Good morning, everyone. Thanks for joining us on the sports symposium. And first I want to introduce our first speaker, Dr. Lou Schoen. He's going to talk about why he doesn't use malarial osteotomies for tail or OCD anymore. Thanks, Lou. Good morning. Good morning. I don't know if you all enjoyed the music before, it was Cantaloupe Island by Herbie Hancock. If I was going to pick my opening song, that would be it. I want to thank my colleagues at Union Memorial, particularly Brent Parks and my fellow at the time, Paul Peters, who helped with some of the basic science behind this project. And my current fellow, Emily Williamson, pulled together some cases, so I want to thank her as well. My partners at IFAR, at NYU, at Hopkins, and my Mercy colleagues, disclosures. I think the most relevant one is that I'm co-inventor of the Zimmer Total Ankle Replacement, and I do talk about DeNovo, although I don't consult from them on that, but this is one of the innovations that I was consulting on initially, but don't anymore. So strategies for articular cartilage restoration, everybody knows these things, shaving, curatage, chiseling, fixation, marrow stimulation, microfracture, surface debridement, resurfacing allograft for allograft, exposure osteotomy, which means that we cut it to get into it for no other reason, and then a realignment osteotomy, which is more purposeful, I think. So this is what I used to do. So this is a osteotomy for a osteochondral lesion that has been operated on many times. You have to make your osteotomy so that you could get perpendicular to your lesion, and that was the key with the osteotomies, is that they had to give you access to get perpendicular. So not only did it have to be accessible in the front, it had to be perpendicular in the front, and certainly in the middle or in the posterior aspect, it had to be perpendicular. So the osteotomy would go something like this. You go down, you spread it, and then you're looking at the lesion. It's quite impressive. You do sometimes fear at some point, did I cut it the right way? Did I cut enough? Am I going too deep? Okay, but you get through it, and then you spread it. You use a laminar spreader, and then you prepare your lesion. This is the way I used to do it with the large lesions. I'd drill it out. You make a nice big cylinder. This is an allograft, obviously, not the patient's other side. Then I put that in this little contraption, and then we take out the plug, cut it, prepare it, and tap it into place. This is very fussy. People do it well. Can I have a show of, in the audience, how many people do this? Okay. Yeah. So, I mean, this is a thing. It can be fun. It can be a lot of work. It can look very good. Sometimes it looks a little high or a little low in a spot, then you've got to fix the osteotomy. I never really loved the osteotomy part, because there can be some problems. These are some papers. This is from Bruce Cohen and Bob Anderson explaining the medullary osteotomy, different ways to do it. You get a distal fibular osteotomy with a chapeaued osteotomy, and Toshigi gave us some demonstration of that. Basically, with these osteotomies, you're really affecting what you're doing for the cartilage, because you can't do the same aggressive protocol. In my hands, we had to do some delayed weight-bearing. They had some pain. They had some complications. Sometimes you didn't want it to shift. You had to fix it really well. Sometimes it gave you hardware prominence, and you could get tendon injury. Now, this is a paper by Nathaniel Gould, who is one of the founders of our society. I had the privilege of meeting with him and talking with him about his role in the society, going back 20-something years ago. He wrote this paper with this guy named Flick, and basically showed this troughing that he made on the front of the tibia to get access to the lesion. I was like, that's so cool. I thought that would be a good idea. I did that periodically when I was just filling a little OCD with some iliac crest bone graft. Some people said, well, let's do that for doing the OATs, because the OATs wasn't really a thing 30 years ago. When we had the OATs, can we go back and do the plafonplasty? This guy, Asim Macher, did do it, and it was successful, and they had good results. Then this guy, Muir, said, well, you can't go too far with it. Plantar flexion doesn't get you all the way, and he demonstrated that with this study. I had a lesion like this, and this is obviously a very large lesion, but it's in the front, maybe at the junction of the middle and the anterior aspect. It was a big lesion. The guy was very flexible. I went in. I did my limited plafonplasty, and I was able to plantar flexus patient and get him perpendicular. This is kind of the limit to what I could do with my plafonplasty, prepare my base, and then take my allograft and tap in the piece. It works well, but again, it does have a limit. As soon as you need to get a little bit more posterior, you can't get perpendicular, and you don't want to remove all of the tibia. That was the problem, is that when you get back further, we needed to go perpendicular. Now I got to do an osteotomy. Here's an example of a plafonplasty. This one was pretty far back, and I did get perpendicular, but I did go a bit deep on my plafonplasty. I might have been about 12 or 14 millimeters deep in this particular lesion, but it worked out well. I took the graft and plugged it in. It was a pretty deep plafonplasty, but then the breakthrough happened. That was the advent, I think, in my life of the biologics for cartilage lesions. With the tissue graft, now I didn't have to be perpendicular, and now my plafonplasty didn't have to be as deep. This was a big game changer. Since this time, 225 cases, I looked up how many de novo cases I had, 225 cases, no osteotomy, because I don't have to be perpendicular. If it's in the back part of the ankle, I could go posteriorly, or I just resect the back edge. This is, for those of you who don't know the product, it is a human allograft tissue. It's living. It's cellular. It has high glycosaminoglycan and proteoglycans. They have living cells. The average age of the donors, they call them neomorts, are three. Here's a case. This patient had had prior surgery, had removal of hardware after the fracture, had scope with debris mount, still had pain. Here's what we had. Pretty bad lesion. Here you can see the scan. I'll show you what I did. I go in. I take my chisel. It's usually about a two to three centimeter incision. You could do it with a smaller incision, with an extended arthroscopy portal incision. I take a little bit of the bone away. Here I am pulling out some of the lesion. Here you can see a little trough. I don't always go ... Every case is different. You basically take away what you need to get access with. If you think you have one way posterior, you may have to go maybe five or six millimeters. Then you could plantar flex. You could put even on a Hintermann distractor to get a little extra plantar flexion if they're tight. I take that. Plafonplasty gives me really good access. I don't put the piece of bone back. I take that out. I use it as additional bone graft if I need to, or sometimes you could use it as additional cartilage graft. I take the Jamshidi needle, these sort of devices. I take Iliac crest and BMAC, bone marrow aspirate concentration on every case. I bone graft the defect by taking the trefine without the trocar and take these plugs of bone as you see over here. I mask them up. I put them in the defect. Then I prepare my grafting material. Then I take that and dump it into the lesion and then put a little fibrin glue and dorsiflex. Then I let it remodel. You can see this is with the foot plantar flex that you could see the lesion right in there. We've had really nice results. This is the patient four years out. You can still see there's no way you ever get a perfectly normal MRI. I know some people say they've had improvements. No question, but you don't get normal. You can get close to normal, but there's always like there's a MoCart score, which is a way to grade these lesions. They're always a little bit off. Here's another case, 47-year-old OCD, kind of central. Here just a small plafond plastic got me in, prepared the base and put it in my fibrin glue, dorsiflex. It molds against the tibia. That's the plafond plastic. It's a very small piece that you remove to get access. Here I was drilling the base. I generally don't drill anymore. Most of the time I'm just doing the scraping and dorsiflex. Here's another case. Here's the plafond plastic. It's just a limited resection like you do for a little osteophyte resection. It's not a lot of bone. You don't want to take a lot because you want to leave as much bone as possible behind because you want it to mold the surface of the underlying talus. Here was this case. This is a really good looking MRI. This was one of the better ones. You can still see a little edema there and you see some lack of homogeneity at the surface. What we found is that majority of lesions are accessible and the limited plafond plastic gave us access to the front 75%. Here's a bunch of cases showing some rather posterior but rather normal lesions that I deal with. You can see the lesion access, the little plafond plastic for the bone grafting and then the cartilage. Another case, just to show you that it is possible, none of these were really challenges and I rarely have to use the laminar spreader. I rarely have to use the Hintermann distractor. Here's that case. Again, still some abnormalities. Clinically these patients do about as well as everybody else's patients do, which can be about 85% that do well. I think some of them are fantastic, but it's pretty much the same. That was a relatively posterior one. Here as well. We did a study looking at the access using a cadaver model, basically plantar flexed the ankle and then measured the angle and then we did a drilling to see where we could get to with that plafond plastic and with a 10 millimeter deep plafond plastic we were able to get 75% of the tails involved. I don't find there's a need for malleolar osteotomy. There's benefits of the plafond plastic because we have the ability to move the patient forward, no hardware complications, no limited access. Thank you very much. If you have questions, you could call my secretary. She's standing by the phone. I know it was a quick talk. Thank you very much. Thank you. Thanks Lou. Our next speaker is Dr. Chris DiGiovanni and he's going to talk to us about what happens when the patient was managed non-operatively after Achilles tendon rupture and now they're weak. What do we do? Thanks Nguyen. I also want to thank and congratulate and acknowledge Fernando Radovan. He's in the crowd. He's a former fellow and now a very recent colleague in Boston and he helped me look up all our patients over the last year who we've treated with this problem for this talk. So I don't have anything to disclose related to this talk. So, Achilles rupture, if you guys could get that video to work, if you don't mind. I don't have to tell everyone that it's the Achilles rupture. It's the Achilles rupture. It's the strongest and most injured tendon in the body. The path is certainly not always diagnosed. This is a famous sprinter, Ana Claudia. That's her actual rupture right there. And these patients, you know, if they come in lengthened or non-healed, I think it's a significant functional deficit. Acutely, these patients can be treated, I think, similarly, up to about 30 days after an acute injury. And I know the data is fairly controversial. We have a lot of papers. I'm hoping James, my good friend, is going to maybe clarify some of this in his upcoming talk. And there are still some things I personally think about, which is how quickly we get to them, if it's truly within a few days, how much that matters. And also about their actual explosiveness. I'm not sure we really know how to measure that and what kind of a difference that makes, op versus non-op. But for the purposes of today, the late and the non-diagnosed Achilles ruptures that come in, which is about, by the way, a quarter of patients, unfortunately. In all cases, the gastro-axillial complex lengthens. And while they can sometimes have heel pain, the big issue is push-off weakness. And it can be more than both you and the patient really can predict. Like, this was a great white shark when my sons were fishing for stripers. And that's what they pulled up from the water. So sometimes it's more than you anticipate. And there is significant functional muscle deficit, which, at least in my experience, is not really well mitigated by rehab. So I think for most of these patients, if they're higher demand, they usually do best with surgical treatment. There are a number of different outcome prognosticators. Certainly gap size and reducibility is one of them. And I'm going to go into that a little bit more and what I think that means. Chronicity, which I actually think we still grossly underestimate and don't truly understand the gastro-axillial muscle quality itself, like in this patient. And scar tissue, where the stumps are versus where the scar begins. As well as, most importantly, skin contracture. These are all patients we've had over the past year. This is a patient where clearly there's a significant deficit there in the skin contractually over time. So this is seven of them. So by the way, we had 12 patients over one year that came to me to be seen. And we had to treat one a month. This is seven of them. And you can see a whole bunch of different MRIs with different defects on the MRI. And my conclusion, level five evidence, is that I'm not sure. The MRI is great for identifying the pathology. I actually don't think it's very good at telling you about the severity or the consequential nature of what you're going to deal with in the operating room. That's my opinion. You should definitely, especially, be aware of people who present with prior surgery, such as the patients who presented like this with infection. And this gentleman ended up losing a lot of his Achilles. And then we had to use antibiotic beads, et cetera. Prior incisions, they can be challenging if they are in a place that you don't specifically want to go through again. And it can end up looking like this. This is another one of my patients that I had to manage. And of course, any patient for any problem that ever gets sent to you by a really good orthopedic surgeon, always beware of those too. So I will give you two summary points for delayed treatment options. Number one, there are no evidence-based guidelines or clear superiority for any of the things I'm going to talk about. And secondly, no matter which choice you make, set expectations with your patients appropriately. Because none of these are going to return your patient to normal. And they need to know that. Certainly, for the ones with significant comorbid factors, you can brace them. And they can guide by symptom tolerance. And there are other procedures that are talked about in literature, fascial turndowns, VY lengthenings. I've done these. I don't like them. I don't do them anymore. And they don't make sense to me. They restore Achilles' integrity, but at the expense of elongation. So you're sort of trading one problem for another, perhaps the problem that they started with originally. So I don't understand that. Isolated tendon transfers, yes, for a few situations I'll go into, I think they're really good. But my problem with these is that they ignore the gastroxoleal complex. And I'm not sure that's the greatest choice. So the three that I usually go to are either direct repair, functional Z-shortening, and some kind of graft. I don't have any personal experience with synthetic or mesh grafts. Maybe some people here do. I usually use auto or more frequently allografts. So I think the best indication for an isolated FHL transfer is mid-substance tendinopathy, a little separate from these patients, because theoretically they have a normal gastroxoleal complex. If they have a poor soft tissue envelope, that's probably another good indication for this. And this is my proposed algorithm for this constellation of patients. If they've got a gap of about 2 to 3 centimeters, most of these patients, I think, once you mobilize everything, you can do a direct repair, plus or minus a strayer, and or an FHL if you think you need it. When you get between the 3 to 5 centimeter gap range, I think I personally will go to a Z-shortening with the surrounding tissue if I can, and I might add a strayer or an FHL. And then for 5 centimeters or greater, I would recommend some kind of graft, whatever your preference is. What's important, three things important about this. These determinations are made game time. They're in the operating room. So the gap is determined after you've mobilized the tissue, lysed the adhesions, done a strayer, and or a vulpeus if you need it, and the time interval after which you can or cannot expect re-approximation, I don't think you can predict. And it's all about the muscle fiber excursion, and that's important. It's not based on your physical exam or your MRI beforehand, in my opinion. So isolated tendon transfer does have a role. You can do it openly or arthroscopically. Some authors have advocated for FHL versus peroneus brevis. This is Mercer Rang's article from years ago. And in my opinion, you should always be doing the FHL. It's stronger. It's in phase. It's local. There's minimal, not no, but minimal donor site morbidity, at least in my experience. You can pulver tap these distally, depending on what you have, or put them into a calcaneal bone tunnel. But look at this. This is the same article. Four to five times higher strength in the gastroc and the soleus. So again, you're ignoring that if this is the only thing you're doing. So this is an example of one of our patients. We did an open FHL transfer. And this is an example of an endoscopic or arthroscopic one. The direct repair is my optimal choice if I can do it. The Strayer, in my general opinion, gives you about a centimeter of extra length. And if I need another centimeter, I'll do a vulpeus, which you can do right through the same exposure very quickly. I'll add an FHL at the very end if I feel like the integrity of my construct is not that robust, or if I need to bridge another maybe centimeter or so of gap. And I think that's a good choice, as you see in this patient. A functional Z-shortening is when you have a slightly longer gap, again, in the three to five range. And so I'll use the stumps and the surrounding scar tissue when it's available, and I think it usually is, to restore gastroc-soleus integrity. You've got to think about the Starling curve and the sarcomere. So you're pulling this muscle tendon unit back. And that restores not all, but a lot of the integrity of that construct. Just like with the heart, with volume output, I think we do the same thing in the calf. This is easy to augment with a stray or FHL once you're done. And that's the final decision you make based on your tissue. This patient came to me as an orthopedic surgeon, actually, from the Middle East. And this was his MRI this past year. And you'd look at that and say, gosh, there's nothing to work with. Oh my god, major defect. But here's him in the operating room. There's actually a fair amount of tissue to work with. And so he wanted me to augment this with an allograft. I told him I could maybe just do a Z-shortening. And he didn't want me to trust that, so I added an allograft to him. And that's the construct. Healed, however. Even with my plastic surgical colleagues, who I did involve beforehand, they didn't use a tissue expander. But you can see I had a little wound healing issue, which I had to watch and sweat out. And thankfully, it finally healed and he's done OK. But a little rocky for a little while. Grafts, when these defects are larger, are usually, in my opinion, necessary as interpositions. Carlson and Maffulli have talked about various different kinds of autografts. I don't think you should add a strayer in these cases. My historically preferred approach is open, because I think that's the best way to really mobilize the gastro-axillary compass and assess scar. But I definitely see, and am beginning to increasingly appreciate, advantages to smaller exposures and PERC and endoscopic techniques. We've seen a lot of that at this meeting, and I think that's probably the future. What does the data say? Kennedy and Arshad, two separate bodies of work, very recently, past few years, have had some nice articles summarizing this. And the bottom line is, there's no direct comparative trials, unfortunately. So nobody's compared open versus MIS, with or without gastro-axillial augmentation, isolated tendon transfers, or grafts. And so we definitely can do a better job in studying this. And I would summarize by saying, generally speaking, our results are improved, but there's still persistent limitations. This is another of my patients. He's got a Thompson there, but it's not great. It's good, but not great. So these patients rarely complain of pain, but they're still 10% to 40% weaker, according to these papers, compared to controls. And there's some residual calf wasting. And the overall complication rate's about 15-plus percent, many of which are wounds. So for the future, in conclusion, I would say that the gastro-axillary complex is about four to five times stronger than any tendon transfer choice you can make. So if you can reincorporate it, I think you should. Never underestimate your ability to do that before you're actually in the operating room. And try to restore that sarcomere length after you get rid of all that interposed scar. And I think you should pre-tension these. I think all of them stretch out a little bit, so pre-tension them. That's partly why we have soft tissue problems, I think, which is why I think we're going to evolve towards less invasive techniques. But my concern with those is that you may not be able to lysol the adhesions as well and or mobilize those. And I think we need better level one comparative trials. And finally, we need to listen to our other orthopedic colleagues. The shoulder surgeons have very clearly shown that rotator cuff outcome can be predicted by the Gouttier classification of fatty infiltration of the rotator cuff musculature. We should be looking at that at the gastro-axillary complex when we do these patients. And we haven't done that yet. So thank you very much. These are my references. Good morning. Our next speaker has come to us from England. James Calder is an MD, Ph.D. who has done a great deal of work in sports injuries. Thank you very much indeed for inviting me here and I I have a Disclosure switch in the handbook and on the website and I disclose that most of this work is courtesy of Tom Clanton So what are we talking about? Why is ankle instability so important and in the UK and in Europe certainly? It's a massive problem When it comes to sports and football, it's a financial cost in the Premier League Which is pretty small league compared to some of the leagues you got in the u.s. Admittedly But they the wages of these injured players cost two hundred and seventeen million in 2017-18 So it's a big financial problem. And if we're not treating them correctly, we've got huge issues So why in these injuries should we consider native tissues? So I'm going to go through when we do native tissues when we do autographed and should we be using something else such as a suture? brace We know that the brostrom or the modified brostrom is extremely good. It's robust You may add the Gould in but the results are excellent in Publications from many many years and even 90% good results at 26 years And if you look at the return to play it has an extremely high Return to play rate even in the elite athlete There have been some concerns regarding Infection risks and perhaps some stiffness if you're not immobilizing them if you're not mobilizing them quickly, which has led to Many arthroscopic techniques being reported. I Was initially a little bit circumspect to this about this not that didn't do it initially but in fact It does seem to be This is the sexy option if you like it is definitely very cool It's much cooler than my open operation, but more importantly it does seem to have very good results and they are reported as very good results You don't do the capitalist shrinkage. That doesn't seem to work, but the reports by Masato by Stefan Gilel who I spoke about a couple of days ago down in Bordeaux He's got excellent results and also Mark Glazebrook Who I did a the traveling fellowship with many years ago, so it is a very good operation It is sexy, and it's cool, but it seems to work But there are no results Because to get this operation right, we have to understand the anatomy. And Pau Gallano did a lot of work initially, and then his protégé, Mickey Delmapasto, when unfortunately Pau died, he's now taken over, and taken over the mantle and has done some incredible work looking at the different fascicles in the ATFL and the lateral ligament complex, so that we can understand why, if you get a single fascicle, it may not give you instability, but it can give you maybe subtle instability. Jordi Vega talks about some subtle instability where you don't get frank instability clinically. I don't know about that yet. I think the jury's still out. But certainly it would understand why in that case, if you do your, you can do an ATFL repair alone, and you don't need to do a CFL repair at the same time, because it goes back onto the footprint, because they are joined by the ossiform ligaments. So that's why an ATFL repair alone will work. Jan Carlsson in Sweden did his thesis and said this in the last century. He didn't understand why he was right, but he was absolutely right. And I think Mickey has now shown why he's correct. So you get those ones, and if you take off that, then you get the gross instability with the subluxation. So the functional anatomy is important. And I think there's some more work that's being done through Mickey showing what happens in the experimental stuff in the lab when you have an ATFL, a purely ATFL injury. He's also looked at the Gould modification as to why some people are getting very good results, many people are getting very good results, without augmenting it with a Gould. And that's, in his experiments and his anatomy, he's shown that actually 81%, so four-fifths of people, So, if you've got native tissues, I think the evidence would suggest, if you look through the literature, that an anatomical repair is very good, and that's what you should be doing. There's a recent systematic review, which Mark Glazebrook led on, looking at the surgical treatments, and the gold standard would remain anatomical reconstruction. The evidence should be there, is there for that. But what about the autographed options? I'm not going to dwell anymore on the perineal tendons. I don't do it. It's probably wrong. It doesn't make any sense at all. And I think most people have moved away from that now. But the hamstring autographed certainly is a very good alternative, if you don't have good tissues there when you get in there, or for revision cases. There are various different ways of doing it, but basically, if you take your hamstring, you can use a gracilis single tendon, very easy, very quick, it gives excellent results in the literature, and it's great for reconstructing when you just open up and there's a whole world of, there's just a gaping window there and you've lost the tissues. And it's either that or you're in revision cases. And the results are very good. There aren't big series out there as far as I can see. 32 patients in Cody's paper from 2018 and 28 patients published earlier this year in Kista with a 96% return to sport. In this paper they also looked at using a half of a peroneus brevis tendon. And they found that the results of that were not as good as when using the gracilis. So in my practice I always use the gracilis and I think that's the way forward and the papers out there would support it. Arthroscopic procedures to do this have been described and they seem to work extremely well. If you do manage to get to Bordeaux and visit Stefan, as I said the other day, there are many more reasons for going to Bordeaux than seeing Stefan, but he's a great arthroscopist and I urge you to go and visit him and watch him do a gracilis. It takes him about 25 minutes including taking the graft. He's an amazing arthroscopist. But his results, he's genuinely, I've seen him in clinic and I've seen the patients in clinic and he's a very honest guy. And he gets great results. Synthetic, so suture tape. That's coming to Vogue. Well, why is it coming to Vogue? Well, the initial results looking at the shoulder and then the knee suggested this was actually could be a great augment for the brostrums. But you've got to ask the question, if a brostrum has a 98% success rate, why should we always do, use a suture tape? Well, there is some work that's been done there, mainly by Tom, so I'd be a bit careful about how I critique this, but he knows his work a lot better than I do. But the repair is 50% weaker than the intact innate ATFL. So, there is an argument that if you use a suture tape, we know biomechanically you can get the repair as strong as the original ATFL. You can use this arthroscopically. This was a paper just many years ago, seven or eight years ago, looking at 85 patients with an arthroscopic repair. There was no difference in laxity on the AFA scores at six months. They did very well with using an internal brace. And it did kind of become a mainstream. Certainly there have been people in the UK who've just used it all the time. And they suggested this was because it's the IB strength versus native ATFL. Also, if you compare suture versus suture brostrum versus internal brace, you seem to get earlier return to sport, reduced risk of injury, and good stability. So, quite a lot of people are going mainstream with it. I haven't done that. And there are some concerns. And the reason I haven't done it is because I think if you've got a good operation that works very well, I don't want to put a load of material in there unless I really need to. There is a concern regarding reduced ankle dorsiflexion from Chris Coetzee here. And there's also been some foreign body reactions that have been reported. Although, I have to say, there aren't many in the literature. And I've only seen a handful of cases myself. There is the concern about over-tightening. And Bill Ribbons and Gordon have written about this in the past. And they've got ways of dealing with this. I'm also not sure. It's a slightly unforgiving suture tape. And I'm not sure that we put it in exactly the right place anatomically every single time. And I think we could do, or maybe Tom could do, a little bit more work on looking for that to find the ideal isometric point to put the internal brace. Because I don't think we get it out there. There are three systematic reviews out there. They have suggested that there may be a lower recurrence in injuries. But overall, there doesn't seem to be a massive difference. And they have comparable results of Brostrom alone versus Brostrom and an internal brace. So it seems to be safe. It seems to be effective. There could be a bit of a nudge up saying there's a lower recurrence rate. But I think the jury's still out as far as that's concerned. But I think importantly, generalized, there are some specific groups where it may be beneficial. And I do use it in certain people. There is generalized joint laxity. There's some good studies out there showing that BITEN scores of, say, over four or over seven, you should perhaps consider augmentation. Because the clinical results would suggest that. And also in revision cases when you may have poor material to play with. So what do I do? I don't use it as a routine placement. I do use it to augment in revision cases BITEN of greater than seven. And if there's a large ossicle that I've had to remove. And in summary, I think the Brostrom gives good results. I selectively use acute repair in young athletes. I'm not convinced about the success rate of arthroscopic techniques. It's great. It's sexy. It's really cool. And I get that. But a Ferrari can spend a long time in a garage. And that's my operation. And that's the car I drive. Which is pretty good over rough ground. Which is what my footballers are doing, isn't it, really? So there we go. So that's why I do that. And I think you can augment it with an autograft if you want to. But I would selectively use suture tape in revision cases, generalized joint laxity, and when you excise a dirty great big ossicle that's been avulsed. Thank you very much. Our next speaker, Ken Hunt, is the chief of foot and ankle at the University of Colorado Anschutz in Denver. And has a lot of experience with sports injuries. And I'm very interested in his talk. Thank you, Tom. Good morning, everybody. Those are some fantastic talks. This is a wealth of knowledge up here. So I was asked to talk about the symptomatic sesamoids. And specifically I was charged with trying to convince you why you should not hate them. So I'm going to take that literally as I approach this. I don't have any financial disclosures, but I will disclose that I, too, on occasion, have developed some dislike for the sesamoid bone. So I'll take you through some of the reasons why. So as I really thought about this when I was charged with this topic, I came up with three reasons to try to convince you not to hate the sesamoids or find ways to maybe hate them a little bit less. The first is that sesamoids are actually useful. I'm going to quote Dr. Chow who said in the green room that God gave you two sesamoids, you should try to keep them for your whole life. So I would agree with that. And when it comes to sport, these are really valuable. Sesamoids like the patella in the knee increase the mechanical advantage of the flexors. So they're actually responsible for a lot of power. They stabilize the first ray, which is really important in sport. They're the main weight bearing focus during the push off phase of gait. And they protect the metatarsal head. So the articular surface doesn't see a lot of load. And they protect the FHL. So these are really important in sport, particularly with jumping, sprinting, and control like in ballet or martial arts. During normal gait, they see a lot of load. 50% of the body weight is transferred through the sesamoid complex. And when you jog, run, or do a running jump, it can be up to eight times of your body weight. So they see a lot of force. They have to dissipate a lot of force. And so that's important. Because of that, an increased magnitude or frequency of force, which we often see in sport, can lead to injury. And that's when we get involved to try to manage this. So the second reason I came up with is that most of these problems we can fix. So as I went through common causes of sesamoid pain, sesamoid problems, these are the five that I came up with. So I'm going to go through each of them individually. Sesamoiditis is the most common. This would be the mild edema or pain that's not associated with a fracture, AVN, or arthritis, or anything like that. These can typically be managed non-operatively. So I like orthotics that offload the area. I like to add a little pad proximal to the metatarsals, maybe a little recess underneath them, a period of rest, a period in a boot, anti-inflammatories. There's some evidence for shockwave and bone stimulators. So you should do what you can to get these to heal without surgery and to try to prevent it from becoming a bigger issue down the road. Sometimes we'll see this thickening in the skin, these intractable plantar keratoses that are associated often with bone spurs. So when we see that isolated thickness of the sesamoid or a bone spur that's kind of sticking out and causing a problem, we can actually shave this down. So you can take down up to 50% of the bone without interrupting the FHB or the ligamentous complex and causing instability. And this will take care of the skin issue that the patients are developing. This planing procedure has been investigated. This was another patient of mine that had this significant amount of HO, which really changed not only the foot posture, but the way this patient walked. So I removed the HO, but retained the sesamoid, and he went on to function quite well. So this has been investigated. There's not a lot of literature on it, but the literature that's available shows that this works. The majority of patients get better. It does not cause further disease to the sesamoid or loss of function or loss of toe alignment. Fractures. Now this is not an uncommon problem that we see, and I would say that the most important factor in treating fractures is to differentiate these from the bipartite sesamoid, which is much more common. So there are three radiographic keys to differentiate between the two. Usually with a bipartite sesamoid, the sesamoid that's bipartite, usually the tibial is much larger than the fibular sesamoid, which is not typically true in fractures. The bipartite sesamoid has this corticated or even sclerotic surface on the border instead of a non-corticated, sharp, radiolucent line that we see with fractures. And if you look at the fracture, you'll kind of see where they'll fit together like a puzzle piece. So those three factors will help you differentiate between fractures and the bipartite sesamoid, and that's going to guide treatment. When they're displaced, that can still be a bipartite sesamoid, and it's a little bit different in its ability to heal. So about 17% of people on average, there's variance obviously in the reported incidents, but about 17% of people have a bipartite sesamoid. The majority of them are the tibial sesamoid, and the majority of them are bilateral. So these are much more common than fractures, and an important thing to keep an eye out because you'll often get that sesamoid fracture referred in, which is not actually a fracture. So this was a defensive back who felt a pop, had all the evidence of a fracture on the x-ray. MRI showed that edema in the acute fracture line. It was not displaced. These can be treated nonoperatively. So I put him in a little plantar flexion splint for a couple of weeks, let him walk in a boot for an additional four, and at eight weeks he had healed and he was back on the field. This was a runner with sort of a chevron pattern fracture of the fibular sesamoid. When these smaller fractures are there, the blood supply is not optimal in the sesamoid, and so these have a chance to either not heal or go on to a symptomatic AVN. So these can be removed in that case. In this case, it was through a dorsal incision where at least the lateral portion of that sesamoid can be accessed, and the sort of smaller fragments can be removed, getting it down to a good functional sesamoid with a sufficient weight-bearing surface. What about the chronic non-united fractures? This can be a plague, particularly in running athletes. Do we have something to address this? Well, these can be approached and bone grafted. There's not a lot of data on screw fixation. I like the idea of putting something in there that's going to add some compression. In this case, the fracture was bone grafted with autograft bone after a really good debridement to get that fibrous tissue out, and then stabilized with a 2.0 screw. I think you can give or take the screw, but adding some biology I think is really important. Bob and Angus McBride published a series on 21 athletes where 19 of them healed at an average of 12 weeks, and all but one of them were able to get back to sport. And that's really important as you're thinking about how to manage this in an athlete, because at this point it can be pretty daunting as they look at their career. Now osteonecrosis and arthritis are sort of a different kettle of fish in my view, and that's because we don't have a viable replacement for the sesamoid, and we don't currently have a viable resurfacing option to address the arthritic surface. So this is a little bit of a conundrum, and really the best option is what I think the third reason that I'll give you for not hating the sesamoids is that you can remove a painful sesamoid, and that's not true for most of the bones that we're dealing with that have chronic fractures or avascular issues. You can remove these in an athlete and get them back to sport. So the indications in my view is this is a last resort. This is where you've tried everything else and they're not able to return to sport, and it's typically because of avascular necrosis, a fracture nonunion that you can't get to heal, or an advanced arthritis against the metatarsal head. The tibial sesamoid is best removed from a medial approach. You want to identify that plantar medial cutaneous nerve, protect it, because that can create issues down the road. And the sesamoids are very easily accessible. I use a 15C blade to just carve that sesamoid out of its FHB, and I get a really good repair of the FHB so they don't fall into valgus. Adductor advancement, this is something that Bob taught me and that I use often. It adds a little bit of strength and a little bit of collagen in place of that sesamoid that you can do kind of on your way out during the repair. I also like the adductor release, just putting a little 15 blade in there and releasing the adductor to keep the toe straight, and again that avoids the toe falling into valgus. The fibular sesamoid I remove through a plantar incision. You can remove it through a dorsal incision. I think it's pretty disruptive to some of the other tissues, and it's much harder to repair. So I like going for the bottom. You'll always see the nerve, so you want to keep an eye out for it as you identify the bone. Remove the bone and get a really nice repair of that FHB. You'll see the FHL, and you want to make sure that that doesn't get injured on the way in as well. So what's the effect of this? Classically, the teaching is from this article that said you're going to get some weakness if you remove the sesamoids, particularly if you remove both of them. It doesn't mean it's necessarily going to be a problem. In an outcome study, this is again from Bob's group at OrthoCarolina, they looked at 92 patients at a median of five years, found improvement in pain. The vast majority would have the surgery again, and the majority were very satisfied, and they had four reoperations. So they measured plantar flexion strength. Now they said statistically there was no difference in strength from one side to the other, but the numbers they report were consistent with that 10% reduction. But there was no subjective weakness. No patient said, hey, I feel weakness or I'm not able to do what I need to do, and they found really no migration of the hallux into a valgus or varus position. Similarly, Maffulli and Saxena published their series of athletes at their two institutions. All of their athletes following sesamoidectomy returned to sport at an average of 11 weeks. They did not experience any varus or valgus, and the complication rate was reasonably low. You want to be aware of late sequelae. Again, I think techniques have improved to the point where we don't see this as often, and I think we're better able to recognize turf toe injuries and sesamoid problems so we can get to them sooner. But you want to keep an eye out for these problems developing and make sure you have tools in your arsenal to address them. So in summary, sesamoids are helpful for athletics and for athletes. Most sesamoid injuries can be treated successfully by some means, and when that doesn't work, sesamoidectomy is a viable option and compatible. Our final speaker in this session will be Sam Adams from Duke. Everyone, I'll try to keep us on time here with a somewhat controversial topic. So I have, I'm a consultant for several companies, but I have nothing to disclose regarding this presentation. And so in this never ending, expanding universe of treatment options for osteochondral lesions of the talus, specifically the shoulder, how are we gonna choose which one? You know, I've used basically all of these. And if you also look at the literature, people have combined. like some of the work that's been done with microfracture that has really tried to tease out what lesions are good for microfracture or bad. And we know about size, and we know about shoulder lesions. They're larger size, and lesions that are approaching the shoulder aren't the best for microfracture. But regarding these other techniques, that really hasn't been done. So what I can show you today is what I do, my recommendations. But I really want you to focus on the aspects of the shoulder lesions, and I think that will help you define in your own practice what you want to do. And I'd argue that the topic of this talk is shoulder lesions. I really don't see non-shoulder lesions. I rarely see a central lesion of the talus. And when we look at shoulder lesions, they're not all the same. They're actually quite different. If you look at these three, obviously, the cartilage surface is different, but what lies beneath can also be very different. And here's two of those lesions. And if we talk about what is the difference, well, you have to think about the cartilage geometry, and the surface geometry, I should say. And if you look at the image on the left, that's really a two-dimensional geometry. If you look at the image on the right, or that patient's lesion, that's now we've got the z-axis, basically. We have three dimensions of cartilage that we have to take care of as the treating surgeon. We also have to focus on, really, what is the most important point of this talk, and that's the sagittal buttress integrity, either that medial or lateral vertical edge. And if that is gone, there is really nothing to contain a lot of the treatment options that we have, and they're going to spill out and not provide a successful repair. And then similar to that is, really, the foundation, right? Everything we talk about in life is based on building a solid foundation. And if you don't have a solid foundation for it, or similar to what I just said. So the osteo portion, we have to factor in how much bony. defect. Again, we have to look at that surface geometry of the cartilage. Is it a two-dimensional or is it a three-dimensional repair that we need to do? And then most importantly, what is the shoulder stability? What is containing our repair? And so I take a look in my algorithm, I look at that sagittal buttress, really that shoulder aspect, and is that intact? And if it is, which I think luckily most of the lesions we treat, it is. Lou gave a great talk about the particulated cartilage, which he taught me to do very well, and you'll see some examples of that here today. But in a lot of those cases, really that sagittal buttress was intact. And so we have a two-dimensional surface problem with maybe some mild bony edema. I think that's one that we can all agree, and I'll show in a second, is a relatively easy one to treat. We can extend that a little bit farther where that buttress is still intact, but now we're starting to get more bony involved and maybe a cyst is starting to appear. That can be a little bit more tricky, and I think really what we want to talk about mostly today is really these ones that have these large, voluminous bone defects. There's no buttress intact, and how are we going to treat those? So we first look at these lesions of the shoulder. Microfracture is still my first choice. Here's just an example of a patient that I did. But the key about, again, the key through this entire talk is really maintaining that shoulder. What is the quality of that shoulder buttress? But for these, when the patient gives you an intact shoulder, you're going to want to make sure that you're doing the right thing. And the reason I moved to supplementation is, the literature would say that we have a 90% success rate for microfracture. I've never seen a, I don't. But I just don't think microfracture is the panacea that it once was and so I often perform supplementation and that can be Sorry, micronized cartilage augmentation was the first row and then minced cartilage for the second row here. And these actually provided, there's a lot of papers that show success. But if you really look at all, I mean again, once again, if we look at all these studies and these are, some of these are comparative to just microfracture alone, we have good results with all of them. I think John Kennedy just did a great study recently published that shows though, if you really look at all these, if you summarize all these studies, there's really limited comparative evidence to recommend any of them over microfracture or any one above the other. And so there's still a lot that we need to do. But I think luckily those lesions do fairly well. And then now if we move into lesions that are still on the shoulder, but the bone is more compromised, it's basically a continuum, right? It's cartilage, bone edema, we're getting cysts, we're getting bigger bony lesions. And so it's basically also a continuum of treatment options in my hand. So microfracture, most likely in this case, I'm gonna augment with something, usually a particulated cartilage and a bone graft. And then you can go to oats and plugs and all have shown good success. Here's a couple options with good results with these larger lesions using particulated cartilage. But the key here is if you just look at these pictures that these authors have published, in every case they've still maintained that sagittal buttress. And it's keeping the graft that they use contained. And then if you look at oats, there's several papers. I think on the horizon we may have different shape, things that, different biologics to look at in the future, but these are far off. So now let's get to really what we're here to talk about, these really, these true shoulder lesions where the shoulder is not intact. And I'm gonna go off the deep end a little bit here and recommend something that probably most of you don't use, but here's the importance of that sagittal buttress, right? It's like a retaining wall, and if your retaining wall for your graft is not solid, it's gonna fail. And so if we just kind of look at these other options I talked about that we might use for shoulder lesions, well, the literature is pretty clear that as you get to these large lesions, that microfracture is not good, and I wouldn't do that with an unstable sagittal buttress. I just talked about good results with particulated cartilage or micronized cartilage, but in these cases, without that retaining wall, this is all gonna spill out. And I've just never been able to do plugs on this three-dimensional cartilage surface. I just don't think that works. And so we'll see in a second what I'm gonna propose that is a very valid treatment option. Here's a case where I kind of got into the weeds a little bit. So an unassuming potential osteochondral lesion to the shoulder, start debriding, and then by the time I was done debriding, I had a problem. So I had debrided away that sagittal wall, and so now I'm trying to recover. I'm packing this with some bone graft, trying to fill it up with this particulated cartilage and put some, Tissiel saves the day every time, right? You can make it look really good, but high fives all around, bro hugs in the OR. But then what I was doing was just putting lipstick on a pig, because that patient continued to have pain. Here I am back in the OR for a second look arthroscopy, and you can see that the cartilage that stayed in the area actually did its job. That mound of cartilage there is the graft that I put in, but most of it has spilled away. And now to really, in my mind, make this patient free, pain-free, I've got to restore that cartilage surface. I've got to figure out what's going on. And so what I did is I took him to, back to the OR, did an osteochondralograft. And that's really been my method of choice for these large lesions where the sagittal buttress is compromised. And so, you know, I think a lot of people don't like this technique. I think the benefits are it's an anatomic match. You get three-dimensional recovery of the cartilage and bone. It potentially has living cells. These are all fresh cartilage. call it sometimes, but what I'd like to dispel is everyone talks about this being technically demanding. I have a higher sweat factor, pucker factor in the OR for some of my fusions, trying to align an MTP fusion rate. I think that is sometimes harder to do than this technique. And then other people would say it's too severe for some of the lesions that we treat, but it's a spectrum, right? You could still do this through a medial malleolar osteotomy and do very similar to what a notes plug would do, but you can see the nice three-dimensional surface geometry that you can get with this allograft. Or you can do what we call a hemigraft and come in from the front, and that is a bigger graft. And so just quick on the technique, there I'm doing, like Lou mentioned, I'm doing a profilonplasty. I will say, never just look at the talus. Almost all the time, these patients have abnormalities in their medial malleolus and their anterior tibia. Make sure to take care of those bone spurs as well. You can put a guide pin in, and then we cut to the corners and we remove that lesion and we have the allograft present and we basically, so there's a lot of publish on the technique of this, but you don't measure what you cut. And so we've published on this quite extensively. Here's a systematic review, and if you look at it, it's actually decent data, 191 graphs and almost 87% survivorship at five years. And then Amanda Fletcher, one of my former residents, put together this study for us. And I don't like to always quote our own studies, but this study really shows the success of it, but also some of our failures and things to look at on x-rays. And so we had eight partial graphs and 23 hemitales graphs. And if you just look, I mean, again, everyone does well, but people did well. At six months post-op, it was our first time point assessing them prospectively, and they had significant improvement. And that improvement was maintained to their final follow-up. What we like to do in this study that's not done in a lot of the other studies is look at these x-rays and assess if patients are going on to have some arthritis. So we modified the Kellgren-Lawrence. One thing we did notice it is quite frequently we saw a little bit of I don't see non-union but a little bit of non-union in this vertical the sagittal zone of the burlet lucency score and that didn't see that did not sorry that did not really correlate with patient outcomes and if you look at our results overall we had no Here are a couple of the. Here's a case, a patient that had pain, so this is one of the ones I was able to go back in and look at, and you can see the graph there. So, in conclusion, majority of OLTs involve the shoulder. There's many treatments out there, no data to support one over the other. You must consider that sagittal buttress.

osteochondral lesions of the talus

OLTs

lesion characteristics

sesamoiditis

non-operative treatment

surgical intervention

fractures

avascular necrosis

bone grafting

medical professional