On behalf of the AOFAS, I want to welcome you to tonight's program, Managing Core Outcomes with Surgery on the Athlete, Why and What's Next. It'll be moderated by Robert Anderson. Joining him is Dr. Martin O'Malley, Dr. Chris Coetzee and Dr. David Porter. You can find their full biographies and disclosures in the program document posted in the chat box and also on the PRC. The 2022 webinars are provided free to AOFAS members and orthopedic residents and fellows with funding from the Orthopedic Foot and Ankle Foundation, supported by grants from Arthrex and Stryker. I'd like to run through a few housekeeping items before we kick off the presentations. For technical difficulties, please try closing your browser and logging back in the same way you did the first time. Registered physicians attendees may earn one hour of AMA PRA Category 1 CME credit by completing the evaluation and claiming the CME at the end of the webinar. You can find the link to claim CME in the chat tab and we'll also follow up with an email at the end of the webinar. This webinar is being recorded and will be available for on-demand viewing on the Physician Resource Center in approximately one week. We encourage you to ask questions during the presentation. To send your question to the faculty, click on the Q&A tab on your navigation bar at the bottom. If we cannot get to all the questions during the live broadcast, the faculty will reach out to you following the broadcast with a response to your question. I will now turn the program over to Dr. Robert Anderson and thank you. Well, hello everyone. Thank you very much to AOFS for helping to put together and host this exciting webinar. And the title, as we mentioned, is Managing Poor Outcomes of Surgery on the Athlete, Why and What Next? This is sort of a fascinating area. I think that as we go forward with this, trying to get my slides to go, you'll see this is my disclosures, which have nothing to do with this particular presentation. This is your faculty. These are my close friends. These are my colleagues. These are my buddies because we oftentimes share numerous cases, particularly on the athletic population. Dr. Chris Coetzee, who is one of the team doctors for the Minnesota Vikings, as well as taking care of a number of other organizations. The same for Dr. O'Malley in New York that helps to keep the Brooklyn Nets running up and down the court, but also is engaged in numerous other college and professional sporting teams. And then Dr. David Porter, same can be said for Dave in Indianapolis, where he helps to take care of the Indianapolis Colts, but also works with the college and professional ranks in that part of the Midwest as well. So as I mentioned, the four of us oftentimes share difficult cases. They usually deal with athletes who have had surgery, but unfortunately have developed less than optimal outcomes. And the question is what to do with those particular individuals. So I think to get us going, let me just talk a little bit about sport foot and ankles in general. I think that as you work through these patients, when you have these patients in your office, the more elite type of athlete, whether it's high school, college, or professional, but somebody who's trying to make a career out of being an athlete, you have to work with the issue at hand and you have to think about, okay, well, how do I need to work this up? What steps do I need to take? And I think that you first need to think about, okay, what pertinent exam findings do you have? What imaging do you need to come to a substantial conclusion? And what is the diagnosis? And then you have to educate the player and everybody around him on what that diagnosis is and what the various treatments are available at that time. Your next thing you have to consider is what's the estimated return to activity, return to sport. When that is that going to be? I know it's hard to estimate that from the very beginning, but you have to at least give them some kind of clue in what they're looking at as far as when could they return and when they do return, what are the risks? And lastly, you have to be able to discuss with them what the overall outcome and expectation will be. Now, the interesting thing about dealing with an elite athlete, again, whether it's high school or professional, as compared to the weekend warrior, is that it is a business. Even in high school, if you have an elite athlete, it's somewhat of a business. They have to think about college scholarships and family pressures and what are their long-term potential. You have to go with what's most reliable. And unfortunately, surgery sometimes is more reliable than non-operative management because it does provide a baseline. I think when you're dealing with these athletes as well, you got to be on the other side of it. You got to maintain perspective. You got to remember that player is your patient. You can't get caught up in the team's needs or outside pressure. You want to minimize short and long-term risk. You want to do what's best for the patient, particularly long-term. You have to have very open communication. You have to have the skills to discuss the player's surgery outcome and rehab concerns with the entire team. That includes your physical therapist, your athletic trainer, coaches, and so forth. And I think the last thing that I've learned is the physicians don't determine return to play. We can orthopedically clear an athlete to go and advance his functional recovery and rehab, but we don't necessarily tell them when it's time to return to the field or return to the court. That basically requires the input of multiple people, including the trainers and strength coaches and everybody else. So there's just some things to think about as you deal with the elite athlete, and that's what my colleagues are going to present to you in the next few minutes. I'm going to start out, though, talking a little bit about acute Achilles ruptures and some of the concerns I've had recently with some of the repairs and some of the complicated, you know, situations we've run across. Because, you know, you see the acute Achilles rupture and pretty much go, you just put some sutures in there, you put the two ends back together, they're going to do fine, right? They're going to do well, no issues there at all. And I think you got to back up and think about, you know, why did these acute Achilles ruptures occur in the first place? You know, there's a lot of theories out there. Is it aging? Is it deconditioned athlete overuse? Dehydration? Is it genetics or is it just bad luck? And the pathophysiology is important. When you think about exactly where the rupture is, what's going on at that level? Is it hypovascularity? Is it a blood supply that reduces with age? Is it repetitive microtrauma or eccentric overload? And the real controversy is, is it just bad tendon? So you got to remember that as we repair Achilles tendon rupture, sometimes you're just dealing with bad tendon and just simply putting sutures in bad tendon may not always, you know, work to a perfect outcome. When we take care of an Achilles rupture in the elite athlete, our goals are typically to restore the muscle tendon integrity of that tendon. We want to restore tension. We want to give that athlete the best opportunity to return to his pre-injury level of activity and regain that explosiveness that these athletes need to be elite. But we want to restore that integrity of the muscle-tendon relationship while avoiding complications and doing the best we can to get them back to normal strength or return to full activity. There are a lot of repair techniques out there. Some of you may use an open repair. Some may have a unique percutaneous method that they prefer. And then of course, there's the mini open type techniques. There's certainly multiple techniques out there described. There's a lot of jigs out there now that can be utilized. The original one there on the left is the Avalon, the next generation jig that I've been utilizing for a few years. It's called the PARS. But these are typical things that you can use if you wish to consider exploring the non-traditional open techniques. So this is the PARS. This is just where you have to, you know, make a longitudinal or transverse incision at the level of the mid-substance rupture. And that's basically a lot of suture management. You have to put the sutures in. You might double lock or lock on each side of the Achilles tendon. And then as you bring all the sutures out, you're going to eventually bring those tendon ends back together under appropriate tension with that foot plantar flex. And this is what we typically do. We secure the sutures with the ankle and maximum plantar flexion. And to be honest, I've never had anybody too tight. So we do secure those sutures of maximum plantar flexion with, you know, the maximum tension applied that can be. And then the post-op protocol is really whatever you feel comfortable with. Everybody's got their own protocol. I prefer to keep people non-weight bearing for the first four weeks, then gradually let them, you know, weight bear in the boot for the next four weeks, gradually bringing them out of a wedge, bringing that heel back to the ground. I try to avoid any dorsiflexion patches, neutral for 12 weeks, while initiating a very aggressive plantar flexion against resistance type of program. And then there's protected running, pool, Alter-G that typically are engaged by 16 weeks. But that's just my protocol. I think when you start looking at the different techniques around, again, my preference has been the mini-open. We found that the mini-open shows a very favorable result in the general population. This was an article we published out of North Carolina in 2015. We also have done a couple of papers and studies looking at my more elite population. This was one we presented to AOFS in 2017, basically showing that NFL players, particularly veterans, had a fairly good outcome and had a fairly high return to play once they had an Achilles tendon rupture repair with a mini-open technique. Basically, I've used a mini-open technique for the past 10 years, regardless of the size of the individual, the sport. I think it has all the advantages of operating on these people while decreasing the risks of a true open repair. I do also think it has the additional advantage of an accelerated healing time, and therefore perhaps an easier or quicker rehabilitation program as well. But, and here's what I want to really spend time on. I've seen people go too quick, and I've had people lengthen through the Achilles repair. So here's a guy that I did six years ago, and you'll see he dorsiflexes to neutral with the extended, but then he had his other side repair and had a little bit of accelerated rehab, and now he has excessive dorsiflexion. With that excessive dorsiflexion on that left side, he has no push-off strength. He has no explosion. This is a very difficult situation. This is basically an over-lengthened Achilles tendon. Here's a case example, 28-year-old NFL defense and classic mid-substance rupture, no prodromal symptoms. He had no contralateral issues, and you'll see there that he has a classic MRI with the mid-substance rupture with the retraction. He had an open technique done to repair this Achilles tendon. The surgeon elected to prep out the contralateral limb and then match the resting tension of the injured limb to the contralateral. No post-op issues, but at six months, he had significant calf atrophy, was unable to perform a single limb heel rise, had excessive dorsiflexion at 25 degrees as compared to zero on the other side. There's really no tension in the Achilles tendon. He's very frustrated, as you can imagine. His biodex showed a 65% plantar flexion deficit on that operative side, which is obviously not good. And the question is, was this inadequate rehab, not aggressive enough rehab? Is the lack of pylometrics? So we attempted three more weeks on an aggressive rehab program, but still no improvement. He'd already missed an entire season. The question is, what do you do? And this is his MRI. You'll see the MRI looks good. And that's the way these over-lengthened, elongated tendons are. The MRI looks good. There's no gaps. The tendon consistency oftentimes will look good, but they're elongated. And this is the Achilles over-lengthening that I'm very concerned about, because I've seen a number of these cases over the past couple of years. This is what I call the Dan Marino syndrome. Dan Marino, the famous quarterback in the NFL, had an over-lengthened repair and played the last five years of his career in a AFO with a dorsiflexion stop. There's not much in the literature on Achilles over-lengthening. Most of the literature will discuss failed non-operative management or missed ruptures. So there's just not a lot in over-lengthening. This is an article on re-rupture following a minimally invasive repair by Dr. O'Malley and his colleagues at HSS. But again, nothing really about over-lengthening itself. There have been articles more recently that says beware of over-lengthening, beware of elongation repair, even up to 12 months after the repair has been performed. So again, they're starting to get some literature out there that even after a good repair and a careful rehabilitative course, the Achilles tendon can still elongate up to 12 months after the repair itself. There's been a newer article by Dr. Mufuli and his colleagues in London about cautioning on an accelerated rehabilitation program for the same reason, the concern about elongation. So again, there's now concerns, particularly if you're doing percutaneous or mini-open repairs, to go a little bit slower with your rehabilitation program to avoid the over-lengthening elongation concern. So not only is there not a lot in the literature about over-lengthening, there's not much in literature about how to manage it. And that's the problem. You've got to avoid over-lengthening because there's just not a very good solution to it. Here's one article that was back in 2003 on doing a Z shortening for elongation. There's another one here in 2012 about utilizing a Z shortening type of procedure. So again, as I mentioned, I've run across quite a few of these athletes and this is what they look like. Here's the video of that person. He's got basically a horrible Thompson and he's now eight months post-op and just basically no tension in that Achilles tendon. So the way we manage this is exactly what has been described in literature. If you think have something new in orthopedics, just go back a few years, you'll find that somebody's already described it. This is one of them. This is the Z lengthening. And so you can see, we've opened that up through his old incision and you basically create a Z in the Achilles tendon. You cut through the entire thickness of the Achilles tendon, creating basically these two arms, and then you cut out the redundancy. So I excise the redundant tendon until I have maximum tension with the foot fully plantar flexed. So that's the way you want to do it is you got to be fully plantar flexed and then you go ahead and you overlap the tendon ends and then see how much redundancy you have and then cut it out. And once you cut it out, you do an end-to-end repair with a non-absorbable suture. And then I do a side-to-side repair with a PDS suture that is absorbable. And that's what you should strive for right there. You aren't going to see much of a Thompson there, but what you can see is I've got maximum tension with that foot fully plantar flexed. So that's the way we've been managing these Achilles over lengthening. Afterwards, it's a very, very important rehabilitation program with significant protection. Non-weight-bearing four weeks, we utilize BFR and other adjuvants. We do some plantar flexion against resistance after the four weeks, but we protect them in a boot with wedges to at least eight to 10 weeks. We really go very slow. It takes a long time to recover the explosiveness of these individuals, but you don't want them to over-lengthen once again. This is that gentleman. He's five months post-op now. This is his second surgery, and you can see he's doing quite well five months. But again, I anticipate it takes him a year to get back to where he could actually be competitive in his football-related activity. So the question is, why does over-lengthening happen? Well, I'm not sure, but I do think there are some concerns with the repair itself. I'm concerned when people say that they match the resting tension in the contralateral limb. I just don't think that that's possible under anesthesia. And as I mentioned before, I've never had a repair that's too tight. So I think that you need to get those repair tight. You need to put maximum tension on your repair and with the foot plantar flexed, and don't worry about what the contralateral limb is doing. I also think a concern is being too aggressive with the post-op course, particularly with these minimally invasive and percutaneous techniques. I think just like Dr. Mufuli said, it's probably better to be a little less aggressive with your post-op course to avoid a lower lengthening situation. And really, to be honest, why is there a hurry? There's not a major hurry to get these guys back. I do think, though, some of these elongations occur because the tissue is bad. You have bad collagen. And again, I think that this may be more of an issue with a mini-open approach than open approach that we'll need to follow with time. But at any rate, the bottom line of these Achilles tendon lengthenings is to avoid if at all possible. Now, Achilles tendon elongation is different than a re-rupture. Re-ruptures can happen. And unfortunately, they happen despite the technique used or the post-op regimen used. I find that Achilles tendon re-ruptures, you know, four, six, eight months out, generally have to do more with the poor tissue, poor tissue quality. Maybe it's due to a suture reaction. Maybe it's due to a low-grade infection. And for that reason, when you're dealing with a re-rupture as compared to an elongation, you may have to consider the possibility of doing a two-stage technique instead of one stage to make sure they don't have an infection. Typically, the re-ruptures will occur with a gap, but the muscle will be viable. In that regard, you need something to bypass that gap, something to bring new collagen into that area. And then the question comes up to use autograft or allograft. And there are multiple options out there. The size of the defect's not a concern because you're going to use some kind of hamstring graft in most instances, with my preference being a gracilis allograft. Just real quickly, this is the case of a re-rupture as compared to an elongation. This is a 47-year-old professional golfer who had an open Achilles tendon repair. Felt a pop three and a half months post-op. They tried to treat him non-optically. Unfortunately, he has no push-off, and he presents at six months for reconstruction because of his inability to play golf. In this situation, this is just an example, very quickly, of a gracilis reconstruction where we do a pulvotaft. We approximately, we still have excursion into that proximal muscle tendon region. And then we go ahead and we put it through a drill hole in the calcaneus and then set that tension with the calcaneus, you know, maximum tension through the calcaneus drill hole with the foot at about 20 degrees of plantar flexion, maximum tension applied. And again, you can augment that with various materials if you want, but that's our typical management of a re-ruptured case. So just to very quickly, I just want to bring this up to you all, is that I am concerned about Achilles tendon ruptures. They don't all do great. Some ruptures will recur, unfortunately, like I said, to bad tissue. But I do think we have an opportunity here to avoid some of the elongation cases. Again, making sure you tie it strong enough in the operative and make sure you don't do too much of an accelerated rehab program in an effort to avoid some of this. So again, we can't prevent all these complications, but we can certainly help. And even when we have to go back and operate, I mean, you still have to tell everybody there's a very guarded prognosis for return to sport. Fortunately, I think we'll find in the next few years, there'll be newer techniques being developed to hopefully lessen some of the risks of re-ruptured elongation, but also how to manage them when they do occur. So again, very quickly, just on that one topic of Achilles elongation and complications. And with that said, I'm going to turn this program now over to Dr. Coetzee from Minneapolis, who's going to talk about Jones fractures. Chris, I'm going to share, I'm going to stop my screen and let you go ahead. Thanks, Bob. Thanks for inviting me. It's a great panel and as usual, a great presentation. So I'm going to talk about Jones fractures and my disclosures on the website. I have nothing to disclose for this specific presentation. So this is one of the more important papers about return to play in the NFL after operative treatment of Jones fractures. And of course it's by Bob's group, so no news there. 25 players with open reduction. They used an intramedullary screw, idler crest, BMAC, and an external bone stimulator. And 100% of these returned to play and it took anywhere from eight to 10 weeks, which is obviously a lot quicker than with the Achilles tendons. But there were three refractors and we will get to that. That's part of the issue if you return them pretty quickly. So we can talk about the starting point and all this just a normal treatment for that. But everybody on the webinar should know all this. So and I can also show you all the good cases and trying to live up to the Joneses or in this case to the Andersons. But I'm going to show you the more complicated stuff. So there are some technical issues that can happen with these that can make a fairly simple operation complicated. And I think this is one of the most underestimated issues that you see with Jones fractures is the sclerotic shaft. If you look at this, this is typical in these cases that happen over slowly over a period of time and they have lateral foot pain and they complain a little bit, but there's no fracture and eventually they fracture. And you can see the reparative attempt of the body and there's this thick lateral sclerotic border. And the issue in my mind with most of the current Jones fracture systems that are out there, it's a cannulated system with solid screws. Now if you put a fairly thin K wire down that shaft, it usually bounces off or skives off that sclerotic lateral rim and it puts you in the wrong direction. To show you an example, this is a case where you can see there were multiple attempts at getting the guide wire down the shaft and you can say, well, maybe the starting point was not perfect. But the real issue is if you look at this, it keeps bouncing off this lateral sclerotic rim. And in the end, that's where you end up at. And this was an interesting case. When I eventually redid this case, the surgeon told him it will be usually about 10-15 minutes and it's quick and easy. And two and a half hours later, came out and said, well, it was a little bit more complicated. And you can see in this case, the lateral wall blew out. There's either a drill bit or a K wire that broke off there. And that entire piece is completely unstable. So how do you salvage this? In my mind, this is what I do with basically all of these Jones fractures with the sclerotic lateral wall is I take a 4-5 drill bit and basically ream out that lateral wall. No different than what you would do for a tibia or a femur fracture or something like that. And once you ream out that lateral wall, it's much easier to get the smaller drill bit or in that case, in a guide pin through the distal part and it makes a complicated problem actually very simple. And you can see where before that screw went medial to that little broke off piece of the drill, but now it's lateral in the correct position and everything went fine. Sometimes it's hard to imagine if you look at some of these x-rays, how people left the OR with a screw in place. And this was a fascinating case, because I actually talked to the surgeon, and this was his comment about it. He said, I'm confident in my ability to find the canal and I never use C-arm for Jones fractures. So my advice to him was maybe start using C-arm, it will help you quite a bit to stay out of trouble. And in fact, with all the Jones fractures, but even more important, so if you deal with these professional athletes, or high profile athletes, whether in high school or college, keep a record. I take with the Jones fracture, I do more excursion about anything else, because I want to document every step of the way. So I know afterwards I was in the right place, if something bad happens. The second technical issue that I see more often than I want to is the screw head position. So in this case, there was pain at the base of the fifth metatarsal and the cuboid, but then also increasing pain over the past few months at the distal third of the metatarsal, and we will look at both of these. So obviously, that's one issue, either due to the placement or just the configuration of the head. And fortunately, there are some of the systems out now where the head is beveled to stay away from that impingement on the cuboid, because that can be a real issue for pain management for these players, if that happens. The second is if you rotate this a little bit, you can see that the screw penetrated medially, but also almost plantarly. And it's again, I'm very serious about that one problem is that sclerotic rim, in this case, it's not only lateral, but it's also dorsal. So it forced the guide pin in the wrong position. And it leaves you with a fairly complicated problem. When I removed the screw, that plantar wall was basically broken through. So I had to be very careful with the rehabilitation after that not to create a new fracture. The next important point for me is the diameter of the screw. And this was a pretty good study, I could have a study looking at the mean dorsal to plantar diameter, but also the mean medial to lateral diameter. And the recommendation out of that was minimum 4.5 millimetre screw you should use or alternatively, the largest screw which will fit which can be a 5.5 or sometimes a 6.5. The screw choice with that is actually obviously important. So even though we try to get the biggest screw in there, you cannot put a screw in that's too big. So this is the typical stress fracture with significant sclerotic changes around the fracture. It was treated non-surgically for three months. And I want to make the point while I talk about that, I personally feel the Jones fracture in any athlete is a surgical indication. If you immobilise them long enough, without surgery, they might heal but they will refracture. If an athlete fixes it, that's the quickest way and most secure way to get them to play again. In any case, if you look at that sclerotic rim now, that's a very narrow canal that you try to get a guide pin through if you use the cannulated systems. So we had an open reduction fixation and this looks like a 6.5 diameter screw. And it broke through the medial wall. So this is now an interesting complication because that entire wall is loose. There's a big sclerotic area. And he was basically told it will heal. So just give it a bit of time. So three months later, still an established non-union. And you can see it moves a lot once that screw is out. Same there, completely unstable. And because that medial wall is still broken, I didn't think I could fix this with the screw. So I put a lateral plate on and I don't think a lateral plate is ideal. But with a large medial fragment, I had to get lag screws across that. And then eventually it healed. So this now it's nine months after the fracture was diagnosed. So you can imagine if you are a senior in high school, there's your college scholarship. Or if you are junior in college, you might not make it to the NFL or the NBA if you missed nine months out of your short career. This is an interesting article that's still quoted a lot by Chris Larson. He's actually one of my partners. And he's best known now as a sports hip and knee guy, but clearly he wanted to be a foot and ankle surgeon. That's why his most important paper ever was about foot and ankle. And it was about cannulated screws. And the short answer is don't use cannulated screws. There's a very high failure rate, 40% of the total cases failed while 83% in elite athletes. So the short is don't use cannulated screws, you will get into trouble. So what about the refractor? This again is by Ken Hunt and Bob Anderson, 21 athletes with refractors and they treated all of them with another intermediary screw, 5'5 diameter or larger. Most of them had otologist bone graft or otologist BMAC, only one with no graft. They all returned to play and there was only one refractor, which is pretty good. But again, this is we have to be somewhat careful how much bone graft you put around that because if you see something like that, that will force you to a second operation, which is likely not a big deal. So to show you a few cases, this is a garden variety Jones, seven weeks out looks pretty good. So is he ready to play? I'm a little old school with that. I still do a CT scan before I let him play. I'm not sure if it's really necessary. But I did the CT scan and it looked perfectly healed. So we let him play. And he did fine for the entire season. So about four weeks into the following season, he came off the field and said that he felt a pop. And that is pretty sure and amazingly enough, the refractor you can see there's a fracture even with the screw in place. And this is what do you do now? So the different options, you can immobilize and keep you nonweight bearing for a while, you can leave the screw and bone graft or use BMAC, you can use a bone stimulator or revision screw or a planter plate. And I think all of these are fine, depending upon the situation with a specific athlete, and what time of the season or the career. I've done a few where I used BMAC and a bone stimulator and they eventually healed, but it makes me very nervous. Most of these I will actually revise. In this case, we elected to do a planter plate and he did fine with that and finished his career. And again, let him return to play once it was fully healed and confirmed with a CT scan. This is another case also with a planter plate. This is interesting. One of my patients fractured in the second week of training camp, again, garden variety, returned to play at nine weeks, he never felt perfect. And so supposed to be re-injured in early December, I think he might have never been completely healed. But the same thing, there's a refractor that's confirmed with a CT scan. And this was two weeks before the end of the season. So he basically just shut them down and said, Okay, let's revise this. And this turned out to be an amazingly difficult artery removal that is not uncommon with these. He had very dense sclerotic bone. And you can see I had to take a fair bit of the base out to get the screw out. And in that case, there's no way that you can use another screw. So I had to use a planter plate for him as well. So that brings me to the point, what do we know about planter plate versus IM screw? And this was a biomechanical study out of Houston. And they looked at 12 cadavers. Planter plate allowed for greater cycles to failure, greater peak load before failure and less gap with load. Remember, that's not a planter plate, that's just a poor fixation. So if you use a planter plate, use a real one. The plate position is important. This was a non-union that was treated with a lateral plate, which is in the wrong position for the forces around it. You have to do a planter. This was also a paper out of Houston that looked at refractors and also primary fractures with a planter plate. And all of them heal minimum of two year follow up and no non-unions or refractors. So the planter plate is obviously fairly new on the block. And I didn't think there's enough evidence that it is as great as what it sounds to be off the bat. And there are more issues with it. It's planter, there can be soft tissue compromise and sometimes a little bit more pain. So for me, my preferred approach with the refractor is a larger screw if possible, either CrestGraft or BMAC, limited weight bearing for six weeks, use a planter plate when a screw is not indicated. So finally, what to do if the screw is broken and you cannot get it out? I've had a few of those. You can always get the proximal part out, it's near impossible to get the distal part out. In that case, you still use a planter plate, it's easy to get screws in the proximal part, you can sometimes bypass the distal screw with screws, but then extend your plate more distally to a much longer planter plate. So in the end, it's like most of what we do, you have to plan, you have to prepare and then execute your plan. Thank you. So I will stop sharing my screen and hand it to Marty. Thank you, Chris. Excellent. So Dr. O'Malley is going to discuss some of the concerns about navicular fracture and the stress etiologies for that bone. Dr. O'Malley. Thanks, Bob. I hope you can hear me. My charge is to talk about the complications of navicular fracture, which is really the bane of my existence. These are my disclosures have nothing to do with navicular. So I'll say I'll start by saying navicular stressors, stress fractures can have a poor outcome, even with optimal conservative operative treatment. These fractures can humble you. And the tumble ended up quite a number of players careers. Here's Bill Walton. He broke his navicular twice in 78 and 79. He never his next player out the same player afterwards. We know Zdrowso Galkus was out for two and a half years with navicular fractures on both sides. We know Yao Ming eventually retired because of recurrent recurrent navicular fractures that in eight season he missed 180 games. And Julian Bede missed the first two years of his NBA career with a navicular fracture and a revision. So here's a 28 year old six foot 10 inch NBA player. He landed from a jump acute ankle plane. Here's his navicular fracture, no protornal symptoms. Here he is at six weeks. Here's the three months. Here's at five months. Would anyone continue to cat scan? No. At five months we cleared him to return. He felt great returned. Eight months he rolled his ankle and they take another cat scan and he has this. Here's division one basketball player 915. So he's this is 915. This is a German case 316. So that's, you know, six months later, looks pretty healed. A year later looks healed. This is two years later has a refraction. So why navicular stretch marks? Why they occur? We know it's low blood supply. It's an area of high compression between the first and second metatarsals with the body weight coming through the body of the talus in the air of low blood supply. They all occur in the same spot in the lateral third of the navicular. The risk factors are cavus foot, adductus, ankle impingement, large size. Classification is important. Point five is the stress reaction. These are the ones we just see on MRI. Type one is one cortex, two is two cortex and three is all the way through. These are which in the, in the operating room, you feel the best about these because you can really get compression versus the type one, but these have the worst prognosis. Don't ignore the navicular stress reaction, the edema on the MRI because there's data out of 2005 that showed 7 out of 9 went back and developed a stress fracture. Treatment options have been debated, non-weight-bearing castor or boot. Joe Torg has classic article, which is great to give us awareness of the navicular stress fracture, but that's about the only utilization of this article. No CT scans utilized, only plain imaging. And he went on in 2010, the conservative treatment for all partial and complete surgery not recommended. He used most of Saksita's data out of San Francisco, and he said they misinterpret our conclusion because of fresh navicular fractures, not the ones that have sclerosis, cystic changes, and partial AVN. And in most studies, most patients it fails conservative treatment. In Saxena studies, 50% failure rate to conserve treatment. And we know that if you have a navicular stress fracture in the NFL, you're more likely to be undrafted and less likely to play more than two years. So these have big ramifications for athletes. So I'm just going to jump to my current recommendation. I think it's RF for all types of navicular stress fractures in the athletic population. At type 0 and type 0.5 and 1, I do non-weight-bearing. I think you should do percutaneous screw as minimum. I have not really seen a type 1 really heal within two or three months. Type 2, we RF bone graft with one or two screws. 3, definitely graft with two screws. Return to play with CT scan documents healing. Then we CT scan them in six and 10 weeks. And we'll get to this in a minute. Again, we'll talk about fixation, a cannulated technique with solid screws. Try and get your screws perpendicular to the fracture line. Make a small separate lateral incision for the screws. I'll use B-MEC and electrosurgery for all open cases. And I'll use an interoperative 3D imaging if available because I've put screws in some absolutely bad positions which on plain x-ray I thought were perfect. So I've gone to this for my 3D imaging. And I try and keep a soft tissue sleeve over the navicular because that way I put bone graft in there. It's not a very big hole. You cut it out with a dental pick. And so you lay the bone graft on top. If you have significant anterior impingement, I think that should be addressed as well because it probably puts more pressure at the tail of the vacuum joint. So this is the technique, the bone marrow aspirate. I get graft through the same EMCD needle. I'll pack the graft with my separate incision. Again, interoperative O-arm. These are screws that come in all different locations I see. But this you'll see, I put the cannulated wires across and I just spin it once. So if I like where the cannulated wires are, if they're far enough apart from each other, if they're parallel, if they're perpendicular to the bone, not like this, then I'll just drill and put the solid screws in. Here's a division one cross-country. That's what the fracture looks like. They like to be non-operative. The cross-country track guys get these very frequently. They're often thin. They often have a little bit of bad bone density. Some of these division one long-distance runners. Six weeks, crutches and boot, the fracture actually gets worse. We put a percutaneous screw, put a speed vac, and it's healed in 10 weeks and goes back. Two years later, it fractures the other side. Here's a 20-year-old type two. Bone graft, pack it in there. This is great. 19-year-old Olympic athlete. She came walking in with this, this fracture. I got lucky here. This was probably 15 years ago. I didn't realize how bad things could be at that point. Post-op care, bone stimulator daily. Jim Nunley taught me to get the vitamin D to 50. He had a couple of patients that did not heal until he gets vitamin D to 50. So I give everyone 50,000 units of vitamin D once a week for four weeks. And to date, we've got everyone at least therapeutic. Therapeutic means 30, which is good for usually older white women. But for an athlete, you probably want to get them to 50. We've never made anyone toxic from vitamin D. We've had some guys on 100,000 units a week just to get them to 50. I non-weight-bearing for six weeks, boot after two weeks, and then non-weight-bearing for six weeks. Get a CT scan and then start rehabbing at 10 weeks. I tell them, again, like Bob said, you can rehab at three months, but if your CT scan is healed, you can sort of return to play around four months if you're doing well. Most players go back closer to five months. So surgical outcome, yeah, nothing spoils surgical results like follow-up. I'll tell you the x-rays are pretty much worthless. You can't estimate the degree of healing, and the CT scans are humbling. So I was doing one today. I was doing a revision navicular fracture with a hand surgeon. And she asked, why are you getting a CAT scan? Because for the scaphoid, if it's 50% healed, they never get it. They'll say that's healed, and they'll never take another CAT scan. Well, if you look at this, does this fracture ever heal by a CAT scan? If you go back to an article in 1993 by Con and American Journal of Radiology, they had 55 navicular fractures. And out of that, firm cortical union in 32% by four months. So that's 68% didn't have a firm cortical union, and a gross non-union, 22%. So these things don't really heal completely by CT scan. And this is the tough thing to do. When do you let a player go back when the CT scan is not completely healed? I mean, that case that I showed you before, the two cases, those guys were completely healed, and we let them go back, and they still refractured. Jeremy and Bob showed this that a few years ago, they had 10 patients, 42 months, plain x-ray all united by CAT scan, eight of 10 reunited. And they defined healing as greater than 50% on the CT scan. Six of eight united fractures displayed residual lucency at the fractured line. So you're always gonna see, or not always, but most of the time, you'll see some little line at the navicular fractured line. And if you look at the biggest, say, Saxena in 2017, he had 11% refractures. But he didn't do CAT scans. So if you, again, for me, a plain x-ray is pretty much worthless. Because if I can see it on a plain x-ray, it's bad. It's gonna be bad on a CT scan. So management of delayed union, non-union refracture, this is what my charge is tonight. I think using a plain x-ray, again, is not really fair to the patient. I think you get a CT scan and just take your medicine. Say, okay, you have to coach the patient. When I get the CT scan, it's probably not gonna be completely united. And you're gonna probably have a persistent fracture line. The diagnosis is pretty straightforward if the patient continues to have pain. But if they have no pain, they have a worrisome CT scan, and that's really the hard part. So how do we manage these surgical non-unions, delayed unions, and refractures? Because it's a spectrum. You know, if you get a CT scan at 10 weeks and it's not completely united, is that a delayed union? Is that a non-union? Because it's only 50% healed. And if it never heals, is it a refracture? They're probably all the same, except the ones that you have documented, 100% healing, and then the refracture. So we work on the biology of it. We work on vitamin D. We work at extra bone stimulant. We do shockwave. We try to do everything we can. In the NBA, you're getting foretailed if you have a navicular stress fracture. All the teams are aware of it. Everyone's afraid of navicular stress fractures. So you'll go on foretailed if you have a navicular stress fracture, because we're worried about the players not being able to return. We've been using a little bit of hyperbaric oxygen as well. It's got good data for avast necrosis and good data on bone healing, but you're really trying to throw the kitchen sink at us. So if you look at bone stimulators, we know that ultrasound stimulation is good for fresh fractures. Electrical stimulator is good for non-union. We don't really know whether they're good for these stress fractures. We do it all the time, but it's hard to get it approved. For Aetna, they're both considered experimental and investigational for that. Foretaile, we've done a pretty good deep dive on this. We did it with the NIH through the NBA. We had the NIH people come in and talk to us about it, and they think it's a safe drug. At one point, there's a black box warning that it causes sarcoma, but we know that foretaile will cause sarcoma, increases trabecular bone volume, increases cortical thickness. And there's a number of case studies of young and elderly adults that support this for axillary fracture. Our rheumatologists at the hospital now are very much more aggressive in prescribing foretaile than they were two or three years ago for young, healthy adults. So that's been helpful for us. Sarcoma has been only reported in rats. There's no incidence of sarcoma in adults. And the black box warning was removed in 2021. So this is much easier to do. The problem is, it's a daily injection. You have to keep it refrigerated. So it is very hard to keep people on foretaile. And then the question is, how long do you keep them on? Elliot Schwartz, who just passed away recently, who really brought all of our attention on using foretaile in this fracture, recommended keeping the patients on for a year. So here's a revision cases. Here's this 21-year-old, seven foot tall, seven, two, two and eight pound player with this fracture, type two. Appropriately treated. It looked like it was going out of the union. This was in 6-14 was treated. This is 3-15. This is six, this is a couple months later. This is six months later. Looks worse. Like they had this reversed, but this is then between six and 8-15, getting worse. So he was treated with revision, open fracture. Actually, by the time we got in there, it looked a little bit better. But we opened the fracture site up. We grafted it. We do shockwave. We put him on foretaile. He had actually been on foretaile and stopped it himself when it looked good. So he stopped the foretaile after three months. And he, we also did BMAC in the office twice post-op. And now he's seven years post-op and he's healed completely. There's no complaints. But here's our guy from before who had the refracture. Eight months post-op. He's in his contract year. He doesn't really have any pain. And this is the really hard one. And you know, this is going to go bad if we don't do anything. So he wants to continue playing because he's in his contract year. So we do, in the office, we do Percutaneous Augment Injection, just the fluid from the augment twice. We put him on foretaile. He does shockwave. He finished the season. He got a new contract. This is his most recent CT scan. He filled in the top and he's now been four years symptom-free and just finished playing in the playoffs on one of the teams. But our go-to really is the vascularized bone graft. This is, Jim Nunley taught us how to do this. It's really taking a vascularized graft from the cuneiform and with a vascular leash. Again, you get a vascular network where the flap will be harvested. I do this with a hand surgeon. It's interesting. I talked to Jim Calder in Europe and he said he was going to, Nunley was supposed to come over. Jim Nunley showed him how to do it. He had a player and he couldn't come over because of COVID. So he tried it himself. And he said that he is going to this more and more as a primary treatment. Taking a little flap, vascularized piece off the cuneiform, rotate it back and put it on top of the navicular for these fractures as a primary treatment for his soccer players to get these navicular stress fractures because he was having such lousy results but he's doing it himself. So you dock it at the fracture site. I use that nice boat. We don't screw it in. I use the soft tissue covering it over to hold it in, lay it in the void and then cover it. Here's some cases. You get a nice graft incorporation here. Here's a six-year-old football player. These are the worst with the osteochondral lesions and the fractures. They had screw fixation somewhere else. We went in before. In my experience, often the cartilage is still intact at these. So I went in behind the fracture, took the screws out, go on top. We packed bone graft down there. We packed the vascularized graft in there as well. And we got him to heal. He's now playing in college. This is four years later. He hasn't been seen back. Here's another elite marathon. Again, this is screws going medial to lateral. So you can blame the screw placement. Didn't get very good fixation with some threads in the fracture site. We redid it, the vascularized graft. And I think he's hanging on by this small thread of bone and holding the bone together. Here's a osteochondral lesion with a stress fracture. This is an almost impossible task. He gets screw fixation for the navicular stress fracture. And he goes on and heals, plays over the summer. Then he refractures. This is one of the cases that all of us will talk about. Bob, Chris, and Dave and I will talk about this. And here's his fracture line and the osteochondral lesion. He got a revision of the vascularized bone graft for the medial cuneiform. Again, we put a laminar spur on to actually look, hinderment to look at the carotid surface. It looked shockingly good. We use a 3D window. We packed it behind it with counterpressure. This is the wires going in, and this is our 3D interoperative imaging to confirm we're in the right place that we didn't put bone into the tail of the vicar joint. And this is him afterwards. I mean, it didn't come in all the way together, but he got a good dorsal bridge on it. The joint itself looks okay. He, six months playing, he played his entire senior year of college, Division I, made it to the NCAAs, and is no longer playing. I actually saw him, and the CAT scan is actually pretty much the same as I saw him recently. He came in for his other ankle, and his CAT scan looked shockingly good. AVN, we see parts of this, and this is probably more common than we've seen. We probably get parts of AVN in a lot of these fractures. Here's a guy. We left the vicar stress fracture. He had a little bit of a line. NBA player. This is the kid who I fixed his other side in 2016. Normal bone density. He healed fine. This is his technique, two screws. Can't see the fracture. Here he is at two months post-op, four months post-op, six months post-op. Looks fine. I think everyone would agree that you would let the player return. He starts working out. He comes in with this. Multiple new fracture lines, sclerotic bone. And in questioning, he had been given steroids for a dermatological condition. He'd been on steroids for about three weeks. He had a big swollen foot. So what do you do with AVN of the navicular after you've fixed it? So we know that osteonecrosis for low-dose oral steroids, it can occur, can cause AVN. Actually, it's usually normal. So for him, there's not much out there what to do. We think AVN occurs. There's three theories. One is lipid metabolism, where it panic-fast, and he gets fatty amyloid. The other is hypochondriacal state. The other is a direct effect on the bone. But you have to think it's low blood supply. So foot and ankle specialist came out in 2021 with June with therapies for AVN, rheumatologic therapy, weight-bearing restrictions, physical therapy, shockwave hyperbaric oxygen, and acupuncture. For this player, we put him on boot and crutches, put him on Forteo. We did bone simmer. We did do hyperbaric oxygen. He mostly got it in Indiana. If anyone knows me, lately I'm kind of addicted to hyperbaric oxygen for my players and my patients. There's good data on femoral head necrosis for fecal stage one and two. There's good data for femoral condyle necrosis. So there's a lot of good data that have been done, randomized control studies on hyperbaric oxygen for AVN. So I think it's a low risk, high reward situation. And these hyperbaric chambers, they're all over the place. You just have to look for them. You never know they're there. And I will just caution you, the low, the mild hyperbaric goes to 1.3. These are the 10th. They won't really have an effect. It's gotta be a hard chamber and you want to get to mostly the two atmospheres. So here he is 10, 21, still has some bad looking bone. We didn't do anything except these biology for this. And here he is in three, 3, 22. He's pretty much healed. Maybe he's got a little residual line over there. This is his 3D imaging, but he's formed new bone. He clearly has gotten better than this with these fracture lines and the white scrotum bone. So was it the foretail? Was it the hyperbaric? We don't really care. At this point, we got him the bone healed. His foot feels good. But it is, if you look at this date compared to where it started, that is 14 months from the time he injured himself. It is a huge amount of time out. So complications of the vicarious fractures, worst ones to treat, clinical healing. You have to use a CT scan and you have to be honest with the patient. And you tell them about it beforehand. Just tell them the CT scan may not be completely healed when we get it. If we go for 50% healing and you have no pain, we'll probably let you go back. I'm very early for the biologics, for a foretail, especially in the elite athlete. Hyperbaric is not that well-studied, but I think it's a low-risk addition. Bone stimulators don't have great data, but we do them anyhow. But I think you have to work on the biology of this. Thank you. Thank you, Marty. That's great. Very complete. The audience should all have a special respect for the vicarious stress fracture, that's for sure. If they can look great and suddenly they don't look so great. So we will get to your questions. If we can't do it online, we'll do it privately afterwards, as was mentioned earlier. Without further ado, Dave Porter's going to present to us the medial ankle issues. Dave from Indianapolis, please go. Let me unmute, there we go. Is everybody seeing that OK? No, we still see you, Dave. OK, sorry. Okay, since it's failing to start, here we go. You see it now? Yeah, that's perfect. Thank you. Okay, all right. So disclosures, I want to talk about medial ankle sprains and mainly this is a little less about failed surgery and a little more about recognition. These are very high energy injuries and I think they're oftentimes confused because they're thought to be somewhat rare but actually they're not quite as rare as we often thought. So I'm gonna talk a little bit about the acute sprain, what to look for, how not to miss it, a little bit about a misdiagnosis and then lastly, I want to talk a little bit about something we're seeing more common which is global instability or combined medial and lateral ankle instability. Again, we have always been taught that about 1% of ankle sprains are medial. However, when you have up to 75 to 85,000 ankle sprains a day, 1% of those are medial ankle sprains. That's up to a thousand medial ankle sprains a day. So we really have to be prepared to identify these. We need to be able to see it correctly and it's presenting itself to us a great deal. The sports in particular that I've seen at the most in this football, gymnastics and basketball but even this two weeks ago, I saw one in a high level track athlete. One of the things we have to understand is the deltoid is a very thick, strong ligament. So in order to rupture the deltoid, it really does take a fairly violent injury. We don't know for sure, but there's somewhere around 10 to 20 times the force to tear the deltoid versus the small kind of thin, wispy lateral ligaments. One of the reasons is because most people have a very valgus hind foot and so the medial side is the tension side and therefore one, if you rupture that ligament, the disability that occurs with it is really high because of the tension and the inability to keep the foot out of further valgus. The deltoid is a fairly complex ligament, much different than our lateral ligaments also. You have the anterior deltoid, which goes and attaches to the navicular and really involved with external rotation. Then you got the rest of the deep deltoid ligament, which is more for abduction stress and all this is incorporated into also the spring ligament. So it's a complex ligament set we have over there. As it seems obvious when you're talking on a webinar that the pain is primarily medially, but sometimes we just get overwhelmed by patients who come in who have an ankle sprain and we see the lateral ankle sprain so often, we don't maybe spend as much time or not quite as adept we are with being close and detailed with their exam. The ecchymosis is much more medially like you see here and you see this is much more medial ecchymosis than you would see with just a lateral ankle sprain. On exam, you kind of see just this lack of end point. You don't always see as much instability itself, we just see a lack of end point and significant pain with abduction stress. Again, you'll have more medial swelling than you do lateral swelling. Again, it's usually some type of a pile up in football or someone landing on the heel from the back, awkwardly in gymnastics landing short with the ankle and dorsiflexion, then an eversion or in basketball as opposed to the medial side of the foot landing on the other ankle, so lateral side of the involved foot landing on someone else's foot and causing a significant eversion injury. We miss it, I think often because the plant x-rays are often normal. You just maybe see some soft tissue swelling or a chip fracture on the tip of the medial malleolus, you really have to be suspicious for a medial ankle sprain. I think this is a time where advanced imaging is absolutely critical. I wanna show you just a little bit of the difference between what you might see with a lateral ankle sprain with medial impingement, where you have signal in the deltoid, but you see the striations of these deltoid very normally, even this portion of the ligaments going from the medial malleolus down to the sescentaculum tali. Then counteract that with a medial ankle sprain, you see this huge disorganization of the medial deltoid ligaments and how that ligament has been almost pulled off the medial malleolus where it was attaching to the sescentaculum tali. Another, again, on this plate x-ray, sometimes the only thing you'll see is just significant medial swelling, but that has to be alarming to us and give us a really clue this may something more than your typical medial ankle sprain. I think I've really found a lot of benefit in the stress x-raying. Sometimes I'll do injection or just local anesthetic only into the ankle to give them a little more pain relief to allow them to do a little better stress x-ray. And here you see just a significant tilting of the talus with a abduction stress. This is one of our high school athletes who's playing a slot receiver, he's doing kind of like a jet screen and you'll see him coming down here, getting ready to go into the end zone. And as he starts to advance, he gets toppled and does a complete flip, which is there. Now watch this and look at his left ankle and you see him land dorsiflexion and eversion, which is just a classic injury. You see how violent that injury is too. The only thing you really saw in his x-ray is a little bit of medial swelling. You saw just a little bit of calcification here in the anterior ankle. He had a lot of swelling medially, no syndesmosis, tenderness, bruising was much more medial, and then a little bit of kind of a soft endpoint of abduction stress. He couldn't walk well, he had been placed in a boot, he was diagnosed with an ankle sprain by his athletic trainer and by the primary care physician who was there at the game. However, when you got an MRI scan, which he was, again, suspicious based on exam, you see this complete disruption of the deltoid. His syndesmosis was normal. You can see that same ligament that goes down to the sescentaculum had been completely ruptured off the sescentaculum. And then what was really worse in seeing this structure here on the sagittal views, which was concerning for some type of loose fragment. Now, how do you treat these? You know, there's been some evidence in the past where you can do cast immobilization and go into some type of a, or customized brace. But I think we're seeing now in the more recent literature that it's a lot more important to be more aggressive with these. Certainly in this situation with the condor injury that he exhibited, we want to be more aggressive, certainly with scoping ankle, assess the cartilage, and then see, we can see here in this X, the scope image on the left, this AITFL was completely intact. Yet when you come over to this right hand side scope picture, you see that the D deltoid is completely ruptured and the anterior deltoid is completely ruptured. And you can see he's grossly unstable. So in this situation, again, we scoped and we saw that condor injury, you can see this very large condor injury that came off actually the distal tibia. We're able to take a little bit of the spurs off the front, reduce the size of it, but there's just not enough bone on here in order to be able to repair that cartilage. So we actually had to remove it, removed a little bit of the distal tibia, which decreased the size of that condor injury. You can see the post-op x-rays show complete resolution of that bony area. We did a anchor in the medial malleolus, also did an anchor in the talus, so we can keep his talus in the correct position so that we can then be very aggressive with his range of motion because of that condor injury. We had a non-weight bearing for four weeks because of the condor injury, biked it two weeks. He played basketball at four months, played his senior year of both basketball, baseball, and football, and went on and played a baseball scholarship. This is him at 14 months, and now he's at 30 months. He's having no complaints. Unfortunately, that condor injury hasn't seemed to be a problem for him. Next, I want to talk a little bit about how, again, it's just easy to miss these injuries. This is kind of an awkward situation. He was a 22-year-old NBA Summer League player. He had a quote-unquote ankle sprain, landed off on another player's foot. In further questioning, he said it might've gone into eversion, but he's not really sure, but he did have ecchymosis and pain, which was medial. He was evaluated there by the team physicians and the Summer League docs, and they felt he just had a lateral ankle sprain. Treated him like a lateral ankle sprain with just an ASL brace, an MRI, and rehab. I was asked to see him. He was on the West Coast. I couldn't evaluate him. They just said, he's probably looking at his MRI scan. A lot of us get these kinds of situations a little bit awkward. I saw the MRI, and when I looked at that, again, you can see laterally, there's some concern for the ATFL and the CFL, but then when you look medially, it really looked like he has a complete deltoid rupture. So, you know, you communicate back and say, are you sure this is not a medial sprain, not a lateral sprain? They said, no, I think it's a lateral ankle sprain. He continued to play the rest of the season, but just didn't play well. And as often happens, he was still struggling at the end of that summer league, came in, reevaluated. His stress imaging, you can see he's got significant instability immediately. His lateral ligaments were fine. He had already signed to play in Europe. He didn't want to have surgery. He was adamant against it. And I was certainly very concerned that just trying to treat this non-operatively, but the only thing I could think of is we could try a cast, see if we can cast him for up to four weeks and get this partial ligament healing that was occurring to heal completely. And he really wanted to try that first. So we did a really good molded short leg cast, put him a little bit of plantar flexor inversion, molded the arch and had him brought him back in two weeks, took the cast off, reexamined him and restressed him. And it wasn't perfect, but it certainly looked like he was actually doing relatively well. Recasted for two more weeks. He then played about eight weeks after that. We used a short articulating AFO just for the training purposes and then had him use a stirrup brace and some heavy taping. And he's actually done very well, played the whole season. I think we got a little bit lucky there, but it's just another thing to say, these can get missed at all different levels. Lastly, I want to talk a little about global instability, combined medial and lateral instability. This was a kid from Illinois. He had two seasons in one year. So they, because of COVID, he has his high school season in the spring of his sophomore year and then had his junior season in the fall. In the sophomore season in the spring, had a quote unquote high ankle sprain. They felt it was stable. He just missed one game, but he was not able to play really up to par, favored the ankle a lot, played the fall season again, played basketball. He didn't feel loose. He said, it just hurts on the inside of my ankle. He just played with the brace and taped. And this is his MRI scan. And you can see in the more posterior part of the deltoid, it doesn't look too bad, but the anterior deltoid, it really looks pretty disrupted. He's got edema in the tip of the medial malleolus. He had on exam, on x-ray, some spurring, some calcifications in the deltoid and was a high concern that he had a loose medial-sided ankle. Therefore, we took him to surgery. His planning was to remove the spurs, do a brostrum of the deltoid if able, or do a more substantial reconstruction. We assessed his medial side and certainly looked unstable, medially. Not severe, but you can see, he certainly opens up medially with external rotation and abduction. What was surprising is on pre-op exam, he really had a kind of an anterior joint that was abnormal. His tailor tilt did not feel that bad, but when we got him under anesthesia, you can see how loose he was laterally also. So what you can see is these elite athletes can really compensate even for very significant instability. Now, this guy was just a tremendous athlete. He's going to be a Division I athlete, and he was able to play at a high enough level against his competition and compensate. But I think we just have to recognize that there's more of this global instability that occurs. The time of surgery, you can see he completely pulled his anterior deltoid off the tip of the medial malleolus, but his tissue was very good. So we really thought we could probably do a brostrum of the deltoid. We did a suture anchor in the medial malleolus, did a trough, brought the deltoid back up into the medial malleolus with good permanent suture and absorbable suture, and then went laterally and also reconstructed laterally. This is his perineal tendons. We put a suture anchor in the fibula. You can use a suture anchor in the tip of the fibula, or you can do it through drill holes, whichever you prefer, and stabilize it both medially and laterally. Sometimes, you know, if you've got really poor tissue, medially it's too chronic, there's pronation deformity. You can't really rely on just a brostrum of the deltoid. You have to bring in other tissues such as this with some type of allograft material, which is my preference. But what we're recognizing is that some of these athletes with global instability, you'll recognize the lateral instability, then you'll do a lateral reconstruction and they fail. And we've always known that, you know, varus alignment or ligamentus laxity can contribute to lateral ligament reconstruction or failure. But now I think we're seeing this concurrent chronic medial instability with unrecognized deltoid lesions can lead to failure of what otherwise would be good results for lateral reconstruction. Hinterman has done a lot of work on this. There's several different studies which looked at concurrent medial instability with chronic lateral instability, and both arthroscopically and examining under anesthesia. And when Hinterman did his study, 20% of the time he could never even pick up the instability except at the time of surgery. I think we just have to be more aware of this and be more conscious of this looking at when we're doing lateral reconstructions that there may be concurrent medial instability. I used to not kind of be a believer in this, I think, but over the last five to six years, I've just seen this more and more. And just in the last two and a half to three months, I've had to treat four competitive athletes, two in football and two in basketball with this global instability. So medial ankle cramps are not rare, especially for those of us who are doing kind of sports foot and ankle clinicians. It's missed and underdiagnosed commonly. Chronic medial instability is much harder to treat than chronic lateral ankle instability. So we got to make a correct diagnosis, the correct treatment. If you can do that, you can really have good results and just be aware that global instability does exist and really look for it more. So thank you very much. Dave, that's outstanding. And I did want to reiterate what you just said is that if you've got a failed lateral ankle reconstruction patient, just look back at them again closely to see if you've missed medial instability. Because I think as Dave mentioned, they can go hand in hand and failed, failure to recognize medial instability can lead to your failed lateral ankle reconstruction. That may be the value, as Dave said, it may be the value of putting a scope in on these patients at the time of index surgery just to make sure they don't have a combined instability pattern. We're up against our time limit. We only have one question. We got a couple of minutes, Marty. I'm just gonna ask you a quick question that came through. And that's, how do you use MRI in your evaluation of navicular stress fractures or AVN? Do you use an MRI? Do you, I assume you use it to differentiate a stress reaction versus a stress fracture where you then include a CT scan, but is there a way to use MRI to determine whether you have a true AVN? That's a great question. I think once you put screws across it, MRI is almost impossible to use, even if you use titanium screws versus steel screws. So we've MRI'd this case that I showed with the AVN three or four times. We can't really see anything with the MRI once this surgery is done. Preoperatively, clearly there's some players who have the AVN OCD at the dorsal cortex of the navicular. And I think that's, I think the MRI is an excellent screening tool for the athlete with ankle pain, because most of these guys do not have severe ankle pain. Mostly it's, you know, vague ankle pain. If you have vague ankle pain in the NBA, everybody has that after a game. And so MRI is a great screening tool, but a CT scan is how I visualize it. If I see something bad on the MRI, I still get the CT scan. Great, we got another minute. Let me ask you guys a question that came through after my talk, and that's, I'll ask you a question in a little bit different way. When do you use an FHL transfer to augment your Achilles tendon reconstructions in an athlete? So Chris, you got Achilles tendon over-lengthening, you got Achilles re-rupture in one of your athletes. When do you use an FHL transfer or do you? I think realistically in that situation, it's very seldom that those people will return to play. If you can get them fairly early on, and so the first six months or a year, I will just do a shortening like you showed. If it's more than a year out, I don't think the muscle itself is good enough to get him where he wants to be. And then you either tell him we'll shorten it, hope you get strength back, but otherwise do an FHL as well. Dave, if you do an FHL transfer in one of your running athletes, do you tell them they're going to notice it when they return to running? You know, I would agree with Chris on that, Bob. I try not to do the FHL transfer in my competitive running athletes. I like what you said. I do the gracilis allograft, and I think, you know, one of the things that's nice about Achilles is Achilles wants to remake itself, and I think you made a really good point. The tension and the length is the critical part. If you can span that gap with an allograft and get things in continuity, I like that better because I just think anything I can do to support the push-off, and I think the FHL on the big toe is just better left on the big toe, and I find another source in my competitive athletes. Non-competitive, it's a different story. Great, great. And I know we're right up against the time, but I got to quit in just 10 seconds, but one last question came in I'll probably answer for all of us because I can reiterate what Marty said, and that's, do you scope when you're fixing the vicarious stress fracture? You scope the ankle, I should say. And I haven't been inclined to do that because I'm concerned about impingement lesions, and Marty, I think you mentioned that, that you got to be careful of anterior impingement syndrome in association with the vicarious stress fractures. That might be a biomechanical reason you're getting the stress on the vicar to begin with. So look for those anterior impingement lesions and remove them, either arthroscopically or through many open techniques. And I think that's just to reiterate what Marty was pointing out too. And that, guys, we're up against it. I want to thank the faculty so much. These were fantastic talks. A lot of tips, a lot of pearls. I look forward to going back to the archive webinar and learning more, just listening to you guys further. So thank you, everybody, for tuning in. Thank you, faculty. You guys have been great, as always. Thanks, Bob. Thanks, everybody, for tuning in. Really enjoyed it. All right, take care. Thank you, guys. Thank you.

navicular stress fractures

CT scans

diagnosis

fixation

screw placement

bone stimulators

hyperbaric oxygen therapy

medial ankle sprains

global instability

deltoid ligament

surgical planning