for their sponsorships. Thank you for the AOFAS staff and the faculty. We're gonna move on. We have two more sessions. Thanks for those who are still in attendance or hanging in there. I know it's a long day. We've got two more sessions. The first one is gonna be a potpourri everyday problems, but traditional and new solutions. So these are things that didn't really fit into any one repertoire, but at the same time or any one division that we had originally, but at the same time, they're all things that we kind of deal with and all things that we kind of see. And so we've got three great experts that are gonna help us kind of guide our treatment and methods to try to take care of these. So we're gonna start with Dr. Jacob Zide for adolescent flat foot surgeries, when to fix and how. Okay, bye. Share your screen, but share it on presentation. No, no, you're good. But share it on PowerPoint if you can. So when you go to share, share the PowerPoint. So bring the PowerPoint up. Sorry about that. No, you're good. I forgot to tell you that, sorry. Let's see, here we go. And how about now? And that was gonna hit the presentation. So hit the presentation one. Yeah, you got to play from the start. Yeah, I think that's good. Here we go. Sorry about that. So no disclosures pertinent to this presentation. By the way, I'm Jacob Zide from Dallas. Moving along. Okay, what's an adolescent flexible flat foot? Well, super common. Number one reason for consultation in a pediatric orthopedic clinic. And so they are seen all the time. And so then that leads to the question, is this a deformity or is it just a normal variation? And I would make the argument that a flexible flat foot in an adolescent is a normal variation. They are almost always asymptomatic. When they are painful, it's almost always because of the tight Achilles sort of driving the talus into plantar flexion and into the floor causing that plantar medial pain. And there's not really a great definition for the adolescent flexible flat foot, but they oftentimes have a component of ligamentous laxity, of family history. It should be passively correctable. You should see reconstitution of heel varus and the arch when they stand up on tiptoe. And so in general, I would just say that this is a normal variation. And that's been borne out in studies. This is a huge study, 800 and some odd feet where they just looked at footprints in people one to 80 years old. And they saw that it's super common in infants and it gradually improves with time, but it's normal in adolescents in flat foot. And just to give you guys some numbers from other studies, in general accepted that about 44% of kids age three to six will have a flat foot. And then that improves to about 12 or 13% by age 12 to 14 years. And so the natural history is just gradual improvement in arch height as time goes. This is just a cool study out of JBJS from 1989 where they made interventions in young kids. They did three intervention groups, corrective shoe, a heel cup and a UCBL and compared them to control groups. And lo and behold, they all improved with time. It didn't matter what you did. And so the reality is that there's really no evidence that any sort of non-surgical intervention will impact foot shape or change long-term disability if that's what's coming down the road. Another really big study, this one showed prevalence of 54% in three-year-olds, 24% in six-year-olds. And so once again, we're seeing this improve over time. Interestingly in this study, about 10% of them were treated with arch supports, but the authors deemed that about 90% of those were completely unnecessary. And so Vince Mosca, who sort of has led the charge in treatment of adolescent flexible flat foot from the pediatric subspecialty side of orthopedics, wrote this in a review paper several years ago saying that the adolescent flexible flat foot is common, familial, rarely painful, rarely disabling, yet generates great interest investigation and controversy. And what's interesting is that for such a common deformity, there's not that much written on outcomes of treatment and how to manage these things. There's a lot of small case series and stuff, but not a lot of great stuff written about it. And so bottom line is that adolescent flexible flat foot is normal development and there is no treatment indicated for an asymptomatic foot. What will often happen is that you'll have a patient come into the clinic, either as a second opinion or they've already been operated on and they're having problems and you say, well, what's going on? Why did you have this surgery? Or they've been indicated for surgery and they're not having pain. And that other provider will tell them, we're doing this to prevent disability down the road, prevent arthritis. You're going to progress to a rigid flat foot at some point and we're trying to avoid that. And I would say that all of that is completely bunk. There is no evidence that that is the case. And I think that there is probably a special place where people who do unindicated operations on children end up going at some point. So why am I giving this talk? What's my perspective? This is sort of my little niche is to deal with adolescent deformity. It's a big chunk of my practice. And I go over and have a specialty clinic over at Scottish Rite and have just sort of developed this interest. And I bring it to you because I see this all the time and there's a lot of nuance to these deformities. And you see flat foot adults all the time in the standard adult clinic, but the examination is a little bit different in children. The things you're looking for are different. And if you're only seeing this once a month or every couple of months, you just sort of may miss those things. And so I think it's important to sort of bone up and make sure that you're up to date on how to treat these. I would also just comment that when you're managing adolescent patients, there's more to it than just deformity. There is a lot of psychological stuff happening in your preteen adolescent age range. These kids come in complaining about foot pain and you drill down. And really what's happening is that they're getting bullied. They're getting called, made fun of for their duck feet in school or whatever, but they're not having any pain. It's not stopping them from activity. And so, believe it or not, I involve a child psychologist a lot in these sorts of things when I don't think that the deformity is actually causing a problem. And so making sure to suss that out can be tricky and oftentimes hard to do in sort of a busy adult practice. So there's more to this deformity than just sort of a list of surgical indications that we have to deal with. So an example of that. So this is a nine-year-old. This is before she got to us. And here's her pre-X-ray. She sees someone else and they say, you should have surgery. You're gonna have pain and rigidity down the road. We should fix your bunion. We should fix your flat foot. And so she gets an Evans and a bunion procedure and you look at it and you go, all right, well, it doesn't look so bad and maybe it'll be fine. And maybe it's no harm, no foul and so on. But the reality is, is it's not no harm, no foul, right? Any surgery comes with complications. This turns into a total disaster. She has an infection. She develops an autofusion of her first MTP from her infection. She's over-lengthened through her lateral column. And so she has a lateral column overload and her whole foot is invarious and supinated. And so her metatarsal head doesn't, first metatarsal head doesn't touch the floor. And so this is a happy, active girl who can no longer do the things that she likes to do because somebody decided to operate for no particular reason. And so anyway, by the time she gets to us, she's had all these skin flaps to the top of her foot and it's just this disaster. And she's got this contracted posterior tip and lateral column. And so we reversed it. We did it all with a sort of a reverse Malerba and decompressed her sinus tarsi where she had had her Evans graft and lengthened her posterior tip, which was contracted and got a good result and got her foot flat to the ground and back to activity and patting herself on the back. But the reality is, is that this is a young woman who should have never had any sort of surgery in the first place. And so I think it's really, really important to keep in mind. Okay, looking at these feet, the assessment, a painful, flexible flat foot. They should have pain in a predictable spot. It should be either in the plantar medial arch where the tailor head is hitting the ground or it should be like a lateral impingement type of a pain, like a sinus tarsi or a calc fib impingement type of a pain. That's what you're expecting. Maybe you'll see some callusing in the plantar medial arch. It's true. I think it's not one of those first two devices you may need to retain your device. You're looking for flexibility, so when they stand up on the kiptoe, you want to see their arch reconstitute, you want to see their valgus convert into varus as their posterior tib fires, and you see that it's a flexible deformity. You can obviously assess this manually as well. If you walk into the room and you see this patient sitting in front of you, you write this left foot is sitting in a sort of normal position, no weight on the foot, the arch is reconstituted. It's not a great view of the left foot, but you understand the point. You look at that right foot and it's dorsiflexed and everted and it's stiff and flat and sitting there. That is not a flexible foot. This is a coalition until proven otherwise. You can impress people by just literally walking in the room and saying, aha, got it, diagnosis is made. So look for this on your examination. Remember that Taylor motion is more of a rotational thing than a true varus valgus, it's not tipping one way or the other, so be good about your assessment of your patient. Jacob, you're just cutting in and out a little bit. I don't know if there's anything you're able to do on your end with your connection. Can you hear me? Yes. You're back now. Oh, was it just this slide or it's been going the whole time? It was back. It was out for a little bit and then back. And then when the slide came on, it was choppy again. Maybe, I wonder if it's the video. Okay, I will. No, you'd be better. Okay. Okay, so how do we treat this? There's a good Cochran review from 2011. That went through these papers and basically show that risk factors, high BMI and hypermobility, they're asymptomatic in their treatment, symptomatic, just a generic orthosis off the shelf. You can use a custom orthosis. I would tell you that most of the time you don't really need to. And if those things fail, operative treatment. If someone comes in and they actually have a painful, flexible flat foot, this is my sort of a standard non-op treatment. First of all, education, education, education, good supportive shoes, soft over-the-counter orthotics, not hard orthotics and calf stretching. And this little thing that you see is this little calf stretcher you can buy on Amazon for 15 bucks. It's hard to get kids to comply with their stretching routine. And so I tell parents to buy this thing and put it next to their sofa and make their kid use it while their video game is loading or their commercial is on or whatever. And it's better than nothing. So going through a case, here's a 14 year old who's failed conservative treatment. She's got daily pain that is limiting her activity. If I run out, obviously a flat foot. Here she is walking. And you may say to yourself, I don't know that I can fix this with the sort of usual procedures, but I will tell you that in a flexible foot, it's almost always your same algorithm and it almost always will be just fine. So indications for surgery, deformity with failure of at least six months of non-operative treatment, expected location of the pain as we discussed earlier, pain that interferes activity. That's what we're working on. There are some procedures that we don't really have to talk about, mainstay osteotomy along with soft tissue management. continual stop procedure where they said they wanted to correct the foot shape and it worked. Two percent of patients had pain post-op, but look only 11 patients had only 11 percent had pain pre-op. So this is unindicated. This is these kids are going to get better anyway and so hard to say in an age range 5 to 18 if they weren't just going to get better anyway as that sort of natural progression of improvement. Arthroaresis screws are not benign, although they're sort of it's sort of led to believe that they are high rates of explantation and then these sort of one-off complications that are really disastrous and I just I'm not interested in doing this sort of experimentation once again in children. I just think that's bad. So I'm not using these. As I said not a lot of very good studies with outcomes, but this is this is a decent study done by Mubarek's group where they compared CCC osteotomy, which is medial slide calcaneus, opening wedge cuboid, and medial cuneiform osteotomy to a standard Evans. They both showed good deformity correction. There were more complications in the Evans group, although I'm not sure that they were complications that would make me stay away from it. A lot of them were the calcaneic cuboid subluxation, which I'm not sure actually makes much of a difference and I'll talk about that in a second. So here's a diagram from a or an algorithm from an article that came out last year from Arisa Bouchard who's out of Toronto and this is essentially the algorithm that I use. First you take care of your acquaintance contracture, usually with a gastroc recession, an Evans osteotomy, a medial soft tissue imbrication, a lengthening of the peroneus brevis, and then a medial cuneiform osteotomy. She brings up that you can do a medial slide if you need, but I'll tell you that in a kid I don't think I've ever had to do a double osteotomy no matter the severity of the deformity. You can put really huge Evans graft in, they don't get as, they don't get that stiff like adults do, and so I will, I'm happy to put a really massive graft in for my Evans to get my correction. So running through a case, the young woman's case that I showed earlier, so your sinus tarsy approach, I do a longitudinal incision. In the pediatric literature they often talk about doing an OEA, which is the more vertical diagonal sort of incision. I really don't like that. I like to be able to make something extensile. Go in and find your peroneus brevis and lengthen it in a Z fashion. It is contracted and it will restrict the amount of correction you can get. Once again, this is not an acquired collapsing, you know, progressive flatfoot. This is a developmental problem. This is a contracted tendon and it's going to restrict you. So do a lengthening of this, of this tendon and then you're having osteotomy. You're trying to put your osteotomy between your anterior and middle facets. Once you've exposed your sinus, you can usually sort of stick a freer across it and it'll kind of fall into the space between the anterior and middle facets and that's going to be the angle of your cut. I don't measure from the calcanea cuboid joint. You can usually just stick that freer in and then follow the line of that freer and it ends up, your starting point ends up about 15 millimeters proximal to the CC, but you're angling a little bit proximal to the decimal with your cut. And then when you put in your graft, it's, it's trapezoidal, but from lateral to medial, but also from dorsal to plantar because that tight plantar fascia restricts the amount it opens plantarly. And so I would tell you this is going to be the shape of your graft. They've got a nice trapezoid on B, but on D, on that picture, it really should be a trapezoidal dorsal plantar as well. Otherwise, you're going to not be touching the dorsal part of your graft. And so this is what should happen. You're going to look for the lateral column to straighten out, the heel to come out of valgus with your, and to reconstitute your arch with your Evans. And so I'm just not going to talk. And then you put it in a graft, you can pin it. And oftentimes in the pediatric literature, this is what they advocate is to pin the CC joint for fear of CC subluxation. You're actually supposed to put the pin across the joint before you distract. And then you put in your wedge and you advance the pin across the wedge. I used to do this. It's a very stable osteotomy and I don't pin it anymore. I actually did a little study with cadavers that showed that it's not really a translational subluxation of the CC joint. It's really a rotational subluxation and it's occurring. And then you get, it looks like a translational one on your, on your lateral radiograph. And so I don't think a single pin is going to prevent rotational subluxation. And I just don't think it has any sort of clinical significance. So I don't tend to pin unless I'm, unless I feel like my graft isn't stable. You do your medial cuneiform osteotomy, like Cesar was talking about earlier. You hold onto the fourth and fifth metatarsal heads, and then you assess your, and dorsiflex the foot to a neutral position by doing that. And then I assess my first metatarsal head position. So I'm going to play these videos real quick. So we've got to go back to the medial conform, and then you're going to imbricate your medial soft tissues. So in kids, it's kind of crazy as an adult surgeon to do this, but you have all this redundancy of the medial soft tissues. And when I was trained, I was just trained to only do the osteotomies, not do anything to the soft tissues, but I think this really adds a lot to the correction. So I'll cut the posterior tib in a Z fashion. I'll leave it attached, it's planar attachment distally, so it's pulling that navicular down. And then I will take a small, strangler chunk out of the spring ligament. And then once you do your evans and push it over, that will close down. And you imbricate it, just with a Vicryl is all I use to get that held together. And then I do a pulvertaft weave and tighten the posterior tib. Once again, just repair it with Vicryl. And then finally at the end, go back and repair the peroneus brevis at about sort of a 50% tension that I don't, I'm not so scientific about that, but about 50% tension, plus or minus, and just tie it together side to side. And so this is your postoperative result for the right side is done. Here's radiographs, both sides done. Nice correction. So in summary, consider treating a young patient with a flexible flatbed. They're symptomatic. Thanks so much, Jacob, really always interesting to hear about your experiences with the adolescent flat feet. And we're going to move on to our next talk, kind of taking a left turn with Errol. We're going to talk about Achilles insertional tendonitis, what are traditional versus newer solutions. So take it away, Errol. Thank you all. And I appreciate all the attendees for hanging in here. This is my topic for the afternoon. Here are my disclosures. This is a young Patrick Haglund. We know him for the Haglund deformity, but actually he was a Scandinavian orthopedic surgeon and he's really known for being the first doctor to create orthopedic treatment centers in Sweden. This consisted of a number of row houses where they had orthopedic technicians and nurses and providers with a specific intent of orthopedic care. 30 years later, after he first started this, the first orthopedic hospital was built at the medical college of Sweden with his concept. He unfortunately had retired, died two years later, and never got to work in something that he actually created. We know him for this, the Haglund's deformity, which he first described in 1928. It's a large posterior bump on the superior lateral aspect of the Achilles insertion that provides a posterior heel pain syndrome, which consists of retrocalcaneal bursitis, tendinopathy, and a large exostosis. This goes by a variety of names, pump bump, Haglund syndrome, retrocalcaneal exostosis, and Mulholland deformity. If anyone can tell me who Dr. Mulholland was, let me know, send me something through a chat. I've been trying to find that for my entire orthopedic career. I have no idea who that is. Basically, you can see here on the anatomy that there's a large retrocalcaneal bursa. There's a large posterior tuberosity. There's inflammation here and tension on the tendon that leads to degeneration. How does this happen? Well, there are intrinsic and extrinsic issues here. We all know that the distal two to six centimeters of the Achilles tendon is relatively avascular. It's got poor blood supply. That's what leads to the intrasubstance degeneration. The converse is the peritoneum and the fat pad are very vascular, and that's what leads to them being very easy to get inflamed. Those are intrinsic. Extrinsically, overuse, jumping, and running, and that's what leads to the ultimate degeneration and breakdown. We put great forces across the Achilles tendon, sometimes up to 10 times our body weight. What's the etiology? Well, sometimes we just don't know why people have it, but they tend to all have an Achilles tendon fracture. It can be hereditary. We're most commonly seeing this in the cavus foot. It can come from sheer irritation as well. Here down in Atlanta, and I'm sure Dominique would agree, a lot of our patients eat a lot of fried chicken, and chicken and dumplings, and bacon cheeseburgers, and obesity is a real, real concern, and overwhelmingly, all of my patients tend to be female and obese. It's more common in females. They get posterior heel pain. They get the large exostosis, the swelling, tenderness, and it oftentimes is bilateral. What does it look like on X-ray? Well, on figure one, you've got a prominent posterior tuberosity, and you don't necessarily have to have calcific tendinosis, but more commonly than not, figure two will show you that there's most often, when it's bad, some intra substance calcifications. MRI, the one on the left is pristine, nice, black, thin, narrow tendon with no issues on insertion. If you've got a Hagelin's deformity or retrocalculoneal bursitis, you're going to see this figure four on the right, where you can see that the tendon is degenerative, and there's some intra substance calcifications. So we all are trained to do this. Most of us hand our patients these sheets that teach them how to stretch. We give them topical creams or oral anti-inflammatories. Some end up in physical therapy. I don't use night splints because my patients don't wear them, but that's an option. We put them in boots with lifts, PRP, and I've even had some people try acupuncture and get better. We try this for about six months. If we don't get anything, we tend to start looking for surgical solutions. If they do get better, I ask for them to be symptom free for two weeks, and then I let them return back to their normal activities. What about eccentric stretching? That really does work. If you can get the patient to do it, none of mine ever really fully cooperate. Here's a study by Baral, who had a six week protocol with heel drop, and in athletes, 82% of them got better if they had missubstance Achilles tendinosis. So this actually works if you can get your patients to do it. But if it's insertional, those numbers drop, and only one in two will get better. In his study, 21% of patients ultimately had to go on to have surgery. The same is true if you read a variety of other studies. I've listed two here. And Palvola study, 29% went on to have surgery. That was in the American Journal of Sports Medicine. And Hartag quoted in his series that sometimes up to 50% of people may require surgery. So it's key if we can get them to truly do conservative measures to try to reduce these numbers. What Burlett showed was that if you do MRI these and they have extensive disease, most likely conservative measures are not going to work. What about PRP? It's controversial. Multiple studies, some say it does work. Some say that it doesn't. Where your symptoms have been there for a long time, it takes a long time to also recover. On occasion, it may take two or three injections. I can personally attest to the fact that in mid-substance Achilles tendinosis, when I do PRP, I can get this to work, and I can get this to work very effectively. This works. When it comes down to insertional paculis deformity, my results are nowhere near mid-substance. So if you've got mid-substance, I would highly recommend this. It's not a fluke. This really works there. What about surgical treatment? That's what we're here today for this talk. If you took a poll of how people approach this disorder, they would be all over the place. I have friends who do foot and ankle, who do medial approaches. I do a central splitting. That's what I used to do for a very long time. Many do laterals. I've never done a dual incision, but some do. Some do endoscopic. And what I'm going to finish the talk with, it's a zetic osteotomy, which I am very, very high on. Let's look at what these patients do. We all had them, and we pretty much know what these results are going to be, but I'm just going to take you through a series of them so that we can establish something. Here's the medial approach. Here's an article with the medial approach and 30 heels, okay? Eventually, these patients get there. They get better. 90% were pain-free, but look at the bottom stat, 83% residual pain for up to two years. I tell my patients when I do an open procedure to not expect to be right for almost a year. What if you compare the lateral approach to the central splitting approach? I used to do lateral approaches back in the early 90s. And then when Don Baxter and McGarvey started doing central approaches, I started doing that. But how does the lateral hold up? Well, in the lateral approach, there are less wound problems, but they take longer to get better. In the tendon splitting group, the recovery was less, but of course, you've seen the picture. You've got a number of issues with nerves and wound healing. So therefore, it's still up to debate, which is the best way to do this. This was a landmark paper. Don Baxter and McGarvey were the first to really write about this. They had 21 patients and only got 13 of 22 to be pain-free. And they say at three months, but I'm not sure that's true. I've never had one of these open, be pain-free at three months, or maybe I'm just doing something wrong. Six had scar issues and there was an 82% satisfaction rate and many would do the surgery again. Other central tendon approach studies kind of mimic this. This particular one by Zahn had a 77% overall healing, no rupture, no infection, and two delayed healings. So you're starting to get the picture, nerve problems, delayed healing, reasonable results. The Oreo describes a procedure and the techniques for foot and ankle just last year, where he does the central splitting approach, which we all do. He resects the retrocapitoneal bursa, which is in the way. He takes a saw blade and resects his Haglunds and then tilts it 45 degrees like we all do on each side to get rid of those lateral and medial prominences, gets an x-ray that looks like this, and then starts his repair with a double row technique. His results, very similar to all of those that I've previously mentioned, the issues are wound problems, nerve problems, and continued pain for long periods of time. So we all try to do this when we need to. FHL transfers, how do those do? Well, when we have greater than 50% of the tendon involved and we resect that, we have to augment this with something. I never quite knew where the 50% number came from, it was just something one of my attendings had told me. I'd never seen a biomechanical study, but I'll present that to you next. These do well. This actually works. And in this particular study, it was shown that when you compared the strength on the operated side to the non-operated side, strength was equal. But here's the problem. They fatigue faster, endurance was significantly less. And then this study, 11 of 21, had some type of complication, infection, wounds, clawing of the toes, et cetera. So where does all this 50% come from, or what study validates that? This was a great study here by Schmittberg. They took 30 matched cadaver specimens and divided them into three groups. They cut the tendon to create a 25% tear, a 50% tear, and a 75% defect. And then to one group, they added the FHL transfers, and then they cyclically loaded these to see what happened. What was interesting, in the group that had the tears greater than 50% or 75%, all of those failed at the tendon defect. That's why you need to supplement this with an FHL transfer to add additional strength. So we've all been here, if you've ever done this. Maybe not to this extent, but it's quite common. If you read the literature, wound breakdowns up to 12%. Many patients have irregular sensitivity, superficial nerves, sural nerve, et cetera. Many of them have numbness. There's a 6% infection rate overall in the literature. And you can get re-ruptures from detaching the tendon. But here's the problem. In most studies, they all have continued pain for long periods of time and have problems wearing shoe wear and up to 23%. That's just simply not good. We can do better. So these wound problems have led to additional approaches. I don't do this. I don't have this arthroscopic skill set to do this. Maybe Dominique, your next speaker, has that skill set. I simply don't. However, this works. There's a great paper in Foot & Ankle in 2007. It looked at 28 patients with 30 heals and 26 excellent and three good, only one poor. So that's a 90% success rate. They did have one Achilles rupture. But look, no wound complications. But the authors talk incessantly about how difficult this is and that there's a long learning curve. Another way to do this endoscopically is to do an endoscopic gastroc release and topaz treatment, microtonotomy radiofrequency to the heel. There are papers about this offering similar quality results. Now, if you really want to get into this, you can do endoscopic FHL transfers. In my opinion, this is fantastic if you can do this. In fact, I think in minimally invasive surgery, tendinoscopy and minimally invasive tendon repairs, that's going to be extremely hot. For all of you young surgeons out there interested in minimally invasive surgery, this is going to be some really cool stuff. In this particular paper, they had a 93% success rate. But here again, this is technically very difficult. But I think this is going to persist. I think this is going to be a way and a wave in the future. So overall, no matter how you look at it, these do okay. The best results I found was a paper by Nunley and Putnam in 2011, where they had a 96% success rate. I love Dr. Nunley. I just can't. I can't make that happen in this particular procedure. The complication rates vary, but tend to be high. My patients are still complaining to me. I tell their husbands or their wives, look, the patient's going to come back at the six-month mark and she's not going to like me. I'm telling you now. But in a year, she'll be fine. And I make sure they remember that. Minimal incision works and it mimics open incisions, but again, it has long learning curves. So what about long-term? I've been doing this for over 30 years and I've had a repeat experience that I didn't understand and it just made me very perplexed. Here's what I saw. People coming back to me 15, 20 years later with other issues and they say, hey, Dr. Brady, remember me? You did this Paglen's thing on the other side. I go, oh, yeah, even though I didn't really know who they were and said, you know, you mind if I take a picture of that? Yeah, how are you doing, by the way? Ah, you know, it's all right, it hurts when I do a lot, but you know, onto the new problem. This is what I started seeing. There you can see the track from the FHL and you can see calcifications forming back. And look at the x-ray on the right, central splitting incision about 18 years later. You can see my suture anchor in there. You know, I don't think I'm necessarily the greatest surgeon in the world, but you know, I just didn't leave that like that. It came back. Here's another one. Seven or eight years out on the left, there's a suture anchor. What are those calcifications doing there? And then here's another one, 16 years later on the right. So I was feeling like this guy on the left and then there was another last straw on the donkey's back. I had another patient that came in, one that I had done about four years ago, but I noticed she never got better. I think the center x-ray is very acceptable. But nine months after I did that, she came back starting having pain and she looked like that on the right. It looked like it's coming back to me. So it finally hit me. I'm like, oh, snap. I'm just saying, what if we got this all wrong? Maybe there's another way. I think we're just buying time. It's been shown we're buying time with our bunions. A lot of those 15, 20 years tend to try to recur. I think Hagelin's incisions recur. And I think it's like ankle fractures where we think they're doing all right, but when I really get in there and look at them, they're not. So I called Ettore Vulcano, who was doing a lot of work with the Zadig osteotomy. And I talked to him, I said, man, explain, does this work? Cause I'm sick and tired of looking at these patients, complaining. And he said, Errol, I'm telling you, this is a good deal. I said, okay. Now, interestingly, if you look on the far right, that's Isidore Zadig's paper. This is not new. This was started in 1939, 80 years ago, where a dorsal wedge, closing wedge osteotomy in the calcaneus to unload the Achilles tendon. Kelly and Keck came along in 1965, made some minor modifications, but basically did this through an open incision as well, and started getting reasonable results. However, they started having similar wound problems as many of the other procedures, central splitting or lateral or medial exposures. So what am I getting at? Here's a good study. I won't go in this in great detail, but Miyamoto looked at the effects of the Achilles tendon moment arm length on the insertion. He did a complex biomechanical study looking at where are the main forces and why are they there? These were the two main points. The increased length of the Achilles tendon moment arm is one of the most important causes of increased pressure at the Achilles insertion. That's number one. And number two, the problem can be avoided if you can find a way to shorten the moment arm. I went, aha. So let's look at these three particular diagrams. On the far right, that's our Fowler-Philip angle that we draw. And then in the center, we have our calcaneal pitch, which we measure, which we see increased in cavus feet. And then on the far left, the bottom line is X. It's the total length of the calcaneus and the top line is Y. We're starting to look at the X, Y ratio. Why? There's an interesting paper in foot and ankle surgery in January of 20, where Tornay looked at his zetac osteotomies and Hagelin syndrome. And here, this is what's happening. If you look on the top left, you can see that X over Y, you can see X over Y, and you can see the osteotomy and then you can see on the top right, you can see it closing. Y becomes tremendously smaller than X. And you can see on B that not only does the osteotomy close, but it shortens and elevates. They came up with parameters to look at this. And the X, Y ratio they came up with based on results was a calcaneus less than 2.5. An X to Y ratio less than 2.5 means the calcaneus is relatively long and it probably needs a zetac. Here is an X-ray from their particular paper and you can see how much shortening of the calcaneus this does and how it affects Fowler's angle, the calcaneal pitch. All of these are dramatically reduced. So this is what it does. You get anterior translation, elevation, and it completely unloads the retrocalcaneal bursa and the tendon. What else is happening? It raises the insertion point of the Achilles. So you're getting a relative gastrocnemius lengthening. It displaces the posterior tuberosity anteriorly. It shortens the calcaneus and voila, minimizes the Achilles tendon libra arm, unloads the retrocalcaneal bursa and subsequently reduces pain. So how did the open zetacs do? Here are two studies as I wind down. One left in athletes where there was 52 athletes. Now you're not gonna do an open Haglund's excision and go through an athlete's Achilles tendon if you can help it. Here's a way to not do that. 52 athletes, 50 with good to excellent results. But the point I want you to see is there was return to sports in 21 weeks. I can't get my household ladies back to normal activity in 21 weeks. Mofuli study, same thing. Back to normal activity at 23 weeks. That has been my experience as well with this particular procedure. This is a study by Ettore Volcano who's done more of these than probably anybody in this country. He had 26 patients at a 92% success rate. And what's the beauty of this? You don't touch the Achilles tendon. You don't touch the spur. It's all a percutaneous osteotomy. And I can tell you, these people come back and they lay on the table on the first post-op visit and their posterior heel is on the table. You never see anything like that with an open Haglund's procedure. Their pain reduction is almost immediate. Here I am, and this is my particular setup. Ettore does it differently. He kind of does it in a way somewhat upside down. I can't do it this way. I have to rest the foot on the CRM like this. And I'm sharing with you my very first one. I was nervous, although I'd done a ton of MIS and calc slides, I'd never done this before. So I measured out what I wanted to cut out. When the average length is anywhere from five to 10 millimeters of dorsal wedge. I measured this out. I drew that out on the skin and I made that small incision. You put your burr approximately a centimeter from the plantar surface, just distal to the insertion of the plantar fascia and you create a wedge like this. You dorsiflex the foot. The Achilles tendon closes that down and you simply fire two screws or one screw, whatever your method of fixation is, and you're done. You can do this once you get accustomed to this in about 30, 35 minutes. There's my incision. Those are my incisions from all of this work. I put them in a cast for three weeks and then they're in a tall walking boot and I weight bear them at three weeks because walking on this actually closes down the osteotomy and the fixation helps and they do fine. Range of motion at three weeks in a shoe at six to eight weeks, and then I start physical therapy. Well, what can go wrong? Well, early on, you know, if you don't know what you're doing, you get bone sludge in the osteotomy and a lot of people think, well, that's just good stuff to leave in there. No, you have to suck that out. You have to get rid of it all and get great bone apposition and keep modifying your osteotomy until you get good bone apposition. The sural nerve. I've had some people with some numbness, but it all went away over a couple of weeks. If you're too plantar, you can break the plantar cortex. If you do, you just reduce it and you put one of your screws very plantar so that you can hold that area well together. I have not had any heart rate issues because I will bury my screws deep to the spur so they're no longer prominent. I have had a few people have plantar fasciitis and I went back and looked at my osteotomy and I'm now making it a little distal to the insertion of the plantar fascia. I've had zero wound issues and I've done maybe 25 or 30 and I don't have a single patient, not a single patient who's not significantly better or happy. So I present this to you to just hopefully allow you to look at yours and rethink this and hopefully you can join us in our minimally invasive journey. That's Tom Hanks and he says, thanks. Thank you very much. Thanks, Errol, for the thought provoking presentation. I'm hoping we can have some discussion about the zettic osteotomy later. And then for the third and final talk for this session, I'd like to invite Dominic Herrera here to talk about OCL of the telus and tibia and what the current treatment algorithm and techniques are. I'm trying to get to my close the screen. There it is. Hey, thanks a lot for this opportunity to speak and I will try and be concise and get us done close to on time here. So we're gonna talk about telus and tibia, osteocondral defects. There's not much on the tibia, so I'm gonna be brief in discussing that. In terms of my disclosures, they're listed here. I'm a member of the CORD committee, which is a multi-center research committee and none are relevant. There's a lot of different phrases that are used to describe osteocondral defects as listed here. I will use the term osteocondral defect in the talk, osteocondral lesions, and there's various terms that are used. The term fracture is a good one and certainly making the diagnosis appropriately when there is an osteocondral fracture is important in looking at options of treatment, including refixation. So one of the challenges of osteocondral defects is the tremendous variability that exists in these lesions. And so this is just looking inside and when you look inside arthroscopically, I think it's the tip of the iceberg a lot of times and you get all these different variations in terms of what you can see. And so that's part of what's made these treatments difficult is the variability and the different presentations. So we have different classifications. We have x-ray, we have CT, we have MRI. Are these classifications helpful? I would say somewhat. If you look at this MRI, I think one of the keys to know about MRI is that the edema in the bone can be significant and it doesn't necessarily need to be treated, meaning that if the lesion adjacent to the edema is treated, that edema can resolve and the entire area of edema does not necessarily need to be treated. So this is from the international consensus meeting from 2017, which I was a part of. And it really went into depth as to what are the different factors that we need to look at in assessing osteocondral lesions. And I think this really forms the basis of the treatment algorithm, which is the depth of the lesion, the superficial dimensions, the location and therefore accessibility, especially as it relates to arthroscopy versus open procedures. Stability of the lesion itself, loose fragments, cystic changes, whether they're present or not, degenerative changes, meaning more diffuse, arthritic changes in the joint, and whether they're appropriate candidates for joint preservation. Edema, as I showed on the MRI, which can in and of itself be a significant pain generator. And of course, alignment and other pathologies that coincide with these osteocondral lesions and specifically and especially instability and impingement. So as we look at non-surgical treatment options, generally it's been a process of progressive mobilization over four to six weeks. Generally, there's been poor outcomes associated with conservative treatment with about a 45% success. But again, based on this consensus meeting, the treatment non-operatively that's appropriate is in patients who have acute symptomatic and non-displaced lesions. Those who are older age and with lower function and the skeletal immature should be given handset non-operative treatment. Sorry, my screen froze. Let's see, we will restart the program. Sorry, this is apparently my PowerPoint. Just went on. Sorry about that, I think we're back. So as we look at the various treatment options in treatment of OCDs, the cartilage refixation is one and acute lesions in particular are candidates for refixation in the presence of sclerosis, this would not be a good option. Acute lesions with a minimum of 10 millimeter diameter and a minimum of three millimeter thickness, and the fixation can be with bioresorbables, preferably over metal fixation. The second option is cartilage debridement, and this is generally done for partial thickness chondralesions, kind of the thought is you're mowing the lawn, you're smoothing out the top surface in a partial thickness lesion, especially in more diffuse lesions, this can be a role of smoothing the articular cartilage out. And the second option is acute injuries after an ankle fracture, third is an elite athlete in season, and there has been a growing trend for debridement and not to micro fracture in the elite athlete, given that the length to recovery, and a question about the durability of these micro fracture procedures, particularly in the high end athletes, the high demand athletes, and then those that are incidentally found at the time of arthroscopy should be considered for debridement alone. The rest of these techniques, I'm going to go into a little more greater detail, but they're kind of broken into cartilage repair, regeneration, and we'll address those specifically. So the extent of the surgery depends on addressing these factors that I mentioned earlier. So the depth, does the bone need to be addressed related to stability and the depth of lesion. So thought to be approximately a four millimeter depth, meaning if the bone is affected three to four millimeters into the depth of the bone, not the cartilage, but the bone itself, considering treatment of the bone when treating the cartilage, and so really treating the osteo and chondral portion of the cartilage problem. The superficial dimensions, it really defines the extent of the articular cartilage treatment, the location and therefore accessibility, is an osteotomy needed, and also is the open procedure worth it? So as we look at different options, we think, should we do this arthroscopically or attempt to do that? Does the open procedure have a significant advantage over the arthroscopic in terms of the ultimate outcome and including as it relates to risk and recovery? Stability, if the lesion is stable, the osteochondral fragment, then consider non-op, and if it's unstable, then we generally do excise and treat or refixate if it's an acute lesion. Loose fragments are generally excised, and there is an option when removing cartilage to particulate the cartilage itself, and so there's a new product on the market that allows for excision of that cartilage and reuse of it. I think that's an interesting development. Cystic changes, consider bone as part of the construct whenever there are significant bony deficits. Degenerative changes, if there's global joint injury, you're going to decrease your chances of success. As I mentioned, alignment is always important in orthopedics and here as well, and then let's treat the associated lesions and injuries when doing a surgery such that we are comprehensive and hope to get our best results. So when I think about the classification systems, I really think of the different imaging modalities help address these different concerns, and I don't personally and I don't think many find the classification system to be that helpful. So I don't really think of them as a to-be, and I don't think most do. So as we look at our access to the joint, arthrotomy versus osteotomy, OCDs may be treated with an arthroscopic approach or medial and lateral osteotomies. Authors have suggested access to be different, and I don't really look at the very specific numbers in terms of the accessibility. Is it 15% as Mura has said, or is it 25% or 30%? But understand that the arthroscopic approach can be limited, especially with grafting procedures, and osteotomies may be necessary. The osteotomies are not without potential complications in the setting of medial osteotomies, posterior tibial tendon injury, posterior tibial artery, tibial nerve, damaging healthy cartilage on the tibial side included, malunions, nonunions, need for hard removal. These are all possible complications, and so it has to be weighed when looking at the different options. When doing an osteotomy, really should pre-drill so that the bone lines up exactly the way it started, and for the medial side, I think Perkel's approach of using a three-screw fixation is helpful. I'm going to demonstrate these two approaches here in the following slide. Kennedy and Murawski demonstrated this chevron-type osteotomy, which is on the top here. You can use a guide pin to establish the location of the osteotomy, and then a Hohmann retractor can be used to, I'm sorry, a retractor can be used to actually access the joint well. Here's a second option, which is a triplane osteotomy shown here in the coronal and sagittal planes, and this kind of gives you an idea of how that access can work for you. This more anterior approach, I think, is not very good for the more posterior lesions, but is an option for more central to anterior. I would describe the current state of the literature to be lacking with regard to basic science research and how it affects clinical outcomes. We know that postoperative imaging doesn't correlate well with clinical results, and there's a study recently by Migliorini with the MoCART scoring. The MoCART scoring is basically a scoring based on MRI of the quality of the cartilage, and they looked at all the knee and talus studies that had been published, and basically there wasn't a good association with outcomes. We have this problem of how does the basic science, how does the highland cartilage quality really translate into outcomes, and it's not good, it's not high. So to me, it's really a call for action. We have few comparative studies for different options. I think we've made very little headway in 20 years. I trained with Brian Cole and Dick Sedman and others who really had done a lot of cartilage work and I was exposed to it in my sports medicine fellowship as well, and I personally believe that collaborative multi-center research is really the only way that we're going to get serious answers about this, and that's really the mission of the core group in the AOFAS and a study group that I founded, which is currently seven centers with 205 of these patients enrolled today. Different cartilage repair strategies exist. There's microfracture, which is a bone marrow stimulation that does not include drilling. The drilling procedure has been criticized potentially for creating thermal necrosis, and so I think that although drilling has been described, the microfracture is probably a healthier way to stimulate the bone. Success with microfracture has been strongly and inversely correlated with lesion size, and basically this has generally been recommended for smaller lesions and some controversy as to what's small, is it 10 millimeter diameter or 15 millimeter superficial diameter as the cutoff, and certainly not deep lesions are as well treated with microfracture. In this study of 105 OCDs treated with arthroscopic debridement and microfracture, there were no failures when the transverse and longitudinal diameter were less than 15, and this generally has been my experience, small tailored lesions with a very detailed approach. I think it is a tedious procedure, microfracture is, it takes time to not injure the adjacent cartilage, it takes time to go through each of these steps. The first is to debride the unstable cartilage and create stable shoulder lesions. The second step is to remove the calcified cartilage layer. This is a deeper cartilage layer that creates like a snowflake like appearance when it's scraped out. Holes are made with a microfracture awl, approximately three millimeters depth at minimum, and then you check for bone marrow extrusion. You can turn off your pump and see if bone marrow elements come out of these holes. And looking at outcomes, this study by Core in FAI in 2021, there were 45 patients, 86% of them stated that they were able to return to sport following this procedure. Another study, which was a systematic review of seven studies, a total of 299 ankles showed a mean postoperative AOFAS of 86, with good to excellent results in 80% of patients. Microfracture has been criticized and appropriately in terms of its durability, and especially in the knee and also in the talus. And these are studies here showing that over time, there seems to be a decrease in its success. This one's showing a 13% need for revision surgery at a longer timeframe. And the second study by Pollat showing that 57% were symptomatic at 10 years post-treatment. How do we treat subchondral cysts? A study by Robinson showed that subchondral cysts who underwent microfracture had poor outcomes, 53% of those patients. Another study, however, did not show significant differences. So I think the role of cystic changes is that it does decrease success rates. Exactly how much, including the setting of microfracture, I think is a question to me. And I've had success in these patients with microfractures, at least in the short term up to medium term. At the international consensus meeting, bone grafting should be considered with a greater than three millimeter depth of bone loss. And there was a recommendation for use of bone grafting if it was greater than 100 millimeter cubed dimension to the cystic change. Retrograde drilling is also a treatment. It's really done in the presence of intact articular cartilage when there's bony defect deep to it. It allows for the treatment of the pathology, which is really the bone and not cartilage. Encourage using imaging such as x-ray, but also a targeting drill guide can be helpful. The targeting drill guide helps to basically aim at the site with more precision. Different bone fillers or voids are used typically in this setting, including subchondroplasty or other injectable bone fillers are also available through other manufacturers. There's minimal data with regard to outcomes. There's a study of six patients and eight patients, basically. It's really quite poor in terms of the data to support this. Another option in treatment is ACI. It can be considered in primary revision procedures. It's typically done for larger lesions greater than one or 1.5 centimeters squared. With or without cysts is an advantage of this procedure, meaning that you can fill bone voids. It also includes shoulder lesions where microfracture has been associated with inferior results in the setting of shoulder lesions. In my experience with this is very limited. I think the US experience is quite limited by the fact that this is not easy to get approved. It generally is just not approved. So I've offered it to patients who want to pay cash and that has very seldomly happened. Basically, the goal in ACI as well as in MACI is to harvest, I'm sorry, in ACI specifically is to harvest the patient's own hyaline cartilage. In MACI you're using allograft chondrocytes. These chondrocytes are delivered and sealed in first generation, which is the ACI with a periosteal patch and hyaline cartilage is regenerated. In a meta-analysis of 458 patients, the success rate was 89% with a mean AOFA score of 86. And it didn't seem to be as sensitive to size as microfracture had been, I'm sorry, has been associated. The complication of periosteal hypertrophy has been reported in this first generation ACI related to periosteum itself as a, as kind of the ceiling or cover to it. And for that reason, many have gone on to the next generation or the second generation, which is the matrix-induced autologous chondrocyte implantation. And this uses a self-adherent matrix instead of a patch. The early, the periosteal patches generally had been sutured into place. And this becomes a much easier technique in that the matrix is self-adherent. Couple of studies here, generally small in number, 15, 10, and 10 patients showing improvements and I would say similar success rates as has been reported in ACI. Other pictures of this essentially are autologous matrix-induced chondrogenesis. It's a one-step procedure and it uses bone marrow derived cells from various sources. And basically microfracture is combined with DMAC or PRP and then within a collagen matrix scaffold. Again, it's been studied and has a similar success rate. We'll see this kind of mid 80s success rate as many of these different procedures have been associated with. Then we get into the osteochondral transfers. So bone and cartilage transfers, these are typically cylindrical in nature, both the autograft and allograft type. And basically in the OATS procedure, the plug is placed into the talus, and it's taken from the non-weight bearing portion of the knee as shown in that picture. You consider it in cystic lesions or lesions that have significant bony kind of failure deficiency of greater than a one centimeter in diameter, but also a depth of approximately a centimeter in diameter. Generally, for larger defects located in the shoulder or lacking a stable cartilaginous rim. The optimal depth of drilling has been 12 to 15 millimeters. I think this is being called into question in part because of cystic lesions associated with oats and with allograft cylindrical transfers. And it may be that less depth will lead to less cystic changes. And in the knee, that's been more of a trend recently. So as we look at transplantation here, there is the concern for donor site morbidity. It has been described in 15 to 20% of cases, 20% in this particular study. And as part of the international consensus meeting, the recommendation to avoid donor site morbidity was to do early rehab and range of motion of the knee, decrease the soft tissue manipulation, avoiding tight closure of the lateral capsule. And another important one was avoiding patients with high BMIs and entering the knee joint in those patients. These are the potential sites for the oats and the lateral femoral condyle is the preferred site. But all of these numbers are options basically. And basically they're chosen because they have low weight bearing and mimicking the surface curvature is important. So trying to line up the area of harvesting with the donor need, meaning the area in the tail is, and trying to match up the articular cartilage is a goal when entering into the knee and specifically choosing the exact spot from which the graft is obtained. Another option is an osteochondral allograft. This is generally used for larger lesions and including the shoulder. Thought to consider the allograft when three or more cylinders are needed. This avoids the risk of donor site morbidity. Using fresh grafts has generally been the approach to optimize the chondrocyte site viability. And it's done by doing measurements to match the size of the talus based on CT scanning. There is a significant rate of complications associated with allograft. But I will say that I think the efficacy really has been confounded by its use in larger lesions. Allografts are used in bigger lesions. And so we really had a problem in cartilage research and outcome studies in that we haven't compared apples there have been very few studies that have done so. This includes the study by, or I'll actually quote that study in a minute here, but here's the difference in cell variability. At three weeks, there is a significant decrease in the viability of these cells. And so getting to the grafting at an early stage early timeframe in terms of the procurement is important. And oftentimes when I've done this, my patients have been on standby, so to speak, waiting for the best, an optimal graft to become available. This is what it looks like. The first step is excision. So using a saw blade, typically making kind of 90 degree cuts to one another. This is what it looks like after a lesion has been excised. This is the donor graft. And the last step is basically re-implantation. In this particular view, the fixation was done from top to bottom. Generally, what's favorable is to do it from the side instead of from the top, so as to not to affect the more weight-bearing portion of the graft. This is a systematic review. They used 12 studies, 190 patients that were fresh grafts only. And VAS scores did significantly improve. The graft survival rate was about 86%. 21% of these patients, however, had minor subsequent procedures, including arthroscopic debridement and hardware removal. This is a study that actually did compare at autograft and allograft. The problem, and it was a systematic review with over 1,000 patients. The problem is that in reporting that autografts did better than allografts, I think despite the fact that they claim the two study groups had the same defect size, when really looking at it, the autografts' size was 1.8 centimeters plus or minus 0.8, and the allos were 2.6 plus or minus 4.3. So to me, this is not a real apples-to-apples comparison, and therefore isn't that helpful. This study by Trimozono and Kennedy, this is Dr. Kennedy's work, really has given me pause on the use of allografts, because this appears to be a well-done study. And although the numbers aren't high, with 25 patients in autograft versus 16 allograft, there was a significant difference between the two with outcome scoring, cyst formation, and a higher rate of secondary procedures in the allograft. For that reason, and because of the knee experience, I have adjusted my allograft technique, and this is really based on what's been done in the knee, and I'll demonstrate it here. So basically, you create the defect with kind of 90-degree corners by cutting it out, and then you can pack the most central aspect of it with autograft. This leaves the remainder of the OCD with the allograft. And so I think the difference in this construct can be that the autograft bone well-packed in may lead to a better incorporation in terms of not having as many bone cysts. The autograft seems to incorporate more readily, and this is especially useful, I think, for patients with larger lesions, such as that shown here in the MRI. Another additional option is a particulated juvenile cartilage allograft, and it uses fresh juvenile cartilage. The graft is secured with fiber and glue, and it can be done potentially arthroscopically without donor site morbidity. There have been some disadvantages, including allograft supply and just coverage by insurance companies. Coverage with insurance companies has been a major limitation in my practice. Outcomes have generally been good around this 86%. This particular study in FAI of 15 patients had a 40% failure rate. I think this study may have led to some lessening of the use of this particular mode of treatment. As we look at all of these options, it's really pretty remarkable. When you look at the AOFAS score, 86, 86, and 86 for the three different forms of AOFAS, it highlights the, I think, our lack of good comparative data and our lack of data to help guide us into what procedure we should actually do. So the AOFAS is probably the most reported outcome, but yet it's not validated for articular cartilage. And so I think we just have a lot more to learn in treating these cartilage injuries. A trend has been the use of adjuvant therapies including BRP and BMAC. And it is based on data, which I've summarized here. Interestingly, if you just inject BMAC alone without a surgery, patients seem to do, have significant improvements in this particular study, even up to 24 months. When BMAC was combined with the Bredemont, there was a significant improvement, except for patients who were arthritic in nature, which is not really a surprise. If you compared BMAC and microfracture versus BMAC alone, there was little evidence that combining the two procedures really improved outcomes in this particular study. BMAC plus microfracture versus microfracture alone, another study kind of changing up these different variables. And the BMAC group had improved VAS and AOFAS scores in comparison to microfracture alone. BMAC plus autologous osteochondral transplants showed a success, although it wasn't a comparative study by Kennedy. And so overall there's a positive of literature with regard to adjuvants, but I think there is a growing trend towards it. And the high-end athletes, I use it, because I think that it's become kind of a norm. If you look at PRP, it has been limited by non-standard preparation, meaning there isn't a standard protocol, but as an adjuvant to microfracture in a systematic review of four studies, it did show improved results in the short term. So at 16 months, it was better. By 42 months, there didn't seem to be a significant difference between the two. Another study by Guni and 35 patients in 2015, 16 were treated with microfracture, 19 were treated with microfracture plus PRP. And the second group, the addition of PRP had superior scores. These are, I think, are limited studies, meaning these are small numbers, in my opinion. I think the verdict is still out. Lastly, OCD of the tibia. It's much less common than OCDs of the talus. We don't really have any well-established treatment algorithms. They're rare. They're most commonly found central medial and anterocentral, and the data is limited. But when pooling several studies, 10 studies had 175 patients, it seemed like osteochondral transplantation did better than microfracture. Again, I don't think that's really good data, but I think it's worth certainly considering osteochondral transplant in these patients. So what's my treatment algorithm? I'd say this is with limited evidence. This is just what I do, and as I was asked to present that as well, and basically injecting with PRP or BMAC at the end of the procedure, or I preferably do it during the early weeks of recovery. I think if there's been a procedure done, especially microfracture, those early healing elements are there, and it's really in the subsequent weeks as the patient's recovering and the tissues are healing that I personally have used PRP. So for OCDs, for small lesions, microfracture is a treatment. In the revision setting, if I believe that a microfracture was well done in the primary setting, then I won't choose a microfracture, but I will do it if I question the quality of the work that was done the first time around. And then lesions that are less than 1.5 centimeters with cystic changes, generally using a dowel or cylindrical OATS autograft. And lesions that are larger, 1.5 centimeters squared, if it doesn't extend into the shoulder, I'll use OATS if it's less than three dowels, and if it's greater than or equal to three dowels, allograft. At the base of the allograft, packing it in with bone, as I described with that shelf technique, is I think an option. In a shoulder lesion, generally allograft with, again, using some autograft bone at the base of it if it's a thick lesion. And finally, large cystic lesions with more of a bulk type of a graft can be used. I use the bulk graft, meaning the shoulder and side, I'm sorry, the weight-bearing surface and the side for the shoulder lesions and large cystic lesions with allografts. I find it effective in really matching up the cartilage effectively. Finally, retrograde drilling and injectable bone fills whenever the intact cartilage is noted. Thank you very much. Great, thank you so much, Dominic. I have one audience question that I think we'll address before moving on, and that's for Dominic. What is your experience with retrograde drilling? If any, I know you mentioned a preference for microfracture, but. Yeah, so my experience with it is that most of the time, if I believe that the cartilage cap will be intact, it generally isn't, meaning that when I probe the cartilage, it just doesn't appear to be stable. And so it becomes a treatment that's not a retrograde, but really a full osteochondral treatment for that lesion. The second I would say is that it's a kind of tedious and difficult procedure to really localize it. I think it takes a lot of time to get the exact spot. The third part of it is that I would say is approaching the lesion, it's being precise and getting to the defect without porcupining it, meaning if you're going to inject it with a filler, if you've violated the opposite cortex, then you don't have the ability to fill the void very effectively. And so I think it's from a technique standpoint, really approaching the lesion and redirecting as you're advancing through the lesion and not kind of taking multiple shots at it would be my technique there. Thank you so much. Did any of the other panelists have any burning questions or comments before we moved on? All right, in that case, thank you guys so very much. A lot of information for us to take back to our practices. And we're going to move on to the final session here, symposium eight. It's a diabetic foot, no escape. Since I'm starting off with the first lecture, I'll get going here.

flexible flat feet

adolescents

asymptomatic

surgical intervention

insertional Achilles tendonitis

Zadig osteotomy

osteocondral defects

cartilage refixation

osteochondral transfers

PRP

BMAC

comparative studies

OATS