Okay, everyone. Welcome and thank you for joining tonight. For those don't know me, I am James Robinson. I'm a family medicine, sports medicine physician at Hospital for Special Surgery. And this is the National Fellow Online Lecture Series presented by AMSSM. It's sponsored by the AMSSM Online Fellows Education Subcommittee, the Education Committee, and the Fellowship Committee. Just a few reminders. This is to serve as an adjunct to your individual program's educational program. It's not meant to take the place of your program's educational programming. And its point is to provide direct access to our fellows with experienced AMSS members and invited guests in a variety of formats. And the main goal is to help assist in CHU prep. So just some housekeeping. Make sure that your microphone stays muted and if you'll keep your camera off to help maximize bandwidth. If you have questions during the lecture, if you can just put them in the chat and we will have time for questions at the end and I will moderate those. And then you will receive a link with a survey. And if you'll complete that, that helps us provide better content in the future. So without further ado, it is my great honor to introduce Dr. Peter Fabrikant. He is an Associate Attending Orthopedic Surgeon at Hospital for Special Surgery and Pediatric Orthopedic Surgery. And he's also Associate Professor of Orthopedic Surgery for Well Cornell Medical College. Dr. Fabrikant did his undergraduate work at University of Rochester and then his medical education at Yale. He did his orthopedic residency at Hospital for Special Surgery and then completed a Pediatric Fellowship at Children's Hospital of Philadelphia and then a Sports Fellowship at Boston's Children's Hospital. So he is both fellowship trained in pediatrics and sports, which gives him expertise on our topic, which is going to be Osteochondritis Desiccans. And so without further ado, I'll turn it over to him. Thanks James. Can you guys hear me? Yes. All right, cool. And let me share a screen here. And then. All right, there we go. Can you see this full screen slides? Yeah, we're good. Perfect. So thanks for the introduction. Thanks for the invitation to speak. We work very closely with our family medicine and primary care sports medicine colleagues. And it's we have a lot of shared patients and there's a lot of cross pollination of knowledge that goes back and forth. So I'm really happy to be doing this lecture for you guys. These are my disclosures. None of them are really related to this talk. So as just kind of an overview of what we're going to talk about, I want to first talk about the definition and etiology of OCD and then talk about my diagnostic algorithm, specifically the history and pertinent examination findings. And then my treatment algorithm with a focus on when to treat nonoperatively and when to consider a referral for possible surgical intervention. And then talk about not only kind of nonoperative treatment strategies, but then treatment outcomes. And just kind of each for each joint, I'm just going to I have one slide just for interest of kind of what different surgical options are possible. But we don't get too much into the surgical side of it. And I'm going to do this in order from knee to elbow to ankle, because there's really the most like the vast majority of OCD literature in children and adolescents is available for the knee and then less for the elbow and even less for the ankle. So I'm doing this kind of in order of decreasing the comprehensiveness of the literature. So this is a slide that's going to be referenced kind of throughout the talk. And I think this is really the takeaway slide. When I'm thinking about OCD lesions in kids who are presenting, the two main things I'm thinking about are, is the lesion stable or unstable? And I'll get into kind of how to determine this on imaging and examination. And then is the patient skeletally immature or skeletally mature? And for the knee, this is the table. And we're going to really obviously focus on the upper left hand corner because essentially all unstable lesions tend to require surgery to stabilize them structurally. And in the knee, there's good data to show that chronic stable lesions in skeletally mature individuals can benefit from surgery. But we'll kind of dig into that a little bit. And as far as the knee goes, this is assuming no other pathology, specifically things like malalignment. And I'll get into that as well. So I think it's first important to really understand what is OCD. And when I explain this to kids and parents, a lot of times we think about it or talk about it like it's a cartilage problem, but it's really a bone problem. The definition is a chronic idiopathic alteration of subchondral bone with risk for instability and cartilage disruption that can result in premature osteoarthritis. And that's the definition from the rock or the research in osteochondritis in the knee study group. And then cartilage involvement is always secondary. So if that piece becomes devitalized and unstable and pops off into the knee and there's a pothole, it's a cartilage problem, but it really starts out as a bone problem and we treat it like a bone problem, unlike adults who tend to have normal bone, but then cartilage defects. And I think that the thing that makes it even more confusing is when you hear the phrase OCD, that some people say osteochondritis desiccans, osteochondral defect, and OCD, it's like the same acronym. So it's just important to understand that OCD desiccans can lead to an osteochondral defect, but it's not exactly the same thing. And so we're going to start with the knee. You can see here an example of a medial femoral condyle OCD that spit out a loose body that's stuck in the notch. So just some epidemiology. So this was a study that looked at over a million kids in the Kaiser Permanente database and noted an incidence of 9.5 children per 100,000 person years. I mean, this number in and of itself isn't necessarily that helpful because it's hard to think about what 100,000 person years are, but their epidemiologic data showed that it was much more common in males than females and much more common in adolescents than pre-adolescents. The mean age of their patients was 13 years old. And at least in their group, they did show a race ethnicity predilection for blacks over non-Hispanic whites, and then Hispanics and Asians. As far as where these occur in the knee, the vast majority occur in the condyles, two-thirds in the medial femoral condyle. We'll get into why that is. And then a majority of the rest in the lateral femoral condyle with some also in the patella and trochlea. But largely these are medial femoral condyle and sometimes lateral femoral condyle lesions. A variety of potential ideologies have been proposed. There's certainly a thought that it's partially kind of disk vascularization and then microtrauma, but it's still somewhat considered to be idiopathic with those two main contributing factors. One of the early studies that was done, essentially surgeons went and did core biopsies to do histological analysis of OCD lesions with the thought that this was going to totally answer the question, but it kind of made more questions than answers. So when they sampled all these OCD lesions, there was a really mixed ideology. And so this started to open up some research as to how certain contributing factors might contribute. Others have reported that there may be a component of discrete macrotrauma. I think this is certainly less common, but kids are certainly injuring themselves with minor injuries all the time. This study should look at a couple of patients who had documented bone bruise on MRI and then later on that bone bruise kind of coalesced into an OCD lesion. I think that's certainly possible, but not the most common cause of OCD. It's more likely due to chronic and repetitive microtrauma that's unable to heal due to the vascularity of certain areas of the knee. A more recent radiographic and even veterinary thought is that there's an insult to the secondary physis. So we always think of the physis as the zone between the epiphysis and the metaphysis, which is the primary physis that gives us longitudinal growth. But in the knee, there's a second, you know, and in bones, there's a secondary physis, which is essentially the kind of outward growth of the epiphysis. And if there's an insult to that soft cartilage as it ossifies, it doesn't ossify normally. And there's a thought that that may contribute to the creation of an OCD lesion. I think this paper is probably the biggest landmark paper for OCD in looking at the reason that humans get them in the medial femoral condyle. So this was a study where they took a pediatric cadaver tissue and placed it in a research magnet, which was a 9.4 tesla MRI. And it was able to do vascular mapping. And they noted that there was a watershed area in the OCD predilection spot in the intercondylar aspect of the medial femoral condyle. And in addition, you can see in these images, a lot of the vessels are running parallel to the joint surface, which puts them at greater risk of shear injury than vessels that go centripetal, kind of outwardly towards the joint surface perpendicular. And then the other interesting thing they found is that when they examined goats and pigs, they noted that the same was true in goats, that they get OCD. And also they have this parallel orientation of the subchondral blood supply in goats. But in pigs, they don't get OCD lesions, and they have a perpendicular vascularity, so less likely to have injury by shear forces. So all this taken together indicates that there's certainly a vascular component to OCD, and it's likely that this area is just unable to repair itself like other areas of the knee can with chronic microtrauma. So as far as the OCD of the knee history and examination, very frequently kids present with knee pain with or without a specific event. Lots of kids and families will say it started hurting after I injured myself on this day, but kids are getting injured very frequently playing sports, and everyone likes to have kind of a beginning, middle, and end to their story. So sometimes people will associate with an event, but frequently it just kind of comes on. And the thing that you want to really think about is, are there mechanical symptoms? So things like swelling, catching, locking, or sensation of instability in the knee, because this can indicate a loose or mechanically unstable piece. On examination, in addition to the typical examination, you want to look for things like effusion, locking or lack of range of motion of the knee, and then condylar tenderness, with the exception being the patellofemoral joint. But with the knee flexed to 90 degrees, in that bottom right image you can see where that red arrow is, that would be kind of a location of tenderness typically for an OCD lesion. An OCD diagnosis is made by imaging, so x-rays and MRI. It's very important to include a tunnel or a notch view in your x-ray series to look for OCD lesions. So simply like AP and lateral x-rays can miss OCD lesions because they tend to be posterior. So a straight AP gets the most distal weight-bearing surface as its best view, but with a tunnel or notch view of the knee flexed a little bit, you can see kind of to the back of the condyle, and it's the best way to diagnose these typical lesions on x-ray. So certainly want to include a tunnel or notch view. I think it's also important to understand that there is this kind of ossification variation. So as kids are developing, sometimes they can have irregular ossification fronts, and sometimes that's confused for OCD. So this table is helpful for me at least in kind of trying to understand what's the difference radiographically. The ossification variants tend to be younger kids and have not as much bone marrow edema and tend to be very far posterior without intercondylar extension. So I'll show you an example of that. These are two patients. On the left, there's a 10-year-old male who did not have an OCD lesion. It's more of the normal variant. You can see it's like a puzzle piece. It's very posterior, and you can see those small white arrows show that the tide mark or the subchondral bone line is really intact, whereas on the right side, the 11-year-old male with an OCD lesion, you can see it extends more anteriorly, more of the distal weight-bearing surface of the condyle, and you can see that black line, the subchondral tide mark, is disrupted. So certainly back kind of here towards the posterior aspect of the lesion, this line just kind of disappears, and that's more consistent with an OCD lesion. So my imaging algorithm is very kind of standardized. So OCD is detected, you know, history, physical examination, and x-ray. So let's say for argument's sake, you diagnose an OCD in the right knee. I'm going to get a couple of different imaging, a couple of different sets of imaging. I'm going to get an MRI of that knee to evaluate the lesion. I'm going to get a standing hip-to-ankle radiograph to assess the overall coronal plane alignment, because this can certainly affect healing, and I'm going to get a contralateral knee x-ray, because up to a third of patients can have bilateral lesions, and of those, 40% can be asymptomatic. So I routinely screen the other side for an OCD lesion with x-ray. Based on the MRI, we'll make a decision for surgery or non-operative treatment based on those factors from the table. So if it's an unstable lesion, which is best determined on MRI, then these are lesions that need surgery, and if it's a stable lesion, then we proceed with non-operative treatment. If we proceed with non-operative treatment, I repeat the MRI in three months' time. If it's looking better or no different, you can continue with non-operative treatment. If it's looking no different, you may consider non-operative treatment with then another MRI in three months so that you go out to six months, and if it's not better at that point or it's looking worse, you can proceed to surgery. And I'll explain where that six months comes from. It is literature-based, although I will say that most kids and families are not keen on the idea of a six-month non-operative trial when there's a chance that they may then require surgery. So a lot of times, if it's not looking better in three months, we could certainly consider surgical treatment at that time. So this is the most commonly used staging criteria for OCD lesions. It's called the HEFTI classification, and it's five stages, but I tend to think of them in three kind of groups. So stage one and two are the stable lesions. These have kind of signal change in the subchondral bone, but it's not so linear. Stage three is when it starts to become unstable. You can see on the top right image here, there's kind of a crack perhaps, and there's certainly linear signal there. Stage four is when that breaks out to the surface, and there's essentially a loose body in situ. And then stage five is when there's a detached loose fragment. So I kind of break them down into three groups, stable, unstable, and loose body. And treatment is based on that lesion stability and if there's a loose body. So if it's stable, then these are the patients who can do well with non-operative treatment. And I'll go over kind of a non-operative treatment algorithm. Those that are unstable tend to have surgery with drilling and fixation, and those who already have a pothole with a loose body tend to undergo cartilage restoration. So the color scheme, I'm going to kind of keep the color schemes going from the first table. So green is our non-operative group, and red is our surgical group. So looking at predictors of success with non-operative treatment in neo-CD, this is one of the original studies that is often cited. However, there are some issues with it which I'll go over. So this looked at 62 patients with 76 lesions. They had activity restriction. The patients underwent activity restriction until they were pain-free. And at six months, two-thirds were worse or had no improvement. And at 12 months, only half, or I'm sorry, half were worse or had no improvement. That's where that six months of non-operative treatment comes from because, you know, 33 percent get better after three months and then another, you know, 16 percent get better by 12 months. But those numbers are really quite low and they're lower than what is likely the true number. If you look at their study, they said that predictors of progression were age, lesion size, and presence of cyst-like lesions. And you can see there on the right side, those cysts in the subchondral bone to me actually indicate an unstable lesion. So I think that this group of non-operatively treated patients had a decent number of unstable lesions which likely, you know, should have gone on to surgery out of the gate. I think if you look at just the stable lesions, then the number of the percentage that heal will be higher. You know, later this was followed up by a more recent study done at Boston Children's Hospital where they looked only at stable lesions and they looked at predictors of healing and they also looked at the impact of bracing and crutches. And they looked at a much larger number of patients of three, you know, almost 300 patients and 333 knees at a mean age of 11 and a half years. And of the whole group of these stable lesions, 57% healed. So I think this is probably a more accurate number of overall stable lesions going on to healing with non-operative treatment. So I tend to quote this number to patients and families around 55 to 60%. Now they looked at the use of crutches and unloader bracing and they found in their group that 56% of patients who underwent unloader bracing for three months were actually more likely to need surgery than those who did undergo unloader bracing. And 25% of their patients were placed on crutches and this tended to be protective against surgery. I don't know that you can place too much stock in these specific subgroups because it's unclear if there's a selection bias where, you know, perhaps the worst more involved lesions were the ones treated with an unloader brace and therefore the unloader brace was kind of associated with a failure of treatment. But I certainly think that this 57% number is real and limiting activity and offloading the lesion can be helpful during this time. Finally, with the non-operative treatment, there is preliminary evidence linking low vitamin D levels to OCD, at least in adults. So there's a study of older patients who had an average age of 31 years and 78% of them were vitamin D deficient. And then separately, there's some early kind of data that's been presented at meetings. I can't find manuscripts quite yet that are out, but it shows improved healing rates with non-operative treatment with vitamin D supplementation. And in my mind, this is a relatively inexpensive, low risk, high possible reward. So certainly incorporating vitamin D supplementation or at least vitamin D testing in patients being treated for OCD is a reasonable thing to do. So what's my non-operative treatment protocol? These tend to be skeletally immature, stable lesions with neutral alignment. I think that these are the ones that really have a good chance of healing. If kids have varice or valgus alignment and it's overloading the compartment where the OCD lesion is, I think those are kind of more doomed to fail, so to speak. And so I tend to intervene surgically with things like guided growth and whatnot. But certainly the skeletally immature stable lesions are ones that really deserve a good shot at non-operative treatment. I tend to supplement with vitamin D and check levels as well. And then I do a three-month treatment regimen before I repeat the MRI. So I do everything I can to slow kids down. That's the ball and chain. So I think the most important thing is taking them out of sports and activities as well as impact. I let them swim. I let them ride kind of a stationary bike, but I'm spending the first half of that time brace and crutches. And then when they come back for a six-week check, I let them choose which one they wanna get rid of, the brace or the crutches. 99% get rid of the crutches and they'd rather just walk around with the brace, but the brace at least reminds them not to mess around on their knee and it kind of slows them down for that full 12-week period. And then I repeat the MRI at that three months. It's important to note that symptoms will almost always improve, even if the lesion is getting worse. So that's just because they've been taken out of their impact sports and the lesion can progress even though it feels better. And so for me, my decision at that three-month point, whether it's been a treatment success or it needs more time or potentially needs surgery is based less on their symptoms and more on the imaging. If the MRI looks noticeably worse at three months despite the rest, then that's a reason to refer for surgery. If it looks better, then they can kind of start progressing back to sports and activities. And if it looks the same, it ends up being more of a shared decision-making discussion. I think it's reasonable to do another three-month trial. I wouldn't necessarily put them on brace and crutches, but I'd certainly keep them out of sports activities and optimize the vitamin D. But some kids and families, they just don't want to wait that long. And for stable lesions, transarticular drilling of stable lesions has a 95% success rate. And it's a straightforward procedure that takes about 25 minutes. So sometimes at three months, patients will opt for surgery. I think it's reasonable to consider at least looping in a surgeon at three months if it's not looking better. And then just for the interest slide, what is all this drilling about? So drilling the lesion, this is a stable OCD lesion. The cartilage looks perfect. It's just the subchondral bone that's affected. So this is not microfracture where you remove the cartilage and do varisimulation. It is simply the varisimulation under the cartilage, so fine wire drilling. For unstable lesions, we do that plus add fixation. You can see three implants there stabilizing that lesion, which has a fissure kind of all the way around it here. And then for lesions that are unsalvageable or for loose bodies or cartilage that's kind of also destroyed, then we tend to do things like cartilage restoration. This is an autologous osteochondral graft. And then finally, don't forget to address the mechanical alignment. So again, I get standing alignment films on all these kids, especially when it's not your standard medial femoral condyle OCD lesion. So in the lateral femoral condyle, this is much more common in kids who have discoid meniscus or valgus, which are two things that kind of overload the lateral compartment. So here's an example of a kid with a stable OCD lesion in the lateral compartment, which if it was in the normal predilection spot would be very reasonable to treat nonoperatively. But when you get the standing alignment film, you can see in the right knee, this mechanical axis, the blue line passes very far lateral and really right through the lesion. So this is one that ended up receiving nonoperative treatment, but progressed pretty rapidly at three months. And eventually was treated with guided growth to realign the limb and then surgical treatment of the OCD lesion. So it's important to look for these contributing factors also. All right, I'm gonna move on to the capitellum now. The capitellum is kind of similar treatment thought process to the knee. So you'll see a lot of common themes here. This is again, the takeaway slide from before. You'll notice the one difference is that in that bottom left quadrant, surgery is kind of a plus minus in the stable lesion. So previously in the knee, there's good data to show that stable lesions in skeletally mature patients benefit from surgery just because of the differential in success between surgery and non-surgical treatment in mature kids. But in the capitellum, there's not that body of data. So certainly a trial of non-operative treatment is reasonable. Again, here's the definition of OCD. It's a subchondral bone problem, not a cartilage problem, but cartilage involvement is secondary. And again, in the capitellum, similar to the knee, there is a component of hypovascularity. So you can see in the top right image there, this is a lateral view of a cadaveric elbow. That has the kind of vascular mapping. They inject latex into the artery. Then you can see where the artery goes. There's the blood supply to the capitellum kind of starts posterolaterally and then profuses. And so the last place to get blood supply is that kind of anterior distal area of the capitellum, which is the predilection spot for OCD. On the bottom left, you can see there's a watershed area between the lateral epicondylar vessels and the medullary vessels, which is again, the area of OCD. And then on micro-histological specimens, you can see a very thin area of subchondral bone. And then again, this kind of parallel architecture of the subarticular venous plexus, which is very prone to shear injury. And certainly in kids who get capitellum OCD, most commonly gymnasts, cheerleaders, pitchers, throwing athletes, there's a ton of shear forces at the radial capitellar joint. And you can see on the top right, this is kind of the loading position of the elbow, tension on the medial side, compression on the lateral side and the subchondral bone layer in the capitellum being typically a non-weight bearing joint is only about a 10th of a millimeter. So definitely more prone to shear injury. Who gets capitellum OCD? We very frequently see it in pitchers and overhead athletes and it's almost always on their dominant or throwing side. And then we see it a lot in gymnasts and tumblers that can get it on either side, regardless of arm dominance or bilaterally. And then less common, but still possible, we kind of see it in random kids. I've had a couple of kids in my practice who were kind of video game enthusiasts who presented with elbow OCD. So it's not just the athletes, but it's much more commonly the athletes, specifically overhead athletes. How does it present? Typically vague posterolateral elbow pain that improves with rest. As it becomes unstable, similar to the knee, you can get mechanical symptoms such as clicking, locking, or swelling. And if there's a loose body, you can get a locked elbow. Sometimes I'll see kids who they say their elbow locked, they couldn't fully extend it, and then they kind of worked through it and they fully extended their elbow and now their elbow is swollen. So a lot of times that's the presentation of a loose body. Imaging, same deal, x-ray and MRI. So x-ray, you get your standard views. You can, similar to the tunnel view in the knee, you can do an AP and 45 degrees of flexion to see where that typical OCD lesion is. As far as contralateral screening, I do it just because I do it in the knee and the ankle also. I'm a little less pushy with additional x-rays in the pitcher, quarterback, tennis player, overhead athlete, that's not a tumbler. But in the gymnasts and cheerleaders, I tend to recommend getting it on the other side because they're loading both elbows pretty equally. And MRI is our workhorse imaging strategy. It helps us understand the presence of loose bodies. It gives us a better understanding of the subchondral bone. And I really like STIR imaging, which is the fluid sensitive type imaging. You see there on the left of the MRI here, and I get it in two planes. And it lets us understand the cartilage status and if there's any other pathology in the elbow. Similar deal, this is again, the knee slide, so I won't belabor it, but I still try to categorize these as either stable, unstable or loose body. And similarly, the stable lesions can be treated non-operatively and the loose body and the unstable lesions tend to require surgery. There's better data looking at predictors of non-operative treatment success. Certainly stable lesions for me is kind of a prerequisite to consider in a course of non-operative treatment. But other predictors of non-operative success include an open capitellar fysis. So that's kind of goes along with the skeletal immaturity. There's more blood flow and metabolism around the elbow. Maintained range of motion is important and also no fragmentation or radial head enlargements. You can see in the bottom image there, the top red arrow shows fragmentation and the bottom red arrow shows this radial head enlargement. You can see it kind of sticks out laterally compared to the image above it. And what that's doing, it's essentially the body's attempt to disperse the forces over the radial capitellar joint. This is a clinical sports medicine update article in AGSM, which is a great additional reading. It was published last year. They really kind of noted, they do a great job summarizing the existing literature they point out as somewhat limited. So they did show however, that low grade lesions or stable lesions have similar outcomes with operative and non-operative treatment, but high grade or unstable lesions really did significantly better with operative treatment. So again, this goes to the concept of stability being a real driver of treatment success with non-operative treatment. And then when they looked at different surgical techniques, there wasn't really a superior surgical technique one over the other. What's my non-operative treatment strategy? So again, it's more of the same as the knee. So rest, so no throwing, no tumbling and no upper extremity weight bearing. So like no pushups or any sort of like loading of the elbow. I tend to send kids to PT, not necessarily because I think it's gonna get the lesion to heal, but I think it keeps the arm strong in a way that's safe for the elbow and can work on the rest of their kinetic chain. If it's a pitcher, three months off can be devastating, but if they spend those three months working on, you know, hips and core and scapular retraction and other aspects of their kinetic chain, once they do get back, they tend to do much better. Same thing with the vitamin D, I will check it and or supplement and then repeat MRI at three months. And then similar to the knee, make a treatment decision at that point if it's either working or not working. If the MRI is worse, again, they go on to surgery. If it's better, they get a return to play program. I have a, just kind of from where I did my fellowship, there was a three month return to throwing program for pitchers. So it tends to be somewhat prolonged to really make sure they're not overloading the elbow, but that can be modified based on the, you know, clinician preference and the patient. And again, if the MRI shows no difference, it's more of a family discussion and sometimes a surgical discussion. So what can this look like? In my practice, there's kind of two different treatment strategies. So the top row of images is a loose body in the elbow, which we remove arthroscopically and then debride the lesion and perform kind of cartilage restoration. You can see there on the right. And then for large or uncontained lesions, like in the bottom row, I tend to do an osteochondral autograft from the ipsilateral knee. And if it's way too big, so I think this one was about 18 millimeters across, I tend to do an osteochondral autograft, but concept here is either cartilage restoration or osteochondral unit transplant. And then lastly, I think we're running on time here. We'll talk about the talus, which if you were disappointed in the amount of literature that's available in the capital, you'll be even more disappointed in the amount of literature on the talus. Again, takeaway slide, very similar, the stable and unstable image are mature. So the unstable lesions tend to get surgery and the stable lesions tend to get non-operative treatment. And then again, same definition, subchondral bone problem, cartilage involvement is secondary. You'll hear these being called OLTs or osteochondral lesions of the talus. And there's a very vast literature in OLTs, but it tends to be in older patients. So for pediatric kind of OCD of the ankle, it's not necessarily applicable. Lots of those studies look at people who are kind of 30 to 50 years old rather than the kids and adolescents. Again, in the talus, there's a certainly a contributing etiology of hypovascularity with the medial talar dome being the watershed area. The talus is a very articular bone and there's few areas for blood supply to enter, but the dorsalis pedis artery, the posterior tibial artery and the lateral tarsal artery through the perforating perineal artery supply blood flow to the talus and the medial talar dome is a watershed area, which is the area of predilection. It's important to know that there's a difference typically between your medial talar dome OCDs, like you see on the left there, and your traumatic injuries, which tend to be lateral talar dome. So lateral talar dome tends to be bad ankle sprains or ankle fractures. And you can see there on the right image, there's a lateral talar dome osteochondral defect or osteochondral lesion of the talus, but you can see that the fragment is there, it's in situ, it's actually flipped over on itself. And you can see the yellow orange arrows show all this edema in the subchondral tissue. So that is a traumatic ankle injury causing a chondral defect, which is very different than the medial talar dome OCD. So who gets talus OCD? This is more kind of anyone can get it. So it tends to be progressive subacute chronic ankle pain. You can sometimes get the presentation that a patient has had chronic ankle sprains, but they're not really spraining their ankle, their ankles just kind of hurt. They may get diagnosed with an ankle sprain and they're constantly in and out of sports because of it, but it could be a brewing OCD lesion. And conversely, you can have kids who were completely fine, get like a real ankle sprain, they get x-rays as part of a workup for that. And then it's incidentally noted, they never had any pain there and it's just an ankle sprain. So it's really important to tease out, is this a classic OCD lesion where it just kind of progressively came on? Was it an asymptomatic lesion that only got found because the kid had an x-ray for some other reason, like an ankle sprain, or is it a traumatic lesion? So it's just kind of important to tease those things out. As far as clinical presentation goes, classically, it's a kind of vague anterior ankle pain that improves with rest. If there's a chondral flap, it can cause some mechanical symptoms such as clicking, locking, or swelling. And again, patients can be diagnosed with recurrent ankle sprains. Now, I think that there is less likely to be mechanical ankle symptoms in the ankle than there would be in the elbow and the knee because the ankle's a very contained joint. And typically through a full ankle range of motion of plantar flexion and dorsiflexion, that lesion is not kind of getting uncovered and covered by the tibial plafond. And so it's kind of contained and it's staying under there and it's less likely to click and catch and lock as opposed to the medial femoral condyle or the patellofemoral joint or the capitellum, the radial capitellar joint. There's a lot more shear force there where through an elbow range of motion, that capitellum lesion can become somewhat uncovered by the radial head and then recovered. And so that's typically the time when they may feel mechanical symptoms. As far as imaging goes, I'm a little more extensive with my X-ray workup. So certainly I get x-rays of the involved side. You can see on the left side in the red circle there, there's the OCD lesion, medial tailored dome. I tend to get bilateral x-rays to rule out a silent lesion on the contralateral side. In kids who have flat feet or high arches on a clinical exam, I tend to get Saltzman-Hill alignment views. I used to get them routinely in my practice, but found that clinical exam is pretty good for detecting high or low arches. So I tend not to quantify it radiographically unless I feel like it's clinically warranted. And then if someone does have a history of ankle sprains, I get stress radiography, both tailored tilt views like you can see here in this third image and anterior drawer stress, which you can see in the image all the way on the right. And the reason is because if someone has a really unstable ankle, they're less likely to succeed with non-operative treatment. MRI then again is the workhorse. So this really helps us understand if it's a stable or unstable lesion. In the ankle, for the reason I mentioned before, it's a very contained joint. It's just much less common to have a loose body floating around. They tend to be more loose bodies in situ and therefore the MRI is even more helpful. Again, the subchondral bone is important to assess. And I really like that fluid sensitive imaging, not the imaging shown here so much, but the more T2-weighted or fluid sensitive imaging in two planes, coronal and sagittal. And then the MRI also helps us understand the status of the cartilage as well as any other pathology in the ankle. Same kind of thing as before as far as surgical versus non-surgical treatment. If it's an incidental finding or it's a stable lesion, these patients do pretty well with non-operative treatment. And I tend to try that first. If it's stable but has refractory symptoms, despite non-operative treatment, then they tend to go on to surgery. And if it's a symptomatic and unstable, loose fragment in situ, they tend to move on to surgery as well. This is really the only article that I could really find or that I referenced in recent literature looking at who does well with non-operative treatment, specifically in osteochondritis desiccans in the talus. There's a ton of literature on OLTs, osteochondral lesions of the talus, in older kind of young adults, young adults and middle-aged adults. But I really don't necessarily think that's applicable to pediatric patients. And so this study essentially found that in stable lesions, younger patient age and a lower BMI were the best predictors of recovery. And they actually created this nomogram, which is kind of cool. So you start across the top here, you plot their age in years and you drop it down and give them a certain number of points. You plot their BMI, drop it down, give them a certain number of points. The third thing was what's the initial treatment modality. So if it's a first-time presentation, they're gonna be non-surgical, so that's zero additional points. And you add their points and then you go down here to the bottom and then you say, okay, they had eight points and therefore they're, whatever that is, 45% likely to be healed at one year of follow-up with non-operative treatment. So I really enjoyed this. I enjoyed this paper and I think it's a good one for understanding what the risk factors are for failure of non-operative treatment or the protective factors for succeeding in non-operative treatment. More of the same themes with regard to non-operative treatment strategies in TALIS-OCD. So again, rest. I okay them to do things like swim, bike, and walk. If I find that if I shut these kids down completely, they're gonna just go run around. And so I'd rather kind of give them some sort of a controlled activity regimen so they can burn off energy without pounding on their ankle. If they're limping when they present and they're in a lot of pain, I will put them in a boot, but I do not keep them in a boot for more than two to three weeks, even if they still have pain. I don't think coming out of the boot, I don't think lack of pain, sorry about this. I don't think lack of pain is the indicator to come out of the boot. I think it's more just letting the ankle cool down because the longer they stay in a boot, they become stiff, they become weak, and then they get other ankle problems. So I have seen some kids who were booted for two months and now their OCD is better, but they're just in a ton of pain because they're stiff and they're weak and it just requires a ton of therapy and strength training to get them back. I do put them in PT for calf stretching in order to improve biomechanics. Again, vitamin D supplementation and screening and then repeat the MRI at three months. Again, MRI is worse, they undergo surgery. MRI is better, they go return to sports. If MRI is the same, we have a family discussion and also look at symptoms. I do lean a little heavier on symptoms for deciding at that three month visit with the ankle more so than in the elbow and in the knee. But sometimes these kids are just like pulling their hair out at three months. They're saying it's taken forever and they just want something done about it. But for other families whose priorities are to avoid surgery at all costs, it's reasonable to give them another three month trial. What does surgical treatment look like? So that top row is a stable OCD lesion with intact overlying cartilage. So that's just an arthroscopic view of the medial tailor dome here and it's just soft cartilage. And then what I'll do is I'll put K wires up through the lateral tailor process into the lesion, drill over the central wire and then bone graft underneath it. So again, this is treating the bone problem in order to support the cartilage. This bottom row is a different patient who had a loose lesion with just kind of destroyed cartilage so to breed it back to a stable osteochondral junction and then similar to the elbow, just kind of an enhanced cartilage restoration technique. This is bone marrow aspirate concentrate mixed with acellular cartilage proteins in order to provide kind of a more stable fiber cartilage type tissue. For really larger or uncontained lesions, you can do osteochondral grafting, but that requires a medial malleolar osteotomy. So contraindicated in kids with open growth plates because you'd have to cut across the growth plate. Also, there's a little bit higher morbidity here, but for these large lesions, it's kind of the only option. And then previously in practice, I had treated these with fixation similar to the knee and it's definitely a possibility and it's an accepted treatment method. However, I found it to be a little less successful than the knee, so I've been doing it less frequently as of late. So again, just in conclusion, then we'll have some time for questions. The takeaways here are this table. So unstable lesions are just gonna go right to surgery. The stable lesions, certainly the immature kids or open growth plates get a good non-operative treatment trial. And then the kids that are skeletally mature with stable lesions, it's a little bit more up in the air, but certainly reasonable to proceed with a trial of non-operative treatment, especially if this is like on your boards, I think it's a very reasonable treatment strategy. Non-operative treatment involves rest, relative rest for three months. And I think that's the most important thing regardless of bracing and crutches and boots and things like that. And then a repeat MRI at three months to help guide treatment either back to sports or for a surgical referral. I think less kind of obligatory is PT and vitamin D supplementation, but I certainly involve this in my practice and I think it can be helpful. I'll give you one bonus just for those who are studying for their boards. There is a familial version of OCD and it's extraordinarily rare. I think I've seen, OCD makes up like 40% of my practice and I've seen one case in the last six years or so of a familial OCD. And it tends to be kids who present with multiple lesions in joints and like multiple joints affected. But if this comes up on the boards, it's the ACAN gene or the AgriCanCorp protein gene on chromosome 15Q and it's autosomal dominant. This did come up on my orthopedic board. So I always kind of put it out there when I'm giving a talk to residents or fellows or review talk for the boards because it's just an easy one to memorize and an easy one to get if it does ever show up. So with that, I'd like to thank you guys for inviting me and for listening. I think we're just about on time and we have a little bit of time for Q&A. Yeah, thank you so much. That was a great review and very, very poignant. So there are a few questions in the chat. If you do have questions, put them in the chat, we'll try to get to as many as we can. One of the questions that I get often asked, especially with our baseball players is, do you allow them to hit if they have a capital OCD? Yeah, that's a good question. Sometimes, I guess I would say. For the first six weeks, I certainly wouldn't. If they do have pain, if their pain is better at six weeks, I will let them take some batting practice and see how they feel and then go based on their symptoms. Great. Yeah, I typically don't let them hit either, but that tends to be not a very popular decision. It's very hard, especially these baseball players. One of the questions was about the MRI for the elbow and whether it's just a regular MRI or an MRI arthrogram, especially if you don't have access to a 3T magnet and you're using like a 1.5T. Yeah, yeah. So at HSS, the institution is very heavily kind of biased against arthrograms. I tend to find that arthrograms are not needed for these cartilage type things. I think it's a little more controversial when you're looking at like labral tears in the shoulder and in the hip. And kind of counterintuitively, I have had this discussion with some of our radiologists. Counterintuitively, 3T magnets, although they're great, they're very high resolution, they're much more prone to motion artifact. And I find that in kids who tend to like squirm around a lot in the magnet, any benefit you might get from the 3T magnet is like a little bit lost because they're kind of moving around. And so I wouldn't worry so much about 3T versus 1.5T. I think as long as you can get good imaging, I don't think you necessarily need an arthrogram. Great, and then one of the questions is about in-season management versus out-of-season management. Does it change whether you go to surgery or not, depending on if they're in-season or out-of-season? Yeah, you're talking about the elbow still? I think it's just generally, but probably elbow would be my guess. Yeah, so for the elbow, the thing for me with the elbow is that the surgeries for me, because that subchondral bone layer is so thin, that it really doesn't do well with fixation. So for me, like if they're gonna go to surgery, they're getting some sort of a, either a cartilage restoration or a osteochondral autograft sort of thing. So for me, it doesn't necessarily change the treatment. So if someone has some pain and it's like their senior season or they're like doing showcases and they're gonna get it, let's say they need surgery, they don't have a loose body or a locked elbow and they just wanna power through a couple of weeks of the season, I tend to let them do that because it won't really change the surgery or the outcomes. If they have a medial femoral condyle OCD lesion that looks loose, I really pull them back regardless of the season, if they're in season or out of season, because if that goes from a unstable, but in situ lesion to a loose body, that really changes not only the surgical treatment, but the potential outcomes and kind of the predictability of the outcomes. So for that reason, I tend to not allow neo CDs or not recommend that neo CDs continue with treatment. However, the elbows, I will let them play a little bit more in season if it's important and same with the ankle. Great, I think we have a little bit more time. So if you have any more questions, put them in the chat. One of the things that comes up a lot in our patient population, I'm sure you get it as well, is like orthobiologics and PRP. And if you augment at all with those in your patients. Yeah, so PRP, not typically, the orthobiologics here would be like those, the pictures you saw of the elbow and the ankle with like that red goop that was going in there. That for me tends to be bone marrow aspiration concentrate. I mean, you can use PRP to rehydrate that, those little like white little specks were essentially like a cellular cartilage proteins. The thought process there is you take bone marrow, instead of doing a microfracture where the bone marrow just kind of bleeds into the area, it's liquidy, it doesn't have any staying power and it's got some concentration of stem cells. You could actually do a bone marrow aspirate, concentrate it down, depending on your system, you're looking at kind of five to eight X concentration of stem cells. And then take that and mix it with this powder, this acellular protein matrix, which becomes kind of like a putty. So now you have kind of mechanical staying power, you can put it in there and mold it and kind of contour it to the surface. And also you have a higher concentration of stem cells and they're living in an environment of cartilage protein. So it tends to make not hyaline cartilage, but not fiber cartilage, it's kind of something in the middle. And for me in the elbow and the ankle where microfracture has been described and has been used previously, I tend to do that. And that for me is kind of the extent of my orthobiologics for OCD. Great. Somebody else had a question about any insight on trying to differentiate between a Panner's disease versus like an osteochondritis desiccans in the elbow. Great question. Great question. So osteochondritis desiccans tends to be very focal. I'm gonna try to like zip back to the slide. Okay, focal. So you can see down here, it's like this lesion and that's it. It's like just from here to here and that's it. And then same view over here, it's here to here, that's it. Panner's disease tends to be a much larger area of the capitellum and it tends to be younger kids. So kind of like eight to 12, let's say, and it tends to not have like loose bodies. So it's not like a very large area of the capitellum not have like loose bodies. So it just looks a little bit more like the capitellum just looks a little more just overall in bad shape but it tends to heal on its own. Whereas OCD, I mean, this capitellum here looks pretty much perfect except for this one area. And again, this is your typical predilection spot. So if this were a clock face, like if straight up was 12 o'clock and this is nine o'clock, it kind of runs from this like nine o'clock to seven o'clock area. And OCD tends to be contained to that area. One question about if there's any recommendation changes on with people that have OCD lesions of the elbow but then also have overall joint laxity like UCL laxity. Yeah, good question. I haven't seen that. Certainly if someone has like a ligamentously incompetent elbow, like they have like, they gap way open on valgus, that would certainly be a reason to address that. So perhaps like simultaneous surgery, UCL reconstruction and OCD repair. But I'll tell you, I haven't really seen that but part of that's just my practice. I mean, the kids that I see tend to be adolescents and most adolescents haven't had time to really stretch out their UCL or develop valgus laxity in their elbow. And the other kind of pitching elbow issue that I see at least that requires surgery is on the medial side would be a medial placondial avulsion. So the kids tend to much more frequently get medial placondial avulsions than they would get, you know, UCL laxity or even UCL tears. Great, I think I missed the second part of that question. I think they were kind of referring to like the hypermobile athlete, like, you know, like connective tissue disorder. Like Ehlers-Danlos or even just like a ligamentously lax kid, got it. Yes. Yeah, no, it doesn't necessarily change the treatment though I guess in the back of my mind, I would worry that there's increased shear forces there across the capitellum. But it doesn't necessarily change my treatment with the exception, I guess, being if it's in the patellofemoral joint and they're like a patella dislocator, they're like so loose jointed that they're dislocating their patella. I would certainly consider doing some sort of a stabilization there if I was doing, you know, an osteochondritis desiccans treatment as well. Great, I think that's most of the questions. Just a couple of points for the fellows. So, you know, when you look and try to find these things, if you have a kid that has an effusion on their knee, that 100% deserves an MRI, even if you don't see anything on x-ray. So make sure that you're ruling out structural lesions. And then if the MRI looks normal, then you can start thinking more about your inflammatory causes of, you know, like juvenile rheumatoid arthritis or Lyme disease or things like that. But make sure you rule out structural causes first. If no one has any other questions, Dr. Fabrikant, thank you so much for that. This was a great talk, very high yield for our fellows as you will see a lot of these in practice, especially if you're in practice long enough, so. Yeah, thanks so much for having me. And if there's any questions, you know, you can reach out to James and we can certainly arrange a response. Yeah, that'd be great. Thank you everybody for joining. Like I said, if you have any questions afterwards, you can get in touch with me and I will get back in touch with you. All right, take care. Everyone have a great night.

3rd Edition, CASE 43

3rd Edition

Pediatric Issues

Osteochondritis Dissecans

pediatric orthopedic surgery

skeletal maturity

diagnostic algorithms

imaging

non-operative treatments

surgical interventions

vitamin D supplementation

orthobiologics