denervation procedures and for other novel musculoskeletal applications. I'm Dr. Brett Moore. I'm a PMR sports medicine physiatrist in private practice in Kansas City Orthopedic Alliance. I'm going to be one of the moderators for today. Dr. Allison Schrader is our other moderator. She is a assistant professor at UPMC in the PMR department. In addition to being one of the co-moderators, she'll be presenting our knee case. Dr. Catherine Alter is a senior research clinician at NIH. She will be presenting on lower extremity dystonia in runners. Dr. Eitan Ran is assistant professor in the PMR department at Kaiser Permanente School of Medicine. He's going to be presenting our shoulder case. And Dr. Zachary Bailowitz is assistant professor in the sports medicine department at Kaiser Permanente School of Medicine. He will be presenting our ankle case. Some housekeeping notes for optimal experience for everyone. Please make sure your microphones are on mute. Use the Zoom chat box at the bottom to share your thoughts and ask questions. At the end of each case, we'll do a panel discussion and open it up for a general Q&A. And so you can, again, use the chat function during that time as well during the case presentations. Make sure to claim your CMEs after the end of the session through the Academy's online learning portal. We'd love your feedback with that process as well. There will be breakout exhibit rooms during the break for the session and the kind of halftime as well as at the end of the session. To access the breakout room, you're going to click on the breakout room button at the bottom of the screen. That will only be available when the breakout room is actually there. A pop up screen will appear. Hit the join button. You can leave that breakout room and come back to the main room at any point. Just make sure you don't leave the entire meeting. You just leave the breakout room. All right. I'm going to stop sharing my screen and we will pass it on to Dr. Alter. So I hope you can see my screen here. And these are to my my case today is talking about runners dystonia or dystonia and runners and. OK, so I'm going to cover actually we're supposed to be doing a case, but I have three runners with a similar problem, all of them with stiff knee gait. These are my disclosures. One of the things and Britt's already mentioned this is the expansion of the STEP program. In years past, ultrasound was used primarily or exclusively by MSK and pain specialists within our PMR specialty. But the advances in imaging have led to other PMR tracks adopting ultrasound imaging for both procedural and diagnostic imaging. And this led to the expansion of the STEP program to include both neuro and MSK focused ultrasound imaging. In my case, it will or cases are going to highlight some issues associated with kind of that branch or or span musculoskeletal problems, as well as neurological problems and talk about human innervation procedures for patients with dystonia. And it really illustrates the need for all PMR specialists to think outside their own box. And although many of us are specialists or subspecialists, we also need to be generalists to to be able to neurology focused practices. PMR docs need to think about MSK problems in their patients and MSK focused physicians need to think about possible neurological symptoms in their patients. So here are my three runners. This is a 50 or four year old woman that was referred for history of two years of an altered gait of a stiff knee gait that was presented presented initially only with running. By the time she came to see me and had generalized to affect walking, and she had self initiated physical therapy multiple shoe changes, she'd seen her primary care doctor who referred her for a malignancy workup. She then saw neurosurgery, a couple of orthopedic surgeons and a sports medicine doctor. She had two MRIs, had at least one arthroscopy and two sets of knee joint injections. Before she was eventually referred to a movement disorder neurologist who diagnosed her with a task specific sports dystonia or runners dystonia. And that's case one, and she's going to be my simpler case to present. The second case is a 63 year old many year runner long distance runner who ran many marathons as did the prior patient who had a four year history of gait problems. And initially she reported problems with clearing her toes, her left foot of her left foot when she was walking or running, but then eventually was reporting problems with a stiff knee. Again, she was seen by several different practitioners, including orthopedics was had x rays that showed that she had scoliosis shed an MRI that showed DJD and some disc disease as well as osteoarthritis in her knee. And she was told that the problems with her gait were due to the disc disease, but she never had an EMG or any testing to suggest that she had a radiculopathy. And again, after about three years, she was referred to us for evaluation of this problem and was eventually diagnosed with runners dystonia. And some of these, what we're illustrating here is task specificity so that the problems that patients report are only present during specific tasks. This is my third case. All again, patients with stiff knee gait, but the top video is interesting. This patient was a control in a runners dystonia study that we did at NIH. One of his friends has dystonia and he had normal gait in 2016. In 2020 he was referred to us with this gait pattern of stiff knee difficulty flexing his knee during swing phase. And this all began several years before when his peers noted some changes in his gait. Again, the same sort of history had been referred to multiple practitioners and had seen multiple physicians was told that he had disc disease that was causing his problems. Eventually referred to neurology and to us in a movement disorder program where he was diagnosed with a task specific runners dystonia. So what the heck is runners dystonia or task specific sports dystonia? Well, the first thing is that dystonia is many things. First of all, there's many types of dystonia and there's multiple causes and dystonia is also can be a clinical sign or symptom like in these patients who have dystonia as a primary clinical symptom or in a patient who has a stroke, who develops post stroke dystonia. But dystonia is also a syndrome or a disease like Sagawa's disease or DOPA responsive dystonia or myoclonus dystonia syndrome, where it's a specific disease entity with a genetic diagnosis. So with dystonia, first of all, it's the third most common movement disorder and the clinical features that it can involve any muscle group. This is a young child with a DOPA responsive dystonia and patients can present with intermittent or sustained postures. The patient on the top has a hyperkinetic dystonia, where the patient on the bottom video has a fixed postural dystonia. Although any muscle group can be affected in the same individual patient, the movements tend to be stereotyped and repetitive involving the same muscle groups. Other clinical features that dystonia can occur at rest, like in this patient who has painful moving toes syndrome or in this runner with dystonia who has a trunk or axial dystonia. And some patients will report a sensory trick or just antagonist that a sensory touch or a movement will reduce their dystonia. And in most of these patients with dystonia rigidity or hypertonia is absent and patients don't have altered tone, they just have involuntary movements. In our cases, particularly in the what we're talking about today is really a task specific dystonia that occurs only during specific activities. So in the patient on both of these are patients, to get my videos to work, are patients with focal dystonia involving the arm and you can see the involuntary movements in the patient on the top. On the bottom, the patient actually has dystonia in his left hand and what we're showing is mirror movements when he attempts to write with his right hand. This brings out the dystonia in his left hand, which is involuntary wrist extension. It can be either segmental or focal and that's what we're talking about today. I'm not going to go over generalized or other dystonias. And in our cases, we're talking about either segmental or focal dystonia that's idiopathic. Involving the lower limb, which is runner's dystonia can involve any muscle joint or region in a patient in the bottom, it's toe flexion. In the middle video, the patient has a segmental dystonia that involves his whole right lower limb and in this patient on the top has an axial dystonia with a trunk tilt. So focal dystonia in the upper limb, like a musician's dystonia, on the top video is a patient who has involuntary movements in the flexor digitorum superficialis of D4 of his right hand. Focal dystonia in the upper limb is very common, but focal lower limb dystonia is rare and it's only 0.7% of patients with the idiopathic focal dystonia. There have only really been about 100-150 cases reported in the literature, and at this point it's a diagnosis of exclusion. It's important to recognize that more often that focal dystonia presenting in the lower limb is actually a sign or symptom of a generalized process. In the video on the left is a patient who presented with runner's dystonia who actually has a diagnosis of MS that was picked up by imaging. And you need to rule out all of these other potential conditions, and so focal lower limb dystonia requires an extensive workup to establish this as the diagnosis. So what are the clinical features of runner's dystonia? This is a disorder of middle age, fourth and sixth decade, and in runners sometimes a little bit earlier. It's a two-to-one in idiopathic dystonia, it's two-to-one in females, but in runners it's a little bit more equal. It's associated with, idiopathic dystonia is associated with many years history of repetitive exercise or training, so a skilled task like running, cycling, golf, or dance. It tends to affect distal more than proximal muscles, although you can see either. And the symptoms at presentation, patients usually have had symptoms for over a year, somewhere between one and five years before diagnosis, and is often associated with a change in training. And the first thing is the peers report a change in their gait with a lot of automaticity and slowed speed, with difficulty in changing direction and a pulling sensation or pain. So I'm going to go, the additional feature that I think is important to recognize is task specificity. So in our first patient, the stiff knee gait that she has in walking forward, when you ask her to walk backwards, her gait is completely normal. And because of this, the test specificity can be lost over time after many years, but because these symptoms tend to be kind of bizarre, many patients are initially misdiagnosed with either MSK or psychogenic problem, so it's important to recognize that task specificity is present. So let's go back to case one. And in case one, our lady with, our runner with a stiff knee gait, it's pretty isolated. The main problem is her knee doesn't flex. And so what we did is we did, sorry about that, a gait study. If you're not familiar with looking at gait studies, I've got circles over the ones that we want to look at. This is knee flexion extension and this is ankle plantar flexion and dorsiflexion. Flexion is up, heel strike is on the left. The mid, middle is the start of swing phase. So everything to the left of the 50% line is stance phase. Everything to the right is swing phase. And if we look here, flexion is up, extension is down, red is right and left is blue. So if you look here, here's her normal knee flexion on the left side, which obviously you can see when she's walking, but on the right side, she lacks knee flexion during swing phase. She has some hyperextension of the right knee during stance phase. And she has limited ankle plantar flexion, mostly on the right side. And we also correlate this to EMG and she has a pretty significant co-contraction and out-of-phase contraction on her quadricep muscles, as well as in her hamstrings. So when we looked at this video, our conclusions based on her gait study and also her clinical presentation, her workup was consistent with past specific dystonia. And we felt that the primary problem, her primary issue was limited right knee flexion and that there were another significant compensatory activities, including right limb circumduction and decreased right hip flexion that some of these were, and the decreased plantar flexion of her right side were compensatory. And we really focused on the out-of-phase activity in her quadricep muscles, including the rectus femoris and the vasti. And so our recommendation was botulinum toxin focused on the quadricep muscles. And we initially did a scan of, when we do muscle scanning for chemodenervation, we really scan in short axis because the pattern recognition for muscle recognition really is best in short axis. And you can see the vasti, including intermedius, medialis, and lateralis, and rectus femoris in these short axis scans. And we will do our injections. In this lady, we ended up injecting her rectus femoris. This is a in-plane, not the best in-plane injection, but an in-plane injection in long axis into her rectus femoris muscle to deliver the toxin as precisely as possible into the muscle targets. So we injected her quads. We started with rectus femoris because of the out-of-phase EMG activity. And we really did isolated, we did several, two injection sites at a relatively low dystonia dose of onobotulinum toxin A. And this was the patient four weeks post injection of about 50 units of onobotulinum toxin A into her rectus femoris muscle. That's a frontal plane view. And here's a sagittal plane view. And I think you can see that directly targeting her quadricep muscles had a significant, led to a significant improvement in her gait speed, her knee flexion, and she was able to return to running. Since then, she's had injections in other muscles besides just the rectus, including some of the vasti, and has done fairly well in maintaining her gait and ability to run. And that's sort of my simple case. I started with a simple case of stiff knee gait due to quadriceps overactivity or dystonic activity. The other two cases are more complicated. The 63-year-old woman who has this position, if you look carefully at her gait, she's plantar flexed at initial contact. And she also has this weird little whip in her left ankle to clear her foot. She's not circumducting, but she has a little whip to clear her foot. When we look at her kinematics, she has prominent left knee hyperextension during all of stance phase. But as opposed to our last lady, she has almost nearly normal knee flexion during swing phase. She also has this abnormal plantar flexion during stance phase. And she has, on the left side, which is blue, she has this variable toe-in, toe-out, excessive toe-in, toe-out on the side. Her EMGs were not very clear because she had co-contraction in a whole bunch of different muscles. And also co-contraction on the other side, on the right side, due to compensation. And we weren't really clear what we thought was the cause of this problem. And we weren't sure if her stiff knee and plantar flexion, whether this combination was due to a biomechanical couple that we call plantar flexion-knee extension couple. If you land with your ankle plantar flexed at initial contact, it forces your knee into extension in stance phase. And we thought that that's probably what this was, but she also had co-contraction of her quadriceps. So it wasn't clear to us. So our next step in this lady was not botulinum toxin. It was diagnostic motor point blocks using ultrasound guidance and E-STEM to a guide for lidocaine motor point blocks. So on the left side, this is, we actually first started with, in series, we did her plantar flexors first. And this is just isolating the tibial nerve. And we went down and did motor point blocks. This is kind of a combination of using, we have Doppler on as well to help us with this outer plane position of the needle near a motor point right here. We use Doppler to help us isolate the neurovascular structures in some of these smaller nerves. But we use STEM and ultrasound together to isolate these structures and then blocked first her plantar flexors. And then we blocked her quads in series. I want to talk a little bit just briefly about out of plane. I'm one of the, probably the few people that prefers out of plane injections, particularly for toxin injections. And we use a different technique for out of plane. Many people use this shallow needle insertion angle. And the concern is that obviously you can insert your tip beyond the beam of ultrasound and be in an untargeted structure. We use this very steep angle of needle insertion that prevents you from inserting your needle across the transducer beam, the ultrasound beam, and keeps the needle tip under the ultrasound beam and within the targeted structure of interest. It's just a difference in technique that some of us are using. So this is an example of a Vassus medialis block. I'm gonna just scan through a little bit of this because it may be taking too long. So this is the use of, again, stimulation and using the injectate. We're inserting the needle here at this point into the motor nerve branch, which we'd already isolated was right in this region. And then you will see the flash of the lidocaine as it goes in and fairly quickly blocks the motor response. So we'll do that at several different sites. We also do in-plane nerve blocks of the femoral nerve if we're trying to block all of the quadriceps at the same time. So this is a ultrasound guided femoral nerve block in-plane when we were trying to block the entire, obviously the entire femoral nerve to all the quads. In this patient, we wanted to isolate just the vasti, two of the vasti that we were targeting on that patient. The end result was that she really didn't, she had better response to the plantar flexors than to the quads. And so we proceeded with botulinum toxin injections in the medial gastroc. This is an out-of-plane view of injection of the medial gastroc. Here's the needle tip within the medial gastroc. This is an in-plane long axis view, again, of medial gastroc in the same patient. Because of the equinus position of her foot, we also injected her tibialis posterior from a posterior approach. This is a short axis view, distal end of the medial gastroc soleus and tibialis posteriors down in this gutter, or some of you that know me, we call this the bathtub view with the tibialis posterior sitting between the tibia and the fibula. And you can see the toxin or the injectate as it's going in and distending the muscle belly. So for her, the issue, she had a series of different injections without really great benefit to with injection of her plantar flexors. We added her quads and that didn't really help at all. And then she had an eight month gap between her injections because of COVID. And when we brought her back, she told us that as the toxin wore off, the plantar flexor toxin injections were off, her symptoms got substantially worse. So we decided to go ahead and increase the dose to the plantar flexors. And unfortunately, this was the result. So if you notice, her left knee is now unstable at this point. And at this point, you can see that she's having difficulty walking. And the reason is we unmasked weakness, although she does have dystonia in her left foot, she also has weakness in her quadriceps. And that was the illustration of, you know, having to use care when you're dosing botulinum toxin because you can unmask weakness in other muscles. So our conclusion was that she was using plantar flexion to maintain the extension. And it made it difficult to treat her dystonia in her left ankle to deal with this. And I'm running out of time here. So I'm only gonna briefly talk about our case three, who is this guy with a stiff knee gait. And we were concerned on his gait that he had significant complaints of knee pain as well as this stiff knee. And so after we established that he had a diagnosis of runner's dystonia, we imaged his left knee. And he had a significant super patellar fluid effusion and also a Baker's cyst, multilobulated Baker's cyst as well. So we referred him to MSK for aspiration prior to us injecting him for his plantar flexor dystonia. And I'm gonna skip this part and just say that, you know, the treatment that not all of the gait issues in runners are caused by MSK issues, but not all gait problems in runners are caused just by neurological issues. So it's really important to consider the intersection of MSK and neuro in these patients because we have now several patients with a stiff knee gait that all had knee joint effusions that improved with a knee joint aspiration in addition to treatment of their dystonia. And we think that ultrasound imaging should be considered in all patients with sports dystonia for both diagnostic imaging and procedural guidance. And then I'm gonna stop my sharing here. Thanks so much, Dr. Alter. Those were wonderful cases. We're going to now open it up to Q&A. So if anyone has questions, feel free to put it into the chat. And then the panel will also be available to answer your questions in addition to Dr. Alter. Thank you. Catherine, do you have, do any different like technique in terms of how many sites you use to disperse it more with someone who their goal is to get back to kind of running or walking activities versus kind of typical post-stroke or post-brain injury where you're really just trying to optimize range of motion? It really depends on what the problem is. If you've got a long muscle, like for instance, the quadriceps, you need to, we try to focus our attention at the site or the innervation zone of muscles because we know it's gonna be more effective. When you're treating patients with post-stroke or MS or something like that, oftentimes you're using much higher dose of botulinum toxin. The dystonia doses are much lower for all four of the approved toxins. It's somewhere between a fourth, about a quarter of the starting dose that we would typically use for spasticity. So you're using a lot of the same dosage So you're using such small volumes that I will use at least a couple of sites in a long muscle, like the quads. If I'm doing a focal hand dystonia, it's gonna be a very small, like 2.4. Let's say if I'm talking about on a botulinum toxin A or incubating a botulinum toxin A, I might be using 2.5 units in a muscle fascicle. You know, if it was a botulinum toxin A, it might be five units. So it's teeny tiny volumes. So that precludes you doing multiple sites. But so I guess the long answer is I still try to do multiple sites if the volume of injectate allows. But I follow the end plate, either end plates or innervation zone. We have a question from the chat. They're asking, how do you bill for a simulation EMG while also performing a motor block with the lidocaine? So are you billing for the simulation EMG without chemo denervation? I'm billing for a nerve block and using ultrasound. I'd bill for the ultrasound guidance. Actually at NIH, we don't bill for anything because the care that we provide is all under protocol. In my clinical practice, however, we would bill for a nerve block and we would bill ultrasound and e-STEM. Some people, some states, some insurance companies, you can only bill for one or they won't pay you for both ultrasound and e-STEM. I never had problems with that. I got paid for both. So I don't know if I was just lucky or what, but we bill for both EMG, or I'm sorry, e-STEM and ultrasound. I document why I'm using both. Catherine, that talk was incredible. I feel like I need to come spend a week with you in your lab. Only if I can come spend a week with you. Yeah, I don't know, I think you'll be all right. I also, I do a lot of my trigger point injections in that sort of short axis technique that you described. And I think it's a really helpful way to identify the musculature as you alluded. I was wondering, I guess you sort of described it as a motor point or an innervation point. Is that mapped out somewhere that you, or you just in your years of experience, you've been able to sort of figure it out? No, it's absolutely mapped out. There are a number of articles that are published both in the anatomical literature and the clinical literature. There's a group in the Netherlands that's published a whole bunch of lower limb musculature and there's a whole bunch of articles that are published in the New York Times and there's a group in the Netherlands that's published a whole bunch of lower limb muscle motor points. And probably the one that I learned the most about was for instance, the hamstrings, the motor points are in the proximal and the distal third of the muscle. There are very few, if any, motor end plates in the middle of the muscle. So if you're doing toxin injections in the middle of the muscle, you are gonna be less effective than proximal and distal. The biceps, brachii, the end plates are in an inverted V with the point of the V being proximal. So the van Kampenhout, I can try to put in the chat, I'll try to put one of the authors, but there's a whole bunch of articles that are published. If you just put motor end plates or motor end plate guidance, you'll find them. And for not every muscle, but for most of the muscles. I'll try to put this in the chat. We have a couple of other questions in the chat as well. One of them was asking, how long do you expect the relief to last after you do the injections and how often can you repeat them? Well, in clinical practice outside of the NIH, most of the insurance companies will only approve botulinum toxin at 12 or 13 weeks. So you can inject more frequently than that. All of what I talked about today is off-label use of botulinum toxin because it's not approved for the use of focal dystonia in the lower limb or in the upper limb, actually. It's approved for cervical dystonia, spasticity, blepharospasm, many other conditions, but not for focal dystonia. Most insurance companies will pay for this toxin injections if you document why you're doing it. You can inject, we inject more frequently and under research protocol, I will inject more frequently. But for instance, my third case, the patient, I booster, I injected him at four weeks. I injected him, brought him back at six weeks. He had benefit, but not enough benefit. So we booster dosed him. I increased, I added a small dose and I made him weak. So you have to be really careful if you booster dose because you can make somebody weak. I anticipate once you get the dose right, that the effect will last for at least 10 to 12 weeks if you've got the dose correctly. Some patients you need to inject more frequently at a lower dose so that they don't develop weakness. And that's that second lady that I showed. I think that it can be challenging to get to the sweet spot of the right dose and to get people, because remember, these are like musicians. I'm tuning pianists who wanna go back to concert pianist playing. And runners that run multiple marathons a year have expectations that they wanna go back to running. They don't wanna swim. They don't wanna ride a bike. They wanna go back to running. They don't care about any of these other things. They wanna, same thing with table. Somebody who's got table tennis dystonia. They don't care about any of the other sports, but their sport. And so their expectations are different. But one of my guys, the guy with that trunk lean, he just completed his 53rd consecutive Boston marathon and he just finished. So he has run for the last 15 years with dystonia. We target his injections around his races so that we time them so that he's past the weakness, but still within a sweet spot of the effect of his injections. So we inject him a little bit more than six weeks before his race so that any weakness that he has will be gone. So for athletes, you really have to, you have a different set of goals than for somebody with post-stroke spasticity. And their demands of you are very different too. Our demands on us are very different. Wonderful. Thank you so much. We're going to go on to the second case. Dr. Alter, if you want to respond, there's two other questions left in the chat. You can either respond to everyone or just to the person specifically to answer the questions. And then otherwise, Dr. Rand, you are up next. Okay. Perfect. So I'm Eitan Rand. I work at Kaiser Permanente School of Medicine in Los Angeles. And I'm going to be presenting a shoulder case for you guys today. I have no disclosures. We're going to start by discussing the specific case, some ultrasound findings and my approach. We'll talk about the diagnosis, management options and how ultrasound altered my diagnosis and management in this case. So a 42 year old male presented with right anterior shoulder pain that was radiating into the upper arm, occasionally into the forearm and had severely limited range of motion. The symptoms started about a week and a half before the initial visit. He woke up with the pain. He denied any trauma or inciting event and he had no other complaints. The pain was quite severe. It happened with any kind of shoulder movement with lifting when he was laying on the affected side. And it was a little bit better with resting in the arm, but still present. So if you can go ahead, guys, I'm going to give you guys a few seconds for typing in. What do you guys think is the most likely diagnosis based on this history? You can type your answers in the chat box. I'll wait for some answers. Great, biceps tendonitis, impingement, wonderful. I'll give a couple other people a chance to respond. These are all completely reasonable based on this history. Impingement, impingement, tendonitis. Okay, great. So rotator cuff, tendonitis, tendinopathy, impingement syndromes is absolutely on the differential. This patient was actually sent over by the primary care doc specifically because they thought he had adhesive capsulitis and recommended that I just inject the patient. So we want to further narrow down our differential by examining our patient. So his vitals were normal. He was mildly hypertensive. He was afebrile. The shoulder was not erythematous and there was no swelling of the shoulder. He was diffusely tender, but maximally over the coracoid process. His range of motion was severely limited both with active and passive range of motion. I couldn't perform any special tests because of his pain and the range of motion restriction and his neuro exam was normal. We've all seen patients guarding their shoulders like this. So let's talk about relevant anterior shoulder anatomy. So on the left side of the screen, you can see an image of the anterior shoulder where we have our humeral head articulating with the glenoid fossa. You can see the subscapularis muscle coming in and inserting on the lesser tuberosity of the humerus. You can see that this image on the right is an axial slice of this image on the left. And you can see that subscapularis muscle coming in and inserting on that lesser tuberosity here. You can see the bicipital tendon, the long head of the biceps tendon running in the bicipital groove. You can also note it on the axial slice here. And then you can see the supraspinatus coming in and inserting on the greater tuberosity. We have our coracoid process. On the axial slice, you can see the conjoined tendon coming in, which is going to insert on the coracoid process. We have our coracoacromial ligament. We also have a coracohumeral ligament, which is not shown in this image. And these are some of the important anatomical structures that we'll see on our ultrasound pictures. So what's my approach to scanning the anterior shoulder? So when it comes to shoulder pathology, you always want to perform a complete shoulder exam, unlike some other regions of the body. The reason for this is that often, even if someone presents with pain or pathology in a certain region, the actual diagnosis can be something that's elucidated by examining the whole shoulder. So it is important to perform the whole exam. For the sake of time in today's presentation, I'm just going to focus on the important areas of the anterior shoulder. So I use a high-frequency linear array transducer. The patient is seated with the elbow flexed and the palm up, so the forearm is supinated. You need to know what your home base is. So the home base for scanning the anterior shoulder here is going to be an image of your long head of the biceps tendon at the bicipital groove. And in this image, your transducer will be short access to the long head of the biceps tendon, as seen in this first image on the left in the bottom. Then you're going to rotate your transducer 90 degrees to view that image of the long head of the biceps tendon in long access. And then you're going to rotate back, translate your transducer immediately, and externally rotate your patient's shoulder, or ask them to externally rotate it, and take a look at the long access view of the subscapularis tendon. In this position, you can see the coracoid, you can see the long access of the subscap tendon and the muscle, and you can actually evaluate the patient dynamically for subcoracoid impingement by asking them to internally and externally rotate their shoulder. Then you're going to come back, rotate 90 degrees at that spot, and look at the subscap in short access. Then you'll complete your shoulder exam. So we start our exam. So basically I've gotten a history, I've gotten a physical exam, and I still don't know exactly what's going on. That's where ultrasound is amazing. So we identify our home base here. So if you look at this picture, we can see the lateral portion of the image is on the left. So the greater tuberosity is on the left, the lesser tuberosity is on the right. We can see our biceps tendon sitting here in the bicipital groove with the deltoid overlying it. Does anyone want to throw something into the chat box? Does the biceps tendon here look normal in short access? Are there any abnormalities that anyone sees in the biceps tendon? I'll give you guys a couple seconds. We're talking about other stuff. Okay, for the sake of time, it looks normal. I agree, guys. So there's our biceps tendon. We're going to then translate inferiorly, following that tendon in short access down to where the pec major inserts on the lateral portion of the humerus. And we can see the tendon located here. Does anyone see anything abnormal in this image. I'll give you guys a few seconds again. Absolutely. So there is some fluid located around the biceps tendon. It's very common to see a little bit of fluid around the biceps tendon. We call this dependent fluid within the sheath. It can also be seen sometimes in a bicipital tenosynovitis, or it can be seen when there's pathology inside the joint itself, because the biceps tendon sheath is actually contiguous with the glenohumeral joint. Additionally, you can see it as an indirect sign of a full thickness rotator cuff tear. Moving right along. So now we're going to rotate our transducer 90 degrees to take a look at that biceps tendon long head in long axis. When we do this, we have to remember that our biceps tendon is going to take a deep dive. So it's more superficial on the proximal portion on the left side of the screen, and it dives down as it runs inferiorly. So in order to try to make this tendon as parallel to the transducer as possible, we'll perform something called a heel-toe maneuver, where we press the inferior portion of the transducer in toward the patient, trying to make the tendon more parallel to the transducer and more perpendicular to the beam, however you'd like to describe it. In this view, we can see the fluid in the sheath around the tendon, which is again dependent fluid sheath. Whenever you're looking at these structures, you want to make sure you turn on your Doppler. This is important for several reasons. So the first is to identify any vasculature. So very quickly here, you can see the long head of the biceps tendon with our fluid, and you can see this little blood vessel here. This is your anterior circumflex humeral artery. If you turn on Doppler, when you're looking at the short axis of the tendon, as it's in the bicipital groove, you can actually see a branch of the anterior circumflex humeral artery coming up as well. So you want to identify vasculature. Additionally, if you do have significant tenosynovitis, you could see significant hyperemia or blood flow in the sheath or around the sheath. If you have significant thickening of the tendon, heterogeneity of the tendon that we often will use to describe tendinosis or tendinopathy, you may see neo vessels or new blood flow located within the tendon itself. So Doppler is invaluable. So subsequently, we're going to now take a look at the long axis of our subscap tendon. So we translate our probe medially. On this image here, you can see on the lateral portion, the greater tuberosity that we're familiar with, the lesser tuberosity more medially, and the biceps tendon sitting in the middle. On the medial portion of the image, you can see the coracoid, and this is where the subscap lies, and it inserts onto the lesser tuberosity here. I just highlighted in yellow an abnormality. Does anyone want to attempt to describe what they see in this image? I'll give you guys a few seconds, but for the sake of time, if we don't get any responses, I'll continue. Okay, subscap tendon retraction. Okay, so good. So that person's describing that perhaps they're seeing a hypoechoic region over here. That's a great point. Anything else that anyone notices in this image? I'll draw your attention to it. So there's a large hypoechoic density, exactly, and it is causing some shadowing under the density, which we call acoustic shadowing, and yes, it does look like it's likely a calcification. When we look at echogenicity, we always like to talk about relative echogenicity, and we can see that this is not as bright, not as echogenic, or not as hyperechoic as the coracoid or the greater tuberosity, but it is definitely more dense than other structures, and so that's why we can't really see this lesser tuberosity as well, and that's why that individual astutely pointed out that there's a hypoechoic region down here. All right, wonderful. So we're going to measure that. So remember, when we're examining the subscap tendon, we want to make sure that our patient has their shoulder externally rotated. We can see that going from medial to lateral, this region is about 1.5 centimeters. Again, you want to turn on your power doppler, and here we can see that there is some increased flow. For the sake of time, I'll describe it. We see some hyperemia, some vessels around this region, which is a very common finding in this condition we'll discuss. So now, while we're looking at that long axis view of the subscap, we're going to take advantage of all that ultrasound has to offer, and so we're going to perform a dynamic evaluation looking for subcoracoid impingement. So here's your humeral head. Here is that region that we see, and it's all, this whole region is moving together, and this region is actually calcification inside the tendon, and you can see, I'm going to play it one more time here, but you can see that it is bumping up against the coracoid, and the patient, as I'm examining him in this maneuver, is telling me that's exactly how it feels when it feels restricted. He has a lot of pain, and that's what feels like it's blocking him. We're going to rotate our transducer 90 degrees and take a look at the subscapularis tendon in short axis and make a measurement of the cephalad to caudad dimensions of this hyperechoic region, and it's two centimeters. So this is a large region. So everyone writes their reports slightly differently. I'm going to tell you how how I write mine. So in this, the findings, I obviously completed the rest of the shoulder exam. So the long head of the biceps tendon had a normal appearance of the tendon. There is fluid seen within the tendon sheath. The subscapularis tendon was severely thickened with large hyperechoic regions seen within the tendon that was two by 1.5 centimeters with some acoustic shadowing. There was sonographic tenderness to palpation, which we'll discuss more in a second. There was hyperemia seen around the hyperechoic region. The supraspinatus tendon, there was no high-grade tear seen. There was a small cortical irregularity at the insertion on the greater tuberosity. It was a very limited view because the patient was in so much pain. I couldn't fully expose the supraspinatus tendon from under the acromion. The infraspinatus and teres minor tendons looked normal. There was some mild thickening of the subacromial bursa. The subcoracoid bursa was thickened and there was a small effusion. The posterior glenohumeral joint was normal. The suprascapular nerve, the AC joint, all were normal. I couldn't perform a subacromial impingement exam because of pain. And you guys saw that there was limited but positive for impingement with subcoracoid evaluation. So in conclusion, this is a case of subscapularis calcific tendinopathy with subcoracoid bursitis. So in our practice, I work at an HMO, we don't routinely obtain x-rays prior to patients coming to see us. But in this situation, I did send the patient after I performed the ultrasound for some basic shoulder x-rays, pardon the underpenetration. But this patient had an AP view, which is relatively unrevealing of the shoulder. Then on an axillary view, you can see zoomed in along adjacent to the lesser tuberosity that there is a two centimeter calcification, two centimeter density that is consistent with the density that we saw on ultrasound. So what is calcific tendinopathy? So this happens for no known reason. It consists of deposits of hydroxyapatite crystals in one or several rotator cuff tendons. Uthoff, initially in 1976 and subsequently in 1997, proposed that calcific tendinopathy has four distinct phases, a formative phase where the tendon undergoes a fibrocartilaginous transformation where the calcification forms and gets bigger, a resting phase where the deposit is stable. This may or may not cause pain. And if it does, it's because of the mechanical symptoms, the resorptive phase, which is really important. That's where macrophages and giant cells absorb the deposit. It can trigger a significant inflammatory reaction. You can get vascular tissue that develops around the deposit. And occasionally the deposits can leak into adjacent bursa. We don't know exactly what triggers it. And then there's a post-calcific phase where the deposit gets resorbed and fibroblasts reconstitute the normal collagen pattern of the tendon. On ultrasound, you can still see some foci of hyperecogenicity in these tendons for a long time. It happens in three to 10% of the general population, seven to 17% among individuals with shoulder pain. Bilaterally, it happens 10 to 40% of the time. Interestingly, and importantly, we've all seen x-rays where we don't think it's relevant. And it's, you know, 50% of the time, these calcific deposits are asymptomatic. Most commonly occurs in women in their fourth to sixth decades of life. There have been associations made between this condition and several endocrine conditions, including diabetes and thyroid conditions. Important to note is that people who do strenuous manual labor or athletic activities are not more affected than those who are sedentary. 50% of the time, patients become pain-free spontaneously with conservative treatment within three months. 20% of the time it takes about a year and 30% have persistent pain with repeated episodes of pain over several years. Pain can be gradual or acute generally without any kind of trauma. And it typically is caused by the impingement, the inflammation, and the intratendinous pressure. Oftentimes it could be a similar presentation to that experience by patients with rotator cuff tendinopathy or impingement syndromes. As you guys all astutely noted, increased pain at night is very commonly seen with an inability to lay on the affected shoulder. Acute pain, as we saw in our case, is very common in the resorptive phase where patients are going to hold their arm in a very guarded manner close to their body and they're not going to be willing to do much of anything. Most of the time this lasts several weeks, followed by significant clinical improvement. So on imaging, what do we see? During the resting phase, you can see a hyperchoric lesion with acoustic shattering, as you see in the bottom of this image here. And you can note that there's a lot more hyperechogenicity in the calcification here and a lot more acoustic shattering than you see on the right in our case, where the patient is in a resorptive phase and it appears less dense, fluffier, and sometimes fragmented. Pain with compression of the transducer on the deposit while it's being visualized suggests that it's contributing to the patient's symptoms. And we call this sonographic tenderness to palpation. And you can evaluate for impingement, which I showed you guys is a wonderful tool of ultrasound. X-rays are routinely done to assess the size, location, morphology, and texture of a deposit. It's important to include the axillary as well as internal and external rotation views because sometimes if the deposit is in the infraspinatus or the subscap, it can be obscured by the humeral head. MR and CT really don't have any role in this condition. So treatment is typical, NSAIDs, rest, PT. You can perform a bursal corticosteroid injection. You can do shockwave therapy and ultrasound-guided barbitage. Shockwave therapy can be quite painful during the acute phase, but it can disintegrate deposits in almost two-thirds of patients. Ultrasound-guided barbitage is what we decided to perform in this patient. And you have excellent results in most patients, resolves the deposits in 40 to 60% of patients. The amount of calcium removed does not affect the outcome. And a decrease in the size of the deposit over time is seen regardless of how much calcium is aspirated initially. In a meta-analysis comparing shockwave with barbitage, barbitage was superior in clinical pain relief and calcification clearance. And surgical treatment, if nothing else helps, is reasonable. So how do we perform the barbitage? The patient is supine. You do an implant injection lateral to medial. You anesthetize the overlying tissue up through to the bursa. And in this case, it's the subcoracoid bursa. Then I use an 18-gauge, one-and-a-half-inch needle, and you try to penetrate the calcification once. And I'll show you what this looks like. As you're performing the barbitage, you'll see the calcification look like this. Essentially, what you're doing is you're pumping the fluid into the calcification, and it's going in and coming back, going in and coming back. And eventually, you have several test tubes filled with half saline, half lidocaine, and you'll get aspiration of the calcification. And this is one of several syringes that we got from this patient. So how I changed my diagnosis and management in this case, so it's a common complaint with a relatively uncommon location. Normally, it's in the supraspinatus here with the subscap. Without our diagnostic scan, some people may have tried a palpation guider or even an ultrasound-guided procedure. Performing ultrasound diagnostically revealed the source of his pain exactly. We were also able to see the cause of his limited range of motion with the dynamic impingement. Given the severity of his symptoms, we decided to opt for the barbitage. He had immediate relief, and I called him as I was putting this together, and it's lasted over a year and a half, and he's been able to resume everything. And essentially, we were able to take care of this all in one visit. He didn't need any advanced imaging, no surgery, and ultrasound rocks were treating tendinous rocks, and I can make dad jokes. And important plugs, if you want to get better at recognizing the normal and the abnormal, pair up with a buddy, use textbooks. The STEP program is wonderful. AMSSM and local PM&R societies have great resources as well. Thank you. Thank you so much, Dr. Rand. Very interesting case. We will now open it up to Q&A, so type your questions into the chat. I already see one in there that just came up, and then we'll bring the panel back to answer those. So the first question, and Zach already gave in his answer, but they asked what size needle you typically use for the procedure. Yes, I agree. I use an 18-gauge needle for the barbatage, and I anesthetize with a 25-gauge needle. In terms of... Yeah, the next question was asking if you have any thoughts about why the amount of calcification removed doesn't affect the outcome. I suspect that you're triggering your... So after I actually perform the barbatage, I'll fenestrate the calcification more, anything that I can't get out. The reason for that is clearly your body has its own ability to absorb, to resorb this calcification, so I just want to facilitate it. And so by doing the procedure, probably we're triggering some of that additional macrophage activation, and the body takes care of the rest. Do you normally do a subcoracoid burst or a subacromial versus steroid injection after the barbatage lavage? I do, so for both. So if it's supraspinatus, I'll do subacromial, and in this case, I did a subcoracoid bursal injection with steroid following the barbatage. And how would you build... Sorry, go ahead, Brent. I was going to say, how would you build a procedure? There was a question in the chat about that. Great question. So I build... I work for HMO, so it's a little bit different, but technically, you could build this straightforward for an ultrasound-guided large joint injection, and that would be totally kosher. So just like you would for a bursal. It is a lot more time consuming than that. So I don't build for the tendonous portion. Does any of the other folks want to comment on what they do? Yeah, the tricky thing is, as you presented the case, you did an evaluation, you did a full diagnostic ultrasound, which is a code in and of itself. You did an ultrasound-guided injection aspiration procedure. Unfortunately, you cannot bill for a full diagnostic ultrasound the same time you're billing for an injection in that same area. And so coding for ultrasound things, I think, needs to get up to speed with how we actually utilize the time when we're seeing a patient. Right now, in my mind, the most accurate way to bill this is, one, do an E&M code for your time, because that procedure took, what, 15 minutes for everything, whereas an ultrasound-guided burst injection is going to be like one minute. And you had to explain the procedure so much more to the patient and whatnot. And so reimburse your time with an E&M code, because you're going through all of that. And then if you want to either bill the full diagnostic code, which is 76881, or more often, what I do is I just bill the injection code with ultrasound guidance for this. It would be the large joint tendon bursa, which is 20611, and that has the ultrasound included in it. But you cannot legally bill that ultrasound-guided injection code with a full diagnostic ultrasound code, unless it's for a completely different joint that you didn't do. And so it's a lot of time and effort, and you get the same reimbursement as like a one-minute injection, which is why, again, in my practice, I bill an E&M code. Yeah, absolutely. Zach, did you want to mention something? No, no, no. I was going to move on to just catch one more question. There's a good one in the chat about side effects of potential tendon rupture. And so just to address that, when I do these procedures, I treat them similarly to how I would if I were doing a tendon fenestration, where I'm actually kind of shutting them down for a couple days, doing some relative rest afterwards for maybe 10 days of just range of motion before I'm getting them started back into any sort of strengthening exercises. So I treat it as a tendon fenestration, but I'm curious to hear your thoughts on the panel. I do the same. Same. Yeah, often I'll give them a shoulder sling for two or three days, have them come out every couple hours and do pendulums and range of motions, and then back to activity as tolerated. And then often I'll get them into an actual like cuff rehab program two weeks after. And then there's another question about, well, how do you know when the procedure's done, when to stop the lavage, barbitage? So when my hands are too tired. No, I'm just kidding. I just, until I stopped getting calcium out, I would say I've never been able to 100% eliminate all the calcium in the tendon from my own experience. Um, uh, not to say that on follow-up there, you haven't had complete resolution of the calcification. Um, many times there is, um, and I think, uh, almost entirely the Barbatos has been a wonderful tool in my arsenal. I, there was a question about 10 X for this condition. I haven't needed, especially when, if you're in the resorptive phase for these really acute cases, they do really well with the Barbatos. Now, if someone has more mechanical symptoms and they're in a resting phase or post-calc or in the resting phase where it's more mechanical and it's really, really hard, that's when perhaps something like a 10 X or a 10 jet, or, you know, um, one of these other procedures may be beneficial. Um, I think everyone should have access to, um, to all the references from the presentations. I think the presentations are shared with everyone. Um, Is that correct? If not, we can please, we can please do that. We'll, we'll make sure. Cause I, there were some questions, um, sent for, for reference. Wonderful. Thanks so much, Dr. Rand. Um, now it's time for our break. So we'd like to, again, thank Allergan and Omby company, our session exhibitor. You can visit their breakout exhibit room to speak with them about their products and services. The exhibit room will again be open at the very end of the session. Um, to access the breakout room, like Dr. Moore mentioned at the beginning, there will be a pop-up at the bottom of the screen that says breakout room, and you can select that, um, to enter. All right. So we're going to restart in just one minute. We'll give it everyone, uh, another minute to get back from the breakout room here. I will, uh, introduce our next presenter at that time. All right. So next case is going to be Dr. Bailowitz ankle case. Uh, whenever you're ready, Zach, you can feel free to share your screen. Okay. Perfect. Thanks, uh, Britt. Um, yeah, thank you all for joining back after the breakout session. Hopefully we can make this second half, uh, as, um, interesting and, uh, uh, great learning like the first half was. Um, so my name is Zach Bailowitz. I'm a sports medicine, uh, PM&R doctor. I work in the orthopedics department at Kaiser in Oakland. Um, and I'm going to be presenting a case of leg pain today. So, um, I don't have any relevant disclosures. Um, so this case is a 39 year old female who presented to my clinic with complaints of acute on chronic episodic left calf pain. Um, there was no trauma or inciting event that she remembered. And she tells me that her pain has been present for a few years, but it seemed to be worse over the last few months. Um, she describes that the pain comes on a few times a day. And I think what was challenging for her is that she struggles to really determine what brought it on. Um, but she states that it's a pretty intense pain. It can be five out of 10, kind of on average and increases up to eight out of 10 periodically. She described the pain as sort of an aching, sharp pain in her calf. Um, and she described a periodic tingling that she experienced as well. Although she said that she occasionally felt this in multiple other extremities and was a bit worried about that because she had a history, a family history of, of MS, um, but she states that the pain is so bad that, that it limits her ability to walk. Um, so, sorry. Um, she was previously seen by her primary care provider and that's how she was referred to me. And I'm sure many of you can relate to this, but, um, a lot of times when people get sent to us, uh, we ended up being sort of a, I don't really know what's wrong with this patient here, go see that person. Um, and, and that seems to be my experience in the orthopedics department anyways. Um, so this, this patient had previously been seen by, um, the, the spine, uh, folks over, um, in a different department. So I work in the orthopedics department, but there's a spine department that also has physiatrists in it. And, and she was seen there. There was thought that maybe there was some sort of radiculopathy. Um, and so there was an MRI of her spine that was done, but it only showed a kind of mild L5 S1 disc bulge. Um, and then she was sent to neurology because of these complaints of paresthesias and her family history of MS. Uh, and they did an EMG, uh, nerve conduction study that did not have any abnormalities. Um, and they did not feel that there was any central nervous system, uh, ideology for her complaints. Um, so she was sent to me. Um, so on physical exam, uh, her inspection did not show any, uh, deformities of her leg or, or atrophy. Um, she had symmetric ankle and knee ranges of motion and good strength throughout her lower extremities. Uh, sensation was slightly diminished over the posterior aspect of her distal lower leg. Um, but her reflexes were symmetric. She didn't have any upper motor neuron signs. Um, she did have some mild tenderness to palpation around the middle, uh, mid third aspect of her posterior lower leg, right around the distal gastroc. Um, but she also had a little tenderness to palpation up at the sciatic notch. Um, but this did not refer any pain into the calf and a straight leg raise did reproduce her calf pain. Um, so I'm going to just kind of pause here. Sorry. I actually shouldn't pull up the chat. Let me see if I can do that. Um, see if there's any updated for you. Oh, perfect. Thanks. If there's any thoughts on a differential, or we can all just kind of stare at Batman here, who's pondering this leg pain as well. Yeah. So, you know, when I, when I approached these, um, these more sort of ambiguous cases, you know, I like to think about the neuromuscular system. Obviously we, we have a, uh, a great way to evaluate this just from our background as physiatrists. Um, and so certainly, um, you know, thinking about the muscular anatomy in that region, um, is there some sort of gastroc strain or a soleus strain that's more chronic and lingering for whatever reason? Um, I've started to look a lot more into the, um, sort of fascial planes between the gastroc and soleus and the aponeurosis that runs in between, and we'll, we'll talk a bit about that. Um, even though her MRI of her lumbar spine was relatively, um, normal, uh, you know, you can still get a chemical radiculitis or irritation of the, of the, of the nerves in the lumbar spine. And so, you know, I always think about this as, as contributing. Um, and then just working my way down the, down the nerve. So is there some sort of lumbosacral plexopathy? Um, you know, the distribution of her symptoms did seem to fit more with the sterile nerves. So thinking about a sterile neuropathy and then, um, you know, she had a difficult time pinpointing what brought on her symptoms, but if this was a more typical exertional, uh, complaint, then we might think about something like exertional compartment syndrome, or even, uh, popliteal artery entrapment syndrome. And so at this point I've done my, um, my history, I've done my physical. And so, um, I'm ready to move on to a diagnostic ultrasound. Um, the AIUM does a really good job of, of outlining practice parameters that they suggest for various body regions. And the AMSSM just updated their, uh, sports medicine curriculum as well for recommended, um, scanning of different regions. However, there, there is no specific protocol for the lower leg. There's an ankle and there's a knee, but the lower leg sort of, uh, has no specifics in either of these. And so this is sort of my approach. This is my protocol. Um, I do spend a decent amount of time looking at the medial gastroc because that seems to be the area where a lot of, a lot of my patients have complaints, um, and it's a common area for injury. Um, I, I do scan the soleus as well and look for any anatomic, uh, abnormality signs of old muscle injuries there. And then again, I'm looking at the aponeurosis, which is that sort of fascial plane in between the gastroc and soleus. Um, I do look at the plantarus tendon as well, uh, as a common area for injury. Um, I do look at the posterior leg as well, uh, and then I'll turn my attention to the neurovasculature and look at the tibial nerve and the sterile nerve, both in the, in the posterior leg, depending on the location of the symptoms, looking down at the Achilles can be indicated, and then making sure you're thinking about the, uh, flexor tendons, Tom, Dick, and Harry, um, and occasionally I'll do a popliteal artery dynamics scan as well, if it's indicated. Um, so I've mentioned the aponeurosis a couple of times here, and this is a here, um, that, that describes kind of some of the types of medial gastroc injuries that you can see and the relationship with the, um, the aponeurosis. And so, um, you can see this on the left here, the gastroc is removed and you can see the soleus aponeurosis. And then when they put the gastroc back on, you've got the gastroc aponeurosis, which blends into this free gastrocnemius aponeurosis, which is an area that oftentimes can get injured in patients that have your classic tennis leg or gastroc injury. Um, and, and it turns out based on this study that, um, we can actually predict the, um, the severity of the, or sorry, we can predict from the severity, how long it will take patients to return to play or return to work, um, as you can see the, the higher grade injury, which involves the aponeurosis, um, it can get, uh, get much longer, uh, return to play times in comparison. Um, and so this is a place that I'll spend a lot of my time kind of looking at this region, making sure there's no kind of remote tears or changes in the aponeurosis, I also do look at the soleus quite a bit, although as I've, as I've scanned it more and more, I've realized that, um, it can be challenging to see specific injuries and the literature supports this, um, you know, this particular article says that ultrasound is not sensitive enough to detect and assess solely as traumatic tears compared with MRI. Um, but the timing of the ultrasound is important. So the longer you wait after an injury, the more sensitive the ultrasound becomes. Um, so I do look at the soleus as well, but I, I like to keep in mind the limitations of ultrasound as well as the advantages, um, and then I turn my attention to, to the nerves and because of the patient's symptoms, both, um, you know, the location of it, and also the, the paresthesia type description, I specifically wanted to look at the sural nerve. Um, and so just, just as a review, you know, the sural nerve is a branch that comes off of the tibial and common peroneal. So it's interesting that it receives branches from both. Um, there is some variability in the anatomy. And so, um, if you look at this, uh, middle picture here, you can see that the medial sural cutaneous nerve actually gives way to the, to the full sural nerve and the lateral sural cutaneous nerve just sort of, uh, kind of fades away. And then in this anatomic variance, you can see that they, they actually just continue as two separate nerves, although they seem to run pretty side-by-side. And when you're scanning this nerve, you know, there's a, it can be pretty tricky to see, but there's usually a vein that runs with it. And this is some papers I was looking at, call it the lesser saphenous vein or the small or short saphenous vein. Um, but it's usually pretty well, um, uh, kind of just right next to it. And so it's usually a good landmark for you. Um, risk factors for sural nerve injury, um, fractures of the lower leg or ankle, and then patients who have had ankle surgery, um, uh, previous trauma compression, and then, and then diabetics can get sural, um, sural nerve, uh, you know, neuropathy that that's more of a peripheral neuropathy. Um, but you can actually use the sural nerve to evaluate, uh, any of these sort of peripheral neuropathic changes. Um, and in this particular study, they found that symptomatic patients had a larger cross-sectional area of the sural nerve as compared to the contralateral side. So here in this diagram, you can see this small, uh, outline here is the sural nerve, and then you can see the vein just next to it. Um, in terms of imaging this, you know, there, there really are not great ways to image it aside from ultrasound. Um, this was a, a paper I found that talks about MRI imaging of intravenous neuropathies at the lower extremity. And they didn't even mention the sural nerve because I think it's probably too small to see. Um, this particular study talks about MRI versus ultrasound. And, and they say very clearly the sural nerve is quite thin and difficult to identify on MR imaging. So this is not a particular nerve that I'll, I'll send patients for MRI. Um, and I, you know, because of how superficial it is, it really is something that's easy to see on ultrasound. So, um, to evaluate it, place the patient prone, um, and using a high frequency transducer, you're going to scan them in an axial plane. Um, the nerve is often easiest to see superficial to the soleus. Um, and again, it sort of travels with that short or small saphenous vein, uh, superficial to the coral fascia. And in this particular study, they found the average cross-sectional area, um, at this location was about 3.5 millimeters squared. So you can imagine that, um, if, if the change in the cross-sectional area from a, from a compression changes significantly, you might even, even something that changes up to six millimeters squared, which is almost double the cross-sectional area. It can be difficult to see. And so you can, you can, you can get a sense that it might be challenging to, um, visualize compression. However, in our patients, uh, when I scanned them at the level, just distal to the gastroc and the soleus here, it was very obvious that the nerve was significantly compressed here within the fascia. And so this video, um, I'm starting distally and scanning proximally. And you'll see, as, as you look at the nerve right here, which looks relatively normal sitting just superficial to the coral fascia, we'll watch it as it, as it becomes, um, compressed as it gets stuck in the fascia. And so you can see there, uh, it just really flattens out and looks totally compressed before I get up into the gastroc belly itself. So I'll play that one more time again, here's normal, normal nerve. And then it becomes very compressed, flattened out in the, uh, coral fascia there. Hey Zach, what frequency ultrasound are you using for these images? There was a question. Yeah, this is a, um, this is a sonosite 6-15 megahertz. Um, so, uh, as you all probably know what the sonosite you can't adjust the frequency. So I don't actually know what, um, exact frequency it's you, it is used, but, um, yeah, it's, it's a 6-15 and when you adjust the depth, it usually increases the frequency. So it's probably somewhere in the range of 12 to 15, something like that. So normal to high frequency range. Yeah, totally. Nothing, nothing crazy. Um, so yeah, so, uh, the diagnosis that I made for this patient was a sural nerve entrapment at the free gastroc aponeurosis. And so, you know, the patient was a little bit confused. Why, why had that nerve test stock? Like, why didn't that show anything? Um, and so, you know, we, we had to talk about a couple of things and as, as we know, as physiatrists, um, you know, a nerve conduction study is subject to the practitioner that sets it up. And, you know, the average, uh, way to set up a sural nerve is 14 centimeters proximal to the malleolus. And it may have been that the entrapment was just a little bit too far proximal for this to have shown in the nerve conduction study. But in addition, there are lots of, there's lots of studies that show that, um, nerve conduction studies are not a hundred percent sensitive. Um, there, there's, there was one paper from 2002 that showed that, uh, about 85%, uh, sensitivity for carpal tunnel syndrome, I was not able to find any sural nerve sensitivities or specificities, but, um, suffice it to say that, that EMG, uh, nerve conduction studies are, are not, um, they're not perfect. And, and so with this explanation, um, we, I began talking to my patient about treatment options. She had done some extensive physical therapy being treated for a chronic calf strain. Um, so we talked about, um, different types of nerve gliding and nerve flossing, as well as some manual therapy, maybe to try and, uh, break up the adhesions that might be causing the sural nerve entrapment. Um, we also talked about nerve hydrodissection, which is something I offer to perform for her. Um, and then we talked about, you know, ultimately she might require a surgical referral given the obvious entrapment there. Um, so the patient elected to do a nerve hydrodissection with me. And so, um, I just wanted to talk a little bit about some of the literature supporting nerve hydrodissection as a treatment for, um, compression mononeuropathies. Um, so this is a really awesome paper that came out last year, Dr. Kentaro Nishi over at Pittsburgh. Um, and some of his colleagues talked about some of the theories behind ultrasound guided hydrodissections. Um, and it's interesting because one of the first things that you read in this paper is that patients may not need to have changes in the nerve cross sectional area or electrodiagnostic findings in order to still have a compression neuropathy. Um, and that's because you can, you can really have minimal compression or irritation, even just something like friction that can cause pain. Um, and so the theories behind why it might work include, um, downregulation of these pain receptors called TRPV1 pain receptors. There's also some thought that you're correcting a perineural glycopenia, uh, which, which may lend itself to the reason that a lot of people use dextrose to do these nerve hydrodissections. Uh, and then even there are studies that discuss improvements in nerve mobility. Um, this is highly discussed in carpal tunnel syndrome where patients with, with carpal tunnel syndrome have been shown to have decreased nerve mobility. You can watch the nerve as you do finger flexion and, and see that it's kind of stuck. And then after hydrodissection, see that it moves again. Um, so a lot of different theories as to why nerve hydrodissection might work. Um, but there's good literature showing that even without steroid nerve hydrodissections can be beneficial. This study showed, uh, patients with media nerve, uh, uh, compression, and they had, um, either a hydrodissection just with saline versus a subq injection. And it resulted in improvement in symptoms and, uh, uh, improvements in cross-sectional area, um, with trends towards improvements in electrodiagnostic studies as well. Um, in this study for ulnar neuropathy at the elbow, uh, patients with mild to moderate ulnar neuritis had either a steroid or D5 injection. And while both groups had improvements, um, the D5 actually showed a larger reduction in symptom severity and cross-sectional area long-term compared to the steroid. Um, and so that again, lends itself to that discussion of perineural glycopenia. Um, so this is a video of just an ulnar nerve injection that I did for a patient. You can see as the, um, needle injects some fluid right around it, you can watch the nerve kind of come right off of the fascia that's surrounding it, which really gets it nice and dissected. Um, so we elected to do a hydro dissection for this url nerve for this patient, um, here, you can see the needle coming in from the lateral side and you can see that I've been able with, with fluid to free up the, um, region underneath, but here you can see the nerve and very small here still suck superficially. Um, but then with, with some more fluid and a little bit of, um, funky needle maneuvering, I was able to get it to free up here. And so you can see as the needles now moving into the nerve is completely surrounded by fluid, which is the goal to get these things hydro dissected. Um, so I guess the, the, the conclusion to the case is that the patient got about four weeks of improvement of her symptoms from this, unfortunately, her symptoms did come back. And so we, we elected to repeat the procedure, which I did and added in a little bit of steroid. Um, and even with that, she still had a, her symptoms come back after about eight weeks, the second time. And so she actually has been referred to the peripheral nerve surgeon that I work with. Um, I don't have a resolution, so sorry. Um, but she, she has, um, has an appointment upcoming with him and, and may hopefully get a release here of her serum there. Um, so takeaways from this case, you know, I think the biggest thing is that the patient presented with aching, sharp pain in her calf, and that doesn't sound like nerve pain necessarily, but nerve pain isn't always numbness and tingling. And I think that's important for us to remember. Um, and it's also important to remember that the nerve can still be affected even with a normal nerve conduction study. Um, so make sure that you do a comprehensive diagnostic ultrasound so you don't miss things and, and keep hydrodissection in mind as a viable treatment option. Thanks. Awesome. Thank you so much. Great case. Um, did for your first injection, what volume did you use? Yeah, that's a, it's a really good question. And I, I don't know that there's, um, that there's really suggested guidelines or, or literature on exactly how much volume we should be using. Um, in places that can handle that much fluid, I tend to use, uh, about 10 mils of fluid, um, sort of for my first injection and I want to make sure I'm including lidocaine for the diagnostic purposes, and then I'll use, um, D five and, um, oftentimes a little bit or no steroid at all. And then the second time I did it, I added steroid in. So the first time it was about eight cc's of D5 with two cc's of 2% lidocaine. And then the second time it was a similar concoction but a little bit more steroid in it. Awesome. Do you remember, did they do nerve conduction study tests on both sides or did they just do it on the left and it was normal, so they called it normal? Yeah, they did do it on both sides. And I think that the, when I looked back at the case afterwards, I think that the velocity was slightly less, but I think it was something where they were both within the normal range and so it wasn't, there was no attribution to that at the time. But yeah, it's a great point, Britton, certainly thinking about these normal values that are just based on studies that were done a long time ago that comparing side to side can be something to think about. Yeah, and with the conduction velocity of these shoes, all you need is one axon that's carrying the conduction at the normal rate that's not compressed and it'll be normal. So it's amplitude that's gonna be more affected and when the amplitudes are like four or five microvolts, you know, it becomes, you know, it can be difficult to look at these differences. The main thing I think Zach is right is that they probably were a couple centimeters below the entrapment site, because that's where, you know, if you're doing it 14 centimeters proximal to the malleolus, you weren't far enough up. And that's why ultrasound makes, why ultrasound plus electrodiagnostic testing would influence where you would stimulate the sterile nerve, because if they had stimulated above where you notice the flattening, I bet they would have seen a difference. And that's why more and more people are incorporating ultrasound into electrodiagnostic testing. And there was a question here, I think, either Britt or Allison, if you saw, from a resident saying that, you know, there seems to be a lot of, that nerves look like little streaks of gray and how do you get better at this? But I'll let Zach take this, but my answer is you just kind of scan, scan, scan, and just keep practicing and practicing. Because, you know, initially that everything just looks like when you look, the first time you look at a structure under ultrasound, everything's just gray and white. And it doesn't look like anything until you train your eye. And once you train your eye to look at nerves, you can see them. I think Jeff Strakowski, one of the points that I've taken away from him is that you actually have to scan quickly. If you scan quickly with nerves, you see them better than scanning, like inching along very slowly, because you can see the differences between the nerve and the muscle or the nerve and the fascia or nerve and tendon much more easily if you're moving quickly. So Zach, what are your thoughts for how do you identify some of these little small nerves, other than getting a really expensive ultrasound machine with a high-frequency transducer? Which I do not have the luxury of a really high-end ultrasound machine. And so, yeah, no, but to your point, Catherine, the idea of scanning fast and then scanning slow, and this is something that I picked up from my fellowship, Dr. Visco, who I think is on here somewhere, but Eitan can attest to this as well. But, you know, scanning fast to see the nerves kind of moving within the fascia. And then once you've been able to kind of isolate it, then you're scanning slow to kind of really see if there's any abnormalities. But yeah, you know, otherwise, you know, it looks like Anthony brought up that question. Anthony, nerves are really tricky, man. Like they're really hard to scan. They're very small, especially these, like the sural nerve and, you know, Britt and Allison, you know, they've just scanned tons and tons and tons of patients. And that's really like ultimately what it comes down to is just getting a sense of where these nerves live and seeing enough normal so that when you see that one weird one, you're like, okay, I get it now. But I don't know that there's any substitute for just reps. I think that's the key. It really is. I think it's repetition. I think as well, just being so familiar where the relationships of what normal is. For sural nerve, and this might be different from how you do it, I think you had mentioned, I always start at the ankle almost, and it should be just lateral to the Achilles tendon. And it's going to be a small little thing. You're either looking at the nerve or the vessel, turn the ocular on, follow it approximately, see if it turns into a nerve. I think you had mentioned, well, for you, it makes sense to start more approximately in the calf to find the sural nerve. So everyone has their own ways where it makes sense to them. Just making sure that you're familiar with, all right, what is normal? When does the sural nerve branch into its sub kind of division branches and knowing that for all the different nerves? And that's something that you're not going to get right away that will come with time and as you start ultrasounding more. And I think just to summarize kind of what everyone said, especially for the residents, understanding anatomy is like the foundation of understanding anything about ultrasound. So I think we've all kind of circled around that point, but the easiest way to find things that you're looking for is to know what normal anatomy is and know where you're expecting to see that. And I think sometimes we kind of skip over that from a discussion standpoint, because our brains are already thinking about the ultrasound anatomy rather than just like the basic anatomy of where things are. I completely agree with the other faculty. I think you need your home base. You need to know exactly like Britt said, where you're starting from. And if you're examining a patient, not just finding your home base, but comparing side to side is really helpful. And that's a tool that you have with ultrasound that is easily at your discretion. Yeah, that's a great point, Etan. Thanks for bringing that up. I didn't include her contralateral side in this, but it did not look like that. And so that was another clue to me that I was approaching the right diagnosis. So yeah, that's a great point. So Zach, a lot of times nerves when they're entrapped are enlarged, proximal to the site of entrapment. Did that nerve enlarge proximal to the site of entrapment or was it dividing already into the medial lateral branches so you couldn't tell? Yeah, I looked for that. I think the times that we can really find those like enlargements is like the median nerve or the ulnar nerve where the nerve cross-sectional area is 10, 12 millimeters. I think for this small of a nerve, it can be really hard to visualize even like a 50% enlargement. I don't know that I had the eye for it. And frankly, my cross-sectional area measurement tool on the Samsung is not perfect, or sorry, on the Sona site. I wish I had the Samsung. It's not perfect. And so I think I was hoping I would have seen that. I didn't, but yeah, that's a good point. Well, I have the Samsung and it isn't, even with that, it's not that easy. And we're doing, because I'm doing research protocols, patients with spinal bulbomuscular atrophy and ALS-4, and we're doing, you know, sural and facial nerve cross-sectional areas in patients that have atrophy of those nerves specifically. And so you already take a teeny tiny nerve and then it atrophies and it can be really challenging, but it's really practice, training yourself to know what that is and using Doppler to make sure that the structure that you're, to make sure, as Britt said, it's not a vessel. You know, start with where you know where the nerve is going to be. If you can't find it proximal, go distal and track it to where you know, as Allison said, anatomically, you know where it's going to go and go back to an anatomy text, a reference guide that tells you what the direction of the nerve is going to be and that will help. Frankly, to me, that was the value of the diagnostic injection. It was like, I think this looks compressed here. I don't see any enlargement more proximally, but let's try the diagnostic injection and see what kind of improvement we get. And that was a really, you know, and impressing that upon the patient. Okay, this is a diagnostic injection. Here's how this works. You have two hours to remember how your symptoms are and then the lidocaine is going to wear off. And trying to get patients to understand the diagnostic injection can be tricky, but I think it's a really valuable tool. Yeah, the diagnostic injections for a lot of things are really useful. With your D5W injections, so there's the anesthetic window that you're talking about. What is your guideline for the therapeutic window in terms of when, once the anesthetic wears off, when are you expecting, or what are you counseling patients as the therapeutic window of when they should definitively start to work if it's going to work from the D5W? That's a fantastic question. I have no idea. I mean, I usually tell people to expect it. I say check in with me in two weeks and let me know how you're doing. I think some of that is because I'll often include a little steroid in there too. And I think by the end of two weeks, the steroid should have helped, but I don't know. I mean, I would be curious to hear your thoughts on that. I'm not sure. I don't know that we know- Yeah, that's part of the reason I asked because I guess I don't entirely know either. With steroid, I always say I judge it at two weeks. With D5W, I lessen it up to, it's a broader, more diffuse injection. So you might start noticing in a couple of days, but I judge it by the four week mark. And at four weeks, if you're no better, no better with the anesthetic phase, all right, we'll go on to the next. If you had transient or partial benefit, I'll often repeat it. And then if you had good benefit, just watch it. Part of the reason I really like this case is because one, it's really smart, fine. So kudos to you. And two, there's so many different, there's no right or wrong way to go forward. Some people would have started with a steroid. Some people would have started like you started. And the importance is knowing, well, what all tools do you have available? Counseling, well, why would we wanna do one versus the other? D5W really has no downside effects, where a steroid potentially, if they've had a lot of other steroid injections, there's those side effects. Last question, would you consider peripheral nerve stimulation for nerve entrapments? Christina, is that in terms of like a peripheral nerve, like implant simulator, I'm guessing is the question? You certainly could, I would guess. Do you have any other, did you think about any kind of external peripheral nerve stimulators for this patient? I didn't. One thing that we had discussed with her was for ablation. And I think her, because her complaints were so pain mediated, I was worried that an ablation might flare her up more. And we talked about it and she ultimately decided she would prefer to talk with a surgeon about a more permanent fix. But Christina, to be fair, I have very little experience with peripheral nerve stimulations. And so that's a great point. And maybe I should think about that and you're up next for the case, great. Just to that point, I think that if there's a focal nerve entrapment, you wanna do everything you can to eliminate the entrapment, whether it's with hydro dissection, whether it's with mechanical techniques through a therapist, or whether it's through surgical release. I think if I'm a patient, I am very reluctant to have something implanted into me if there is a solution to the problem. And most of these are very low risk, even the surgical is relatively low risk. So I think that before we have implants considered, it's sexy, it's interesting, it's wonderful, and it's incredible tools for the right patients, but in entrapment situations, I would be reluctant. And it has a lower chance of being successful if you've got an entrapment because you still have a focus of what's causing the problem that you haven't addressed. You need to address the entrapment. Perfect. Well, thank you so much for that case. We are gonna move on to Dr. Schroeder's knee case now. Okay. So the last case of the day, everyone made it. This is a fairly simple, straightforward case that I think any ultrasonographer is going to encounter in their time here. So we had a few more zebra cases, and this has a little bit of a twist, but it is something that you will probably see if you are holding an ultrasound transducer and getting referrals for this. So I don't have any disclosures. The patient was a 68-year-old female. She complained of left posterior knee discomfort. It started about five weeks ago. She was helping a friend move, or sorry, she was helping a friend clean their house, and they had a lot of stairs. So she just went up and down stairs for two straight days. She couldn't recall an injury, but after that, she had a lot of pain in the posterior knee region. She described it as an achy, sore, almost a fullness, would get up to a five out of 10. She didn't have any mechanical symptoms, no locking, popping, catching, clicking, no true giveaway symptoms, but she felt like the knee was a little more wobbly than typical. It was worse with stairs, kneeling, prolonged standing or walking, and better with rest. She'd tried ice, heat, ibuprofen, helped a little bit, nothing significant. Her past medical history was most significant for her history of breast cancer, which was in remission, and she had been on a Remedex for the last five months. She was obese with a BMI of 36 and had a couple of other medical problems, but no past surgical history and no prior injuries to the knee. She was working as a pediatric nurse. On exam, as I mentioned, she was overweight or obese. She had slight varus alignment to the knee. There was a mild effusion anteriorly, but I couldn't appreciate any fullness in the posterior region in the popliteal fossa. She did have tenderness over the medial and lateral facets, as well as pretty diffusely in the popliteal fossa region and proximally along the medial hamstrings and distally along the medial gastroc. Her ligamentous and meniscal exam were normal, and she had intact strength, but pain with resisted hamstring and gastroc testing, and she was limping a little bit. She had x-rays prior to coming to my clinic. They just had an AP and a lateral, maybe very mild osteophytes on the patella and a quad calcification, but fairly unremarkable for someone who's 68. She had also had a diagnostic ultrasound performed by radiology to evaluate the Baker's cyst area that was read as normal. So she self-referred to my clinic, and given her symptoms with the posterior fullness and pain, the first thing on the differential that I was thinking of is does she have a Baker's cyst or a cyst in the posterior knee? So that was where I started with my ultrasound evaluation. So throughout the presentation, I'll have the transducer location here on the right side. In this image, medial is on the right side. You can see the medial gastroc tendon, this anechoic cystic structure, and the semimembranosus tendon here. I'll play the video. This is just scanning proximally to distally along that location. And here's just the anatomical correlate to the medial head of the gastroc and the semimembranosus tendon. And that typical Baker's cyst location sits in between the two. However, I was a little bit puzzled by this very small cyst contributing to what seemed like fairly significant symptoms. And whenever I'm scanning the Baker's cyst, I always look for a stalk coming from the joint. So I scanned a little bit more, increased the depth and scanned farther distally. And you could see, I'll replay here again, this small cystic structure communicates with a deeper cystic structure here. And that's kind of the motion of the transducer that I'm making in that. So I measured this deeper popliteal cyst as I felt like this was what was contributing to most of our symptoms. So on this side, we're looking in an anatomic transverse view measuring medial to lateral about 2.35 centimeters. And here in an anatomic longitudinal view, measuring 2.5 proximal to distal. And in this view deep, you can see tibia here and femur here. So this would be like the meniscus region in this location. And given the depth of four centimeters, it's very difficult to evaluate the meniscus of that location. And of course, anytime you have a anechoic cystic structure in the posterior knee, you want to utilize Doppler. There was no flow within this structure. And I confirmed that the vessels were entirely separate from the cyst. And again, whenever I see a cyst in the posterior knee, I also evaluate the anterior joint for, so this is an image over the suprapatellar recess where you have lateral on the right side of the image. The anechoic joint fluid is fairly prominent with the quad tendon, more superficial, pre-femoral fat pad, and femur. And that's also the view I'll use for a joint injection anteriorly. So the findings of the diagnostic scan, I didn't include images of the full scan, but there was a small amount of fluid in the typical Baker cyst location that communicated with the deeper cysts within the popliteal fossa. There was no Doppler flow in either region and these did not communicate with the vasculature. There was a moderate amount of fluid in the suprapatellar recess and the tendons about the medial and posterior medial knee region were normal. I didn't visualize any meniscal tear, but again, that was not fully assessed in my scan. So for the diagnosis here, it was a posterior knee pain, secondary to popliteal cyst in the setting of mild patellofemoral osteoarthritis from a clinical standpoint. So thinking about next steps, and here I'll have people type into the chat what they think is going on. At this point, do we need any additional imaging? Or can we proceed with a procedure? And if we're going to proceed with a procedure, what procedure would we do? Aspirate the Baker cyst region, aspirate deep the knee joint, inject the cyst, and where do we inject the joint itself? Do we do a combination of the above? And then what is the choice of injectate, which I'm not going to get into too much because that's a whole nother discussion in and of itself. We've got a vote for MRI to further evaluate if this is a parameniscal cyst. Great thought. And then in any of these patients, I will also refer to PT, especially if there's fluid in the knee joint. And so I did not pursue an MRI. I talked with the patient about that. The rationale was she's 68. She did not have an acute injury. She did not have any locking complaints or other complaints that would necessitate surgery. So even if this was a parameniscal cyst, would my management change with an MRI? And my thoughts were that they wouldn't. So I discussed the possibility of aspirating the cyst with her, specifically targeting that deep cystic region as I felt like that was contributing most to her symptoms given the fact that it was much larger than the fluid within the Baker cyst region. So anytime that I'm performing an aspiration of a cyst in the posterior knee region, I typically go from a distal medial to proximal lateral approach to avoid the tibial neurovasculature and any other structures. And so here you can just see the needle tip in the cyst prior to aspiration. For this procedure, I chose the curved linear transducer just because of the depth of that cyst for better visualization. But when I aspirate fluid in the typical Baker's cyst location, it's usually much more superficial and I use a linear transducer for that. So we aspirated about four cc's of fluid from this deep cyst and the superficial cyst also decompressed with that aspiration. And this was under fairly significant pressure when we, the fellow that I work with was with me. He performed this procedure and did an awesome job. He, when he inserted the needle into the cyst, it almost decompressed with back pressure into the syringe without him even needing to aspirate. And anytime that I perform an aspiration in the posterior knee region, I typically also target the knee inter-articularly as that's usually the root cause of the problem with the fluid leaking out posteriorly from the knee joint. So here we also performed an aspiration and injection anteriorly. So here's just the corticosteroid injection. And for this procedure, again, I'll go from a lateral to medial approach. And I typically do a few cc's of anesthetic with like a 27 gauge needle followed by an 18 gauge for the aspiration. And so after the procedure, she had immediate complete pain relief of that posterior pain. And I did just recently see her back for followup. She continued to have relief of her posterior pain. She was getting some almost like posterior thigh hamstring and posterior calf pain on the day after physical therapy, likely due to muscle soreness from just not being used to using that as much as she was being challenged in physical therapy. She continued to have negative meniscal testing on examination. And she did have some tenderness over the distal semimembranosus and the proximal medial gastroc. But on ultrasound evaluation, her effusion and cyst had resolved. So just a bit of a discussion, and whoever said parameniscal cyst, that's definitely something I was thinking about. And it also still could be true. However, you can see kind of a lobulated baker's cyst, both deep and superficial to the gastroc tendon. So just a reminder that like a true baker's cyst is found between that semimembranosus and medial gastroc tendons. There is usually a one-way valve for fluid to pass into that bursa. The effusion and interarticular pathology are almost always present in 94% in the literature. And usually ultrasound is the imaging modality of choice here. For the approach, like I talked about, I use the distal to proximal primarily. That's been most commonly described. Others have talked about a medial to lateral or lateral to medial approach, but you have to be very careful about avoiding neurovasculature and also kind of coming cross-fiber to some of the medial hamstring tendons, which can be painful if you're not able to avoid them. And then the thoughts about corticosteroid injection is really kind of up in the air in the literature. There have been studies that compare injection into the baker's cyst region versus injection into the joint, and both are beneficial. Some have compared injection into the cyst versus no injection of steroid, also helpful. And then there's even a study that shows that interarticular injection without aspiration of the cyst can be beneficial. So I think the jury's still out there, and I'd be interested if anyone wants to put into the chat with their experiences with that. Yeah, I see someone already did put into the chat that if you give the interarticular injection, the cysts will diminish. So there has been a report of that in the literature as well. From a parameniscal cyst standpoint, these are usually associated with a meniscal tear, and the fluid typically tracks up through the meniscal tear. Commonly these are fairly small, less than nine millimeters, although a larger cyst has been reported. And most commonly those larger cysts are reported in the posterior medial knee region. For the parameniscal cyst, MRI is the gold standard, though ultrasound also has a high specificity and sensitivity of over 90%. And then in the past, the treatment of parameniscal cysts was often arthroscopic or open excision with a partial meniscectomy. But the ultrasound-guided drainage has been utilized more commonly as we progress with ultrasound technology and comfort. And I just briefly wanted to touch on other things that we always have in our mind on the differential, and these are things most of the time that we don't want to miss. So popliteal artery aneurysm, cystic adventitial degeneration of the popliteal artery, popliteal venous extasia, hematomas or solid masses, tumors, sarcomas. I do have the ultrasound findings here that you can look at on your own. The biggest thing for these is most of them will have some sort of Doppler flow. However, I do caution you that if someone has like a partially walled off aneurysm, they might not have Doppler flow. So if it is directly adjacent to the artery, I would still be, I still would not drain that without further additional imaging or confirmation that it's not communicating with the artery. So just a couple of quick ultrasound pearls. From a diagnostic standpoint, evaluate the medial gastroc and semimembranosus bursa region for Baker's cysts in any patient that's complaining of this posterior knee fullness. You really do need to make sure that there's adequate depth, one to confirm the stock, but also to evaluate the popliteal fossa further. And that is why this case was missed earlier in radiology. Utilize Doppler to confirm that this is non-vascular and also confirm that it's not adjacent to any of the neurovascular structures during your scan. From an interventional standpoint, I talked a little bit about the transducer selection, which is important. And you want to ensure that you can adequately image and plan your trajectory and target prior to the procedure. The thing I didn't mention previously is for both Baker's cysts or any paramunicipal cyst drainage, I typically will enter subcutaneously and tunnel through some subcutaneous tissue before entering directly into the cyst. So if you kind of poke straight into the cyst through the skin, you could create a track And so thankfully it hasn't happened to me, but I've heard of people talking about how that cyst directly communicates, and then it just will continuously drain. So going into the soft tissue before entering the cyst can help prevent that. And then in my case, the cyst collapsed very quickly, but typically if I am draining a cyst, especially if it's multiloculated, I will aspirate the area that's farthest from my needle point first. So the more proximal part of the cyst, that way, as the cyst collapse, you can slowly back the needle out with the aspiration. And that is it. Just a couple of references, and then I can stop sharing my screen and open it up for discussion. Awesome. Fantastic case. It's like you mentioned, something that everyone is going to see. The other thing that you mentioned as well is there's so many different ways that you can approach this. And a lot of it depends on who the patient is. Is it a traumatic high school in-season athlete, in which case, yeah, you might be more apt to get the MRI imaging sooner than later. And this patient, again, unless you thought there was definitive like vascular communication, I agree with you. I don't know that I would have gotten an MRI right off the bat, but that's a good point that you made. And just for anyone, if you're thinking down that line, you'd have to get an MRI with contrast to definitively see if there was vascular communication or not. Again, where this cyst was, it wasn't anywhere near the vessels, but if it was next to it, you'd have to. I know you kind of danced around if you did a steroid injection in each place. I'm just curious, what did you end up doing? I only did the steroid injection into the joint. So I think that into both places is probably overkill. The question is, one, do you need the steroid injection at all if we're just aspirating? Two, can you just inject the cyst? Or three, can you just inject the joint? And my thought process is behind the fact that the pathology is in the joint and the cyst is secondary. And so targeting that primary pathology is the place to start. And I typically don't do more than one steroid injection in most patients. And so I even upfront had the discussion of like, this is the one injection to kind of try to get things calmed down. And if this recurs or comes back, we need to think about other options. Yep, I think that's a great point. I feel like a lot of times when Baker's cyst patients come in and they say, oh, I have a Baker's cyst, it's more because that's a scary term and they don't understand what a Baker's cyst is. And so having that educational discussion with them can be helpful and saying like, why is it there? Oh, it's from the knee and managing that. Sometimes if it's all posterior predominant pain and they really don't have any like peri-joint pain, I'll start with a steroid in both if they have steroid load where I'm able to do that, meaning they're not getting everything else injected. But otherwise, I think it's safest to be cognizant about how much overall steroid you're giving them and the risks and benefits. Anyone else have any pearls in their practice of when they do or don't inject Baker's cyst? Allison, there was actually a good question in the chat or a comment in the chat about if you do an intra-articular injection, you can use Triamcinolone. And I was curious if your injectate changes, if you have a Baker's cyst, does that make you not want to use a particular steroid like, like Kenalog? Just curious how you, how you feel about that. So I typically try to avoid Triamcinolone only in really superficial locations. So I used Depo in this case, and that is solely based on what we have available in clinic. Not based on my steroid preference. The literature for like fat atrophy and skin hypopigmentation is a little bit stronger correlated with Triamcinolone than some of the other steroids. So if I'm injecting something really superficial, a small joint in the hand, potentially even Baker's cyst location, though I tend not to do steroid there, I'll avoid Triamcinolone just for that reason. But I, what I used in this case was solely dependent on the fact that only Depo was available in clinic. The other thing that you kind of touched on is, one, you can aspirate the cyst, two, you can aspirate and inject the cyst with steroid. You can also do a fenestration procedure where at this stalk where it's coming from the joint, you, before you aspirate, you kind of take your needle and you just like scrape at the outside of the cyst with the theory being that you're kind of wanting to create a little bit of an inflammatory bleeding reaction to wall off that one-way valve. So that's something else you can do. With that theory, if you then inject steroid around that area, would that reduce the chance of it wind off? Absolutely no studies to show any of that. But just when you're talking about, well, what's the goal of me doing this or that procedure or everything altogether, things that you can think about. Anyone injects sclerosine agents for Baker's cyst, like doxycycline or ethanol or anything like that in our presenter group? I never have. I think I always worry that there could be some communication with the joint and I'm not aware of how the sclerosine agent would affect the joint, especially doxy. So I have never done it in that, in that setting. I don't know if others have. In my mind using a sclerosine agent, you would want to do it in a place where you can make sure to keep that cyst compressed fully. And so it seems like it would be hard to fully do that in case it starts to form again. But to be fair, I don't, it's not something I use in my practice, so I'm sort of just making stuff up here. All right. And then there's a question about, can we differentiate between fat pad versus synovial hypertrophy in the knee joint? From my standpoint, synovial hypertrophy is going to be just a lot fluffier. It almost looks like they have a knee effusion, but when you stick a needle in it, nothing comes out and then you have to turn the gain all the way up and you're like, oh, nope, that's synovial hypertrophy. Fat pad hypertrophy, I guess I don't know that I've seen that in of itself. The fat pad certainly can get kind of inflamed and irritated, but most often what I appreciate if there's going to be something going on with the articular tissues, it'll be synovial hypertrophy. Any other thoughts on that from your guys' end? I wonder if they're asking that question just because my steroid injection picture, there was a significant amount of soft tissue, which was synovial hypertrophy that once we kind of took that fluid out of there, that like piece of synovium was pulled a little bit more immediately. And that can be a little bit better appreciated sometimes in a long longitudinal view where you are long access to the quad tendon and look deep. So, you know, sometimes it is difficult to distinguish, you know, what, where exactly does the fat pad end and where does the synovial tissue start? But just knowing based on kind of location where you would expect it can be useful. And I guess I was assuming that the needle entry on that picture you showed was a little more distal than kind of the, like you had both the super patellar fat pad and the pre femoral fat pad in the view. Whereas a lot of times we show pictures with just the pre femoral fat pad and there's not anything above that, no fat pad above the needle. Was that not that important to answer that, but that was just what I was thinking as well. The other piece I would say to address that question directly is just that synovial hypertrophy is something we sometimes see in rheumatologic pieces when we think about the knee. And so if you have synovial hypertrophy, putting on Doppler to see if you have any synovitis might clue you in that that's hypertrophy versus just your fat pad. So that can be another tool. But I think Allison, in your case, I think it was just that this was a kind of pissed off knee that was a little hypertrophied and you could see it once you got the needle in there and got the fluid out. The other thing I have seen kind of in that super patellar recess region is something called lipoma arborescens. And that's just like a fatty tumor that kind of it, the name means like tree, yellow tree fawn, and it almost has these little prongs that kind of stick up. And so that looks pretty distinct from synovial hypertrophy as well. And sometimes I find that those patients don't respond quite as well to like interarticular steroid injections and viscose supplementation and any of the things that we typically use to treat arthritis. I don't know what it is. And there aren't many cases in the literature to support, you know, what to really do with those. And I've had some patients who are elderly enough, they just kind of deal with it. And I've had a case where the surgeons went in and took that out too. Just out of curiosity, how much volume did you get out of the knee joint versus the cyst? If you remember? Sorry. Oh yeah. Sorry. So I should have mentioned that it was four cc's out of the cyst and 19 out of the knee. And did the knee look, it was like normal colored. It wasn't completely like normal synovial fluid colored. Even the cyst was? Yeah, they both were. The cyst seemed like it was fairly what I'd call fresh. Like sometimes you can get more congealed fluid the longer it's kind of sitting in there. But I think the fact that it was probably really only there for the five weeks still appeared very normal. I didn't send it for analysis just because it looked so normal and I typically don't send everything unless I'm concerned. I'm going to start using fresh in my documentation. That's fantastic. I completely understood what you're talking about though. Right? Yeah. Yeah. And that's, that's another important thing to note about Baker's cyst is you, what the pictures you showed were of a relatively simple anechoic Baker's cyst. You have all flavors of that where it can be much more complex, multi-lobulated, multi-septated more hyper-echoic. A lot of times when I see that, I'm assuming a lot of it is synovial hypertrophy in that area as well. Sometimes it can be hard to say, all right, this region looks giant, but is it, is there enough free fluid that I am actually going to get anything beneficial if I poke them with a giant 18 gauge harpoon and try and aspirate it? And when I'm kind of on the fence about that, a couple of things you can use just probe pressure. If there's displaceable fluid, you'll see it crank up the gain and you'll if there's synovial hypertrophy again, it'll be sparklier, more hyper-echoic than just anechoic. Any other tools that you guys have or tips you guys have in differentiating, all right, is this something that actually is going to have frank free fluid I can aspirate versus not? I think you mentioned everything. The compression is pretty key. Sometimes I also can almost like milk it. So instead of transducer compression, you compress on the soft tissue, either proximal or distal to try to see if you can milk any fluid under the transducer. Yeah, that's a good point. And then Doppler, like we've talked about can, can be helpful as well. And your comments about the soft tissue, going through soft tissue before going directly into the cyst is appreciated. As I did see a case where there was a tract formation. So please be careful guys, when you inject steroid directly into a superficial cyst, because you can get a tract that's formed. Yeah, superficial cysts, Versa's, olecranon Versa's, one that I think about all the time because of the color Versa, make sure you're buried in soft tissue to some degree and that you're going against the opposite of gravity. So for like olecranon Versa, if you go proximal to distal versus distal to proximal gravity is going to want to try and keep that open versus it's not going to go up your, your arm the other way. Great point. All right. Also for the parameniscal cysts that you'd see like medial or lateral, always try to drain that from the proximal side. Yeah. Because it was so deep that there's so many layers of muscle and soft tissue that it wouldn't have mattered. And in my opinion, well, thank you all the people who attended for coming to tonight's course and thank you to the faculty for all of your fantastic time, expertise, the cases that you presented. Remember to claim your CMEs, provide feedback, and then there will be a breakout exhibit room open for the next 30 minutes sponsored by Allergan and Abby V company. So feel free to check that out if you're interested, have a fantastic conference, otherwise. Take care.

posterior knee pain

medical attention

swelling

tenderness

diagnostic testing

ultrasound

MRI

cause

treatment options

rest

physical therapy

surgery

follow-up

prolonged stair climbing

Baker's cyst