On behalf of AOFAS, I want to welcome you to tonight's webinar, Why is the foot still turning in after surgery? Tonight's moderators are Drs. Greg Guyton and Glenn Pfeffer. Joining them are Drs. Bruce Njorzian and James Brodsky. You can find their full biographies and disclosures, as well as disclosures for program planners, in the program document posted in the chat box and in the AOFAS on-demand education center. 2023 webinars are provided free to AOFAS members and orthopedic residents, fellows, and medical students with funding from the Orthopedic Foot and Ankle Foundation, supported by a major grant from Stryker, and additional funding from Arthrex. To support education programs like this, make a donation to the foundation on our website, or by texting GIVEAOFAS to 41444. I'd like to run through a few housekeeping items before we kick off presentations. For technical difficulties, please try closing your browser and logging back in the same way you did the first time. 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Space is limited, and this meeting has sold out for the past two years. I will now turn the program over to Dr. Guyton to begin. Well, good evening, everybody. Welcome to the webinar tonight. This is a terrifically complex topic, which we're going to try to work our way through in about an hour and a half, and hopefully leave a little bit of time for questions. That's a challenge. My fellow panelists really need no introduction. Bruce Sanjorgin is going to start us off with his protocol for how to deal with the cavus foot, both how to deal with it and how to deal with it, what he's learned when things go wrong. So, Bruce, I will turn it over to you to share your screen. This is a brief algorithm for my approach to cavus foot, and it's based on all the things I've done wrong in the past that led to an incomplete reduction. I have no conflicts. The term cavus, cavoveris, cavocoenoveris are all a little bit complex sounding, but really the part that matters the most is does your heel hit the ground in a neutral position at heel strike, and as you rise up to toe off, does it stay balanced? Those are the only key issues. The clinical complaint are instability and overloading of the fifth metatarsal. So, the goals of surgery are number one, two, and three, correct the heel varus, get the heel in the plumb line. That will increase the stability and decrease the adduction thrust, and ideally rotate the forefoot so that the overload of the fifth is corrected, and the abduction is corrected. But you can only truly rotate the forefoot if you fuse the subtalar joint. If not, you have to do something compensatory. So, the most important point I think tonight from my standpoint is recognize that the subtalar joint itself needs to be corrected, it needs to be shimmed, it needs to be realigned, and most importantly the calcaneus needs to be translated laterally. In the severe cavus, but you can't get enough correction unless you translate that heel laterally. So, how do you correct the heel varus? If it's easy peasy, soft tissue release, simple lateralizing calcaneal osteotomy. If you need more than a centimeter and a half coronal plane correction, then you have to go to a triplane osteotomy or a subtalar realignment infusion. And sometimes on top of that you have to use a supramalleolar realignment osteotomy. So, to unwind the talocalcaneal position that allows you to correct the varus and the forefoot at the same time, that's done through repositioning of the subtalar joint. It allows dorsal flexion of the medial column without an additional osteotomy or treatment. But if the patient's too young and you have to do a compensation, you can't fuse the subtalar joint, then you can correct that forefoot through shortening lateral column or a cuboid osteotomy. So, think back to the original. So, left, middle, and right are a flat foot, a neutral foot, and a cavus foot. In green, the talus is on top of the purple calcaneus. And as you look at the front of those models with the, this is a weight-bearing CT with the forefoot removed, you can see that that talar head is right on top of the cuboid, or I'm sorry, right on top of the calcaneus, or more correctly, the calcaneus is right under the talar head. That forces the navicular up on top of the cuboid. So, the only way the medial column can get to the floor is by hyperplanar flexing and twisting a little bit. If you put the forefoot back on that same patient's diagram, you can see how that navicular is on top of the cuboid, and that's forcing everything in front of that to be out of position. And you can do that on your own on a plastic model. It just rotates the calcaneus under the talus and the whole medial column goes up. So, step one of the algorithm is to correct the varus, figure out how to correct it. And I know Glenn's going to talk about motor imbalance, so I won't spend any time on that. But first, find out, is this a forefoot-driven cavus or an intrinsic hindfoot varus? You can use all the standard imaging to help, but clinical exam is kind of critical. So, you can do a Coleman block test. If this is forefoot-driven hindfoot varus, then a Coleman block test will allow the hindfoot to correct into a neutral position. You can do it this way with the lateral border, or probably more correctly this way with everything but the medial border on. In this case, the hindfoot is in completely neutral alignment because the forefoot plantar flexion has been neutralized by the block. And this is what it looks like when it's truly forefoot-driven. You can see how prominent the first ray is. The peroneus longus is driving that down. It's way too strong. And again, on this wireframe model, you can see that most of these first metatarsals are not only plantar flexed, but they're translated plantarly on the cuneiform. So, keep those in mind when you're doing it. So, a mild, this one is a mild forefoot-driven case. There's a little bit of an angle on the Mary's line. You can see a little bit of plantar subluxation on this first tarsal metatarsal joint. But the midfoot's not too rotated. A simple dorsiflexion of the first ray and lateralizing the calcaneus was enough to correct this one. This one's slightly worse. You can see that the midfoot is much more angulated. There's more torsion there, meaning the navicular is more dorsal to the cuboid. But again, this can mostly be done with soft tissues and a little bit of bony work. And don't underestimate the power of the soft tissues On the top, you can see where that first metatarsal is going after we have moved the heel over. On the bottom, you can see where that first metatarsal is after we've moved the peroneus longus to the peroneus brevis and done a small plantar fascia release. You no longer have to do anything to that midfoot because the soft tissues are neutralized. So, the three parts to fixing major cavus is, one, derotate the subtalar joint. That corrects the varus and unlocks the metatarsal. That corrects the varus and unlocks the midfoot. Two, dorsiflex the midfoot on the hindfoot and find out if you still need to abduct the forefoot when you're done. So, when the dorsiflexion is not enough and the calcaneus is not enough, you have to go to more significant steps. These slides are not supposed to be showing up here. So, the cavus foot is defined by Mary's line, but the foot shape is primarily driven by the talocalcaneal relationship and the bone morphology like we just talked about. When you look at the AP position with this talus on top of the calcaneus on the right, you can see how that's rotated the whole midfoot. So, you have to determine the contribution of the shape of the bone itself. And I'm sorry these hidden slides are showing up for some reason. So, a varus heel that's fixed, you have to move the heel. That's different than a varus heel that's part of planar first ray. Subtle cavus is something Art Manoli used to talk about, and that can be corrected often with just soft tissues. Dynamic varus is a moderately new concept that's been around just for about 10 years, but we'll talk about that in a moment too. So, let's look at the medial column. Here's the medial column. Here's the lateral column. Here are the same things from the side, straight Mary's angle. Here's a neutral foot with all the bones put back together. And here's a pseudo-recreation of a varus foot where we've rotated the calcaneus under the talus. And you can see on the computer model, the third and fourth metatarsals just get superimposed, but that's not what happens in the real world. So, in this complex model where the hind foot is intrinsic to the varus, look at the shape of the calcaneus. You see where the plumb line's coming down from the tibia, and you can see that the calcaneus, even after it leaves the surface of the talus, is bent into a position of additional varus. The varus can also come from above the ankle. This is usually fairly straightforward. This one we managed. The patient was eroding the medial malleolus and was unstable. We managed this by doing an inverted dome osteotomy, tipping it into valgus. The nice thing about this approach is that it heals quickly. It's very stable, and you can just keep dialing the correction until you have what you want. On the right is the patient six months after surgery where she has reconstituted that medial gutter. These are the ones that are really problematic. So, on your left, you see a subtalar axis of a flat foot. On the right, you see the subtalar axis of a cavus foot. You look at the axis of that cavus foot on the upper right corner and imagine where the plumb line is from that axis. So, you know that that heel is not going to ebert. It's only going to invert. And when you want to correct this, that red line on the talus shows where you need to shim bone. You have to actually take your saw, remove part of the lateral process, and then free up the medial soft tissue so you can translate that calcaneus and move this edge of the calcaneus all the way to that edge of the talus. It's a long way. It'll correct three plus centimeters of hindfoot misalignment. And this is just that morphology once again with a line showing, sorry, what you want to do is turn this cavus subtalar axis into a neutral axis or a planus axis where that line of the subtalar axis drops a plumb line straight down to the floor. So, intrinsic avarice like this one can also be managed by a triplane osteotomy. This is the technique Malerba described. This allows you to tilt as well as angulate. So, you can get three plus centimeters of correction with this one too if you can't go at the subtalar joint. So, here's another shim line. Here's the patient's lateral CT. So, on the left, you see where his standing ankle view is. The red line represents where the calcaneal wall should be. And on the intraoperative photo where we've pinned it, you can see that that same line actually goes through the substance of the calcaneus because we've translated it. And this also corrected the talocalcaneal angle on the AP view because we pulled those two apart. So, here's that patient at three months with a corrected hindfoot position. There's bone under the fibula now. And here's the pre-op plan. And here's the alignment. Here's the three-month view. And here's the clinical view. So, we did the left side first because that was the more severe avarice. And you can see how much correction we got simply from repositioning that subtalar joint. So, we've talked about this morphology already. And the twisting midfoot corrects when you realign the talocalcaneal position. But in a young patient, you can't do that. You can't sacrifice that subtalar joint. So, you have to do something to compensate the midfoot to get that fifth metatarsal up off the ground. So, if you can't unwind it, like you can look to see what the elements are that's keeping that long. On your right is a coronal weight-bearing CT showing the navicular trapped entirely on top of the calcaneus. And this is a 20-year-old football player who's had recurrent stress fractures of four and five. So, we can't give up a subtalar joint in a 20-year-old. So, we have to get our correction distal to the subtalar joint. We can move the heel over to correct the varus. And in this case, we shortened the cuboid. We did an inverted cuneiform osteotomy of the cuboid that took more off at the top than at the bottom and took more off laterally than medially, so that we could shift the midfoot laterally and shift the distal segment dorsally away from the floor. Here's the post-op view. You can see we still haven't changed the arch, but the fifth metatarsal is no longer driving down on the floor and the forefoot is abducted. So, this is the pressure mat you see on the far right with these severe cavus feet where all the weight is on the fifth metatarsal. And correcting the hindfoot varus doesn't fix that. You have to get that midfoot up and you can either do it through the cuneiform or through the end of the showparts joint. So, I mentioned dynamic varus, which is a more subtle problem. This is a patient on the upper left who has had multiple recurrent ankle sprains, has failed an arthroscopic ankle ligament repair than an open ankle ligament repair. He continues to get stressed. On the right, I am trying to evert his hindfoot. That's maximum eversion. So, he has no varus when he stands, but he has very little valgus. I think I'm going to play a video here. I hope I'm going to play a video. Let's try it again. This video I hope will play because it's worth looking at. So, here he is in maximal eversion. He inverts about 45 degrees and everts nothing. But when he's standing, he does not have a high arch and he does not have valgus. So, this is a dynamic varus because the alignment of the subtalar joint is off. This is a relatively simple fix. That is, if I could get the slide to advance. This is just a simple calcaneal osteotomy combined with repairing the ligaments. I'm skipping through these because they're marked as hidden, but for some reason they're coming through. So, one thing that can trick you is a fake Mary's line. So, the foot up on the left is a lateral view of the foot. It makes it look like the talus is off because the foot's so abducted the x-ray tech has rotated the cassette. So, that's the patient post-op showing the ankle's actually just fine, and that's just a fake finding. So, this is just a pseudoposterior. So, one more soft tissue, a little throw-in for soft tissue. This is a patient we've corrected again and then moved the peroneus longest to the peroneus brevis, and this highly plantarflexed first ray comes up to a neutral position without any dorsiflexion of the medial column. I'm sorry, these are supposed to be blinded. So, you can also correct that forefoot through the calcaneal cuboid joint. Here's a patient, again, very young but with severe cave ovaries, overloaded fifth metatarsal. You can see that Mary's AP talometatarsal line is about 50 degrees off. The forefoot is completely twisted. Here's the CT showing the angle between the calcaneus and the cuboid also being off. So, we can't give up the subtalar joint, so we can pull the cuboid laterally to the calcaneus, and that unwinds the midfoot so the navicular can come down a little bit. This is the post-op at three months, and the lateral at three months. So, this adaptive morphology is the most important part of causing failures, my own and patients that I see. So, when you're fixing a severe cavus, if you can fix, if you can give up the subtalar joint, get that wedge out of there and use your cob elevator to pull the calcaneus laterally from under the talus, and that'll unwind the midfoot. In this particular case, that even wasn't enough, so we had to do an opening, had to do an opening wedge of the tibia above that plafond. So, the summary is internally rotated subtalar joint with the calcaneus under the talus prevents shock absorption, creates varus and instability, and it rotates the whole midfoot. And the varus midfoot balance forces the patient to balance on the lateral side. So, number one, two, and three, get the hind foot varus corrected. Secondarily, make the forefoot meet the floor. And I'll leave it at that. Thank you. Greg, I think if I go next, it'll follow very nicely from Bruce's talk, if that's okay. Can you hear me okay? Yeah, here we go. Sorry, I've had a lot of people concerned. I've had a power outage at my house. I'm not doing Halloween. So. All right. Well, you still shine through. Bruce, I have a question, Bruce, myself. Vince Moskow and I, Vince, you know very well, he and I have talked about this a lot and he'll make the point, and I don't know the answer, that you really can't correct that transverse tarsal joint by doing a cuboid shortening because the axis of the cuboid shortening is distal. You understand this, of course. And he's always saying, you really have to fuse the CC joint, which is essentially shortening the lateral column. How do you decide? So I agree that you can't change the midfoot. So I use that when I'm unable to include the talocalcaneal fusion. So it's an adaptive change. It's not a correction like a subtalar fusion is, but I just don't feel comfortable doing subtalar fusions in 20-year-olds. But I agree, it doesn't change show parts. It just gets the fifth metatarsal up off the floor where it's causing pain. And these patients that you're showing, do you think they all have CMT? No, I was going to leave the CMT concept to you to discuss, but certainly some of those did. It's interesting. You know, there's a lot of people say that all moderates of your cavus is from CMT. All right, I certainly don't know the answer. Let's see if I can do this. I'm sharing the screen. Yeah. And let's see if this works. Do you see my screen? Yes. Okay, good, thank you. Let me get rid of this. Who can see? Okay, good. Well, good evening. I'm going to talk specifically about recurrent problems with Charcot-Marie-Tooth disease. But again, maybe all moderates of your cavus is from CMT. If you're interested in this topic more, a very nice review was just published by Eddie Haupt and my previous fellow and I in JAOS. And I would also point you to the published 2020 consensus statement that all of the panelists were on. And we owe so much to all of them for their understanding of CMT. I think I was reading Bruce's papers when I had no idea what he was talking about. So I have no disclaimers. I'm on the Medical Advisory Board of the two large CMT organizations in the United States. Now, you'll see that Bruce and I approach this differently, I think, in some ways, but there's no right way of doing it. There are hundreds of different variations. If you think of all the necessary steps in a cable varus reconstruction. I'm basing what I'm talking about on a lot of CMT surgeries since I first went into practice and a lot of research that we've published on this. All right. Now, the goal is to get a plantar grade foot that's stable in the hind foot and has balanced muscle. One of these feet has had surgery on one side and the other one's just coming up. I'm not talking about dorsiflexion and gaining dorsiflexion because our topic specifically is recurrent cable varus. Now, why do we have postoperative failure? And that's really what it is on the short term. Why do we have a persistent deformity within months of the surgery? Unaddressed soft tissue contractures, inadequate corrective heel varus, persistent plantar flexion of the first grade, which goes under different names. Forefoot pronation, I call this forefoot valgus, but we understand what we're talking about, forefoot plantar flexion of the first grade. And then muscle imbalance. But true muscle imbalance is very rare to cause a recurrent or persistent cable varus immediately, but it certainly causes cable varus on a chronic basis. Because remember with CMT, we're dealing with a progressive disease. So let's start with soft tissue contractures first. And I would just take this away most importantly, almost from what I'm saying. You have to release all soft tissue contractures first before you do anything else. If you do any type of bone work first, you're gonna end up with a problem. Now, I know there's some differences of opinion on this panel about this topic, but most of these patients, the CMT patients, have a contracted Achilles. Yes, it could be a gastroc, but I think it's the Achilles. And why shouldn't they? Their talus is horizontal. They can't dorsiflex to stretch out the Achilles. Their hind foot's inverted, right? They have a cable varus, and that leads to Achilles contracture. And then they have a foot drop. So why wouldn't they? And when I was very confused about all this, I remember asking Art Minoli, who was really one of the people who popularized strayers and gastroc lengthenings. And I said to Art, Art, what's going on here? He said, everyone has an Achilles contracture with CMT. So that sort of led me in this direction. A hope, triple cut. And oh, so I can have this. Why don't I have this? Action. Oh, so you told me how to get rid of my sound. How do I do that? Can I still do it? No? Okay, I'll just have to mute these as I go. So take a look at this and try it at surgery. All soft tissue has been released here. And as you dorsiflex the ankle, there's still a persistence of pulling it into varus. Once the Achilles has been released, the hind foot moves very freely into dorsiflexion without moving into varus. Look for it. I think you'll see it. This is not really an Aquinas contracture, the Achilles, so much of it is as a contracture causing the varus. We'll talk about the posterior tibial tendons later. But once the posterior tibial tendons moved out of the way, you need to release the talonevicular joint. Look how that causes the foot to spring back. And it makes sense that this capsule would be contracted. So you go into the joint, protect the neurovascular structures, and I'll release the spring ligament in most cases and that are moderate to severe. Now, when you release the talonevicular joint, please avoid releasing the subtalar ligaments unless you're planning on doing a subtalar fusion. But if you release these ligaments, you end up with my biggest problem, which is not recurrent cable varus, but overcorrection. I've done a lot of these surgeries and I do not like to see these patients that are overcorrected. This person had identical surgeries on both sides. Why did that happen on the right and not the left? And these people did not have subtalar fusions. Release contracted tissues, release the abductor, lengthen or release the FTL or FHL, especially if they're dysfunctional. Release the plantar fascia. The question here is if you release the plantar fascia under the heel, is that sufficient? I don't think so. If you're planning on bringing up the first ring, you want maximum release. Now, the biggest problem that I see from others, and I've seen it for myself, is a persistent heel varus. As Bruce mentioned, you want to get this calcaneus plumb line or ideally lateral to the weight-bearing axis of the tibia. And this is frustrating for people. And there's a reason it's frustrating. There's good reason. It's a very complex deformity. This is not a simple two-dimensional coronal or axial deformity of the calcaneus. You've had abnormal muscle pull for their life on these kids, on people, and the morphology of the calcaneus is not normal. And we proved what everybody knew in this study using just your software that was published last year with my brilliant young partner, Max McCallistee. I'd encourage you to look at that if you'd like. Now, I plan these osteotomies out very carefully. Somebody once said, this is not plastic surgery. Well, it is to me. And I think it should be to you because how you make the cuts in the calcaneus will determine how you correct this complex deformity. And I think one could perhaps use preoperative weight-bearing CTs or CTs to determine this, but mostly it's done clinically. I'll put a blade in, I'll attach it for a trial cut. If you're going to do a closing wedge wire, I see people doing it posteriorly. It's perhaps slightly more in jeopardy of the neurovascular bundle if it's done more anteriorly, but you get a lot more bang from your above when you take out a wedge slightly more anteriorly. And how you angle this wedge or cut will completely determine what rotation you're correcting, what deformity you're correcting in the calcaneus. And it's not easy. I'll release the plantar fascia below the calcaneus. I'm doing this not for what I showed before. I've released the plantar fascia usually in the midfoot, but I need to do this to get this calcaneus moved adequately. I can't move the calcaneus much more than about a centimeter tops. I never do a tarsal tunnel release. I don't understand quite how people can do it more than that. And that's not an adequate correction for most of these patients. So I don't want to have the sounds on here. So if you take your wedge, it's a triangular cut and this, I haven't had problems with shortening the heel. You don't have to do this on all patients, but perhaps 50% of patients and certainly all patients with a severe deformity will have this type of wedge removed. And look what you can do once it's removed. You can put that heel anywhere you wanted to put it. It's remarkable that what you can do. And you can also rotate the heel so that the weight bearing aspect of the heel is lateral to the plumb lines. Very powerful osteotomy. Beware of overcorrection. Now let's just get rid of the sound again. I wish I had done that before. Take your time with where you're positioning the osteotomy. I don't take intraoperative x-rays. I'm just very carefully clinically where we put that heel. Now, persistent plantar flexion of the first ray, it can happen. This person was operated on by a very talented surgeon, but the first ray was still depressed. This is a video that we made with Dysior years ago. It's very primitive, but you can just see as the foot desupinates or rotates through the midfoot, what happens to the first ray. So you really can't determine what you're gonna need until everything else in the hind foot's corrected. It's a lot of audibles to use a football term. You can't plan this out the night before. There are too many variables. And as Bruce has pointed out and just did again, you have to release the soft tissues. It's remarkable to me, especially in younger people, once you release the plantar fascia and the peroneus longus, you may find that first ray doesn't need correcting when you think it did. All right, so here, again, you wanna take your time with this. The hind foot's been corrected. Get the midfoot as reduced as possible, and then look where you're gonna put your forefoot, keeping in mind that the forefoot and the hind foot are completely related in their corrections, Bruce discussed. I use a 3.5 screw and a 22 gauge wire, fast, effective, inexpensive. Roger Mann popularized this years ago. I've had to hardly take out any of this hardware. It's a very nice correction. I understand that the CORA for this is probably proximal. I'm quite sure it's within the cuneiform, but this is still a very effective osteotomy to do. You can grade it. You can take out three millimeters, then four millimeters, then five millimeters if you have to. I've never used a plate. I see Bruce had several fusions. It's biomechanically makes more sense, but why fuse a joint if I don't have to? It's just harder, non-unions, things like that. If I have to, I'll do an osteotomy second. It's not common. If you have to do more than an osteotomy the first and second, that's the role for the midfoot osteotomy. I like to call osteotomy. I don't find myself doing many of midfoot osteotomies, but if you have a significant midfoot cavus so that when you've corrected everything, that forefoot is still plantar flexion. You can't correct it with the first and second metatarsal osteotomy. That's when you need to take a wedge out of the midfoot. Not hard to do, but it's just more surgery. I fixed that with staples. These are power staples. These are not $1,000 apiece Nidenhall staples. The whole set of five staples cost $25. In a child, if the physis is open, Bruce had given one technique, a technique that's been popularized by Ms. Moskowitz, and I think it's just great, is an opening wedge osteotomy of the cuneiform. Specifically addresses the plantar flexion. It's not a technique that most of us have seen. You go through the mid portion of the cuneiform to the base of the second metatarsal, and you can very nicely open this up and correct it, but you have to have the entire fascia divided. I'll use a fresh frozen, sort of customized in the operating room, Iliac crest graft. You can put anything you want in there. It should be triangular, so we're not done fashioning this graft yet. There you can see a very nice correction. All right, let's just talk about muscle balance, which is a more chronic problem. You don't often see a patient wake up from surgery within a few months develop a problem with recurrent cable layers because of muscle imbalance. We're not talking about dropped foot. We're talking about recurrent cable layers. So that has to do with hind foot stability. Bruce seems to like subtalar fusions in these cases more than I do. I understand that. I like to avoid it, especially in a younger person. So I'm sure all the panelists will agree that our work horse is the longest to the brevis. We can use a flexor hallus as long as the brevis. I think Jim, or maybe it was Luz Schoen had published on a flexor. You do a digitorum long as it's not strong enough for my liking. So these tendon transfers are not available because of weakness. I'll use, forgive me, I'll use a subtalar fusion. Some have used bridal procedures. I really have no experience for a bridal with the CMT foot. I think it's fine for a foot drop from trauma, but I've not used it for a CMT foot. Now, this is important. And everybody seems to think this is easy except for me. So perhaps there's somebody out there who thinks it's not as so easy or perhaps people are missing it. How do you evaluate peroneus longus strength? Because if you don't get it right and you think the peroneus longus is strong and you transfer it, this is not gonna work. Now, you can really, you can really pull by the foot if you let the, sorry about the sound, if you're not careful to look for extension. When the toe is extended, as I just showed, that will tighten this, that tightens the plantar fascia with the windlass and it'll depress the first ray. This person actually had hardly any peroneus longus strength. So you have to be very careful with that. In terms of how to do the transfer, and we can discuss this briefly at the end, I will do a pulvotaft weave. I know that Greg says you can do this in the leg and I completely agree with that. The pulvotaft weave is a robust weave and they're basically solid the moment you're done with the three throws. I don't think you get much eversion and inversion after these cases. So I'll take that weave and make it quite tight. For me, it's almost a soft tissue subtalar fusion. Now, if you don't have a longus and you don't have a flexor hallus that's strong, I'll do a subtalar fusion. I don't really ever do subtalar fusions for deformity. I think it's a very weak correction for varus deformity. You can't take a wedge that's big enough out in my experience, unless it's a recurrence after a previous fusion and you have to do that. I'll use the fusion for stability. This person no longer will invert, revert and stable. But note that the deformity, you'll still almost always have to do an osteotomy of some type. These people to finish all had previous surgeries and these people all had recurrence years later. They had one surgery, they didn't want to go through another. Their perineal reconstruction has weakened, their posterior tibial strength has stayed and they've developed this deformity. Most pediatric orthopedic surgeons don't do posterior tibial tendon transfers. It's not needed. You don't have to do a transfer in everyone. Members of our society will say, you always have to do it. You don't. But in some patients, this is what will happen, that the posterior tibial tendon will go on. Typical pediatric surgery, as you all know, is the longus degrebus plantar fascia release and maybe Achilles release and the posterior tib is left intact. So what can you do for these people? Well, they often need some type of fusion and you can use the posterior tibial tendon if it's been Z lengthened or even split transferred to gain adequate dorsiflexion. This is one of the people afterward, but even if you do a triple, you have to correct the deformity. You have to leave with a plantar grade foot. You'll often need a calcaneal osteotomy and an osteotomy of the foot, right? I want to end on the issue about the posterior tibial tendon. It's usually a deforming force in an adult. You can see this spring back, but the problem we have with the posterior tibial tendon is that there's not enough length, all right? John Su was at Rancho, he did a lot of CMT. He's now retired, showed me this, and I would strongly encourage you to do this. You have to take the posterior tibial tendon and dissect it all the way out onto its excursion on the cuneiform. And you really create an extension of the tendon. It's not fat, it's not weak fibrous tissue. There's a tibialis anterior, but this will gain you a critical extra centimeter and a half when you read about papers on posterior tibial tendon transfer, you'll often hear people say, well, if we can't get it into the cuneiform where we really want it, we'll put it someplace else. I maintain they're usually putting it somewhere else because unless you do, I'm telling you, you really can't get into the lateral cuneiform or one of the cuneiforms. And people will say, well, I'll put it into the neck of the talus. That's not where you want this. And if you do, when you do transfer, I try to go below the retinaculum. It's more cosmetic, but if you go superficial and I've done several hundred of cases, just subcutaneous, you'll get an extra length, a centimeter of length if you need it. I put it into the lateral cuneiform, it's lateral to the sub-tailor access, so it'll cause some reversion of the high foot, because again, I'm not fusing the sub-tailor joints if I don't like it. At the end of the case, you wanna leave the operating room with a foot that's gonna look like a foot you wanna see two weeks post-op and three years post-op, plantar grade and with adequate tension in your transfer. And that's it. Thank you. All right, great. Thank you, Glenn. I think next, we're gonna go to Jim. Jim, hopefully you're ready to go ahead and share your screen. Jim's gonna talk to us about perineal tendon pathologies. Now, do you hear me? Mm-hmm. Very good. I don't know. This is where I work. This is a lady with a rheumatoid, juvenile rheumatoid with severe cable varus deformity. It's not hard to imagine that she has a perineal tendon problem based upon that. And when I did the reconstruction with a triple and a few other things, you see this is what her perineal pelvis looked like. It was shredded. Now, this guy, Michael, was a runner, long distance runner who had initial pain three years ago, saw some other folks in my neighborhood and had three prior surgeries and came because he had severe persistent weakness, pain and enlargement posterolaterally. And this is what his perineal tendons or what remained of them look like. And these are the kind of cases that I often see associated with cable varus. We'll get back to what this really means, but I wanted to show you severe cases and recurrent cases and previously operated cases represent a particular challenge. These are his x-rays preoperatively. And I think you could say, well, he doesn't have valgus foot, but it doesn't look like a very bad cable varus. These are the things I wanna tell you about. One, perineal tendons are important in the diagnosis and treatment of cable varus. Sometimes, maybe more times, it's important to be aware of cable varus when you're treating obviously symptomatic perineal tears. The association has been proven. We did a paper published a couple of years ago, I think in 2020, and we quantified and correlated to the type of tear. Wanna go briefly over some pathomechanics and the types of tears, and then look at some surgical techniques for the perineal tendons in general, and of course, also in cable varus. We all have observed that cable varus is associated with perineal tendon tears. The eye only sees what the mind knows. What becomes more challenging is to recognize mild deformity, as the previous speakers have alluded to, when you're looking at posterolateral ankle pain and swelling. Here's a gal who has what I think you would agree is probably a moderate cable varus foot. She has a high arch. She looks like she has a plantar flexed first ray. On the poster view, her heels are in mild varus, but when she is lying on her tummy prone and the foot is hanging free, her subtalar joint easily comes into varus. This is the equivalent of a Coleman block test, which is, you know, he was a lovely man, Dr. Coleman, I met him as a resident, and I had the blocks in my office for a very long time, but this is just the same thing. The test says, basically, if you remove the weight-bearing element of the first ray, is the hind foot flexible enough to move into valgus? So if it's in valgus non-weight-bearing, lying or sitting, and it's in varus standing, that's the same as a positive Coleman block, and it means that the hind foot varus is forefoot driven. Even in some cable varus feet, of course, they still have abnormalities where they don't get a lot of valgus, but as Bruce shows, related to the morphology anatomically, and that was a great demonstration. This is a paper that I did with Kira Taniguchi, who's a fellow from Nara, Japan, and we looked at a large number of surgically proven perineal tendon tears to avoid the conundrum of saying perineal tendon pathology. These were all patients with proven tears, and they were compared with age and gender match controls. The distribution was about the same as in other studies that we've done on perineals, that about 70 to 75% of all perineal tendon tears are the brevis, that 10% or a little bit less are longest tears, isolated, and about 20% are tears of both. The radiographic parameters we looked at, which you can easily use in clinic, are calcaneal pitch, the AP talofirst metatarsal angle, and the talonevicular coverage angle, and these are the numbers, and the differences with the controls were all statistically significant. So one of the points of the study was not only to show the association, but also to quantify and identify which radiographic measures of CAVUS correlate. We also did the same analysis, separating them into the different groups, and found, according to the universal Brodsky principle of orthopedic classification, that the bad ones are worse. So the people who have brevis and longest tears both had higher numbers in most of these categories. Each comparison, though, was statistically significant when compared to the controls. So calenvarious deformity is definitively associated with perineal tendon tears. Now, biomechanically, eversion is a multi-plane action. It includes external rotation, dorsiflexion, and coronal rotation or pronation in the coronal plane. When the foot is in varus, the hind foot is in varus, you get a vector of combined forces which pulls the perineals against the distal fibula. The varus position itself stretches the tendons against the fibula, and the perineus longest, which sits behind the brevis, compresses the brevis against the fibular edge. But in addition to the pressure that pushes the brevis laterally and forward, it has to sublux against the posterolateral margin of the fibula to create the typical perineus brevis tear. Now, this is the subtalar axis, which if you imagine it holding a pencil in your hand, looking at your foot from above, the pencil is angulated about 45 degrees from the horizontal and about 25 degrees from the midline. And your hind foot rotates around that axis. Now, the question gets to be, do we really need to be concerned with the perineals if, as part of cable varus reconstructions, we do hind foot fusion? This is a lady who had a triple arthrodesis done as a child for reasons she doesn't know, although I suspect she probably had a coalition. And it was done by the senior partner of my group when I was in middle school. And over time, her ankle became symptomatic enough to have this total ankle. And after the total ankle relieved her pain, she then got posterolateral pain, which was typical of perineal tendon tear. But she doesn't have a hind foot that really moves, although there's a lot of degrees of freedom in the star ankle. And at the time of surgery, she had a very significant perineus brevis tear. We looked at the data, the preoperative gait data, on a group of surgically proven perineal tendon tears using the opposite leg as a control and then analyzed the data according to the pattern of tears. Was it brevis, was it longus, or both? And in this study, we classified them as irreparable or reparable isolated tears of either tendon or irreparable tears of both tendons. And the distribution was about the same. The type of tear corresponded to age, but not to patient sex. And what you see in this graph of ankle moment, which is basically ankle power times the vector, is that the affected limb at peak moment was significantly less than the affected limb. What we interpreted this to mean is the perineal tendon tears are symptomatic not only in terms of their pain, but they do create a diminution of ankle sagittal motion, power, and moment. So one should just be aware that even when we do hind foot arthritis, treated by fusion, that perineal tendons can continue to be symptomatic and should be addressed at the time you do the subtalar fusion through the same incision. So I've talked to you now about the association of cavovirus with perineal tendon tears, a little bit about the biomechanics and function of the perineal tendons, not just the evert, but also plantar flex. And I'm gonna go back just a moment. This is the same illustration I showed you earlier. And it's obvious, as Glenn also alluded to, that when you know where the axis of the ankle is, which is angled a bit according to the malleoli, with the lateral malleolus being a little posterior, and you know where the subtalar axis is, you know that any tendon that crosses the ankle can be classified as a plantar flexor, dorsiflexor, or inverter, or evertor. So the calcaneus is not only a plantar flexor, but it's also an inverter, as Glenn was saying, because it's medial to the subtalar axis, which you see here at the bottom. It also, of course, makes sense that the perineals are plantar flexors. So now I wanna talk about the different patterns of perineal tendon tears, what they look like, what their main characteristics are, and some of the surgical ways to treat them. Brevis tears constitute the vast majority of perineal tendon tears, and in the groups and studies that I've done here, it's usually between 70 and 75%. Most perineus brevis tears are centered on the lateral malleolus. Acute tears are not common. The vast majority of perineal tendon tears are chronic and are due to chronic subluxation of the brevis against the posterolateral margin of the distal fibula, associated with some mechanical factor that's also consistent with the problems of a varus hindfoot that allows the tendons to move and slip against the fibula. So that would be either gross or more likely subtle incompetence of the superior perineal retinaculum or associated ankle ligament instability, because as the ankle shifts forward with each step, it's pulling the perineus brevis against the distal fibula. This is a paper that we did, the first paper I did on perineal tendons when I just started noticing these in the mid 90s. And at the time that my fellow John Kraus and I published the paper, a series of 20 patients was the biggest around. And that's where we did a little research in terms of the biomechanical literature and came up with the idea that you could repair the tendon if there was less than 50% involvement. I don't think that anymore. And I'll show you photos of why, but in summary, it's because repaired tendons have a very high likelihood of continuing to degenerate and to be painfully adhered and scar. And when they do and become immobile, they're painful. Now, this is a classic perineus brevis tear. It's centered on the post-lateral edge of the distal fibula. You see that it's shredded into two major portions, but each of the two portions is multiply shredded in itself. That's a non-viable tendon, and in my experience, is not successively repaired by suturing it together. This is another example of it where the brevis is actually split directly on the lateral malleolus, and yet another. What's difficult is when you have a subtle perineus brevis tear, that's not entirely split. So sometimes you look at the perineus brevis, and it looks like it's intact. It's not changed in morphology. And you need to take the brevis tendon and flip it over with a pair of Adsens and look at the undersurface, and you may find a chronic shredding, fraying tear on the undersurface. Now, there are other ways to tell that the perineal tendons are torn. It's not just a matter of finding a split in the tendon surface or the tendon substance. It's also the fact that if the tendon tear is sufficiently chronic, that you lose the normal characteristics of the tissue. In a chronic tear like this, the tendon is patchless because it's stretched out. And while most perineal tendons don't stretch with interstitial lengthening the way posterior tip tendons do, as a chronic tear gets substituted by this type of opaque, shiny, white scar, it becomes essentially non-functioning, and it's a source of pain. You notice that there is a very white appearance to that chronic scar. A normal tendon has a more ivory color, and you can see the individual fibrils of the tendon. And when this tendon is flipped over, you see the undersurface where it's been shredded over time, and then healed and shredded, and that's why it's grossly misshapen in a fusiform pattern. And this just shows that the replacement of the normal fibrils with the scar. So the role of subluxation in Brevis tears is the emphasis. And in some cases, if you have an insufficient retinaculum, there are opportunities to be challenged in how to reconstruct the soft tissue. Even in the cases that worked very well, it's surprising how flimsy the superior retinaculum tends to be. And in those cases, you can also detach from the perineal tubercle, where the two perineal tendons split into separate sheaths, the band of very tough tissue that goes over the perineal tubercle and holds the tendons, and do a reconstruction of the inferior retinaculum. This is a technique where the remaining tendon can be placed underneath a Z-lengthened or split calcaneofibular ligament. And the benefit of this is that it medializes the tendon more than anything else against the synovial tissue on the side of the calcaneus. And that's what it looks like when it's re-approximated and sewn. In a case like this with a chronic split tear, the retinaculum has been elevated off of the lateral malleolus. And in this case, the bone surface has to be roughened in order to adhere the flap. The tendon has to be treated as we would otherwise. And then I do it in a multiple layer where drill holes were used to suture the posterior portion of the retinaculum to the bone, and then the anterior portion sutured over that to adhere to the bony surface and then reinforce the inferior or posterior flap. Now, this is a patient who has a typical brevis split centered on the lateral malleolus. And in this case, the plan is to do a tenodesis of the brevis to the longest and then excise the damaged portion of the brevis. This is a slide to remind you that this may be associated with ligamentous instability and we need to check for that and fix it at the same time. Now, in this slide, you see the tenodesis is completed. My steps are to do the proximal transfer and tension the brevis slightly to then reconstruct the retinaculum so that we have the shortest line of pull of the remaining longest tendon, and then to reinsert or establish a lateral insertion of the peroneus longest to the lateral border of the foot to get the maximum eversion moment. And that can be done by suturing into a viable stump of the brevis or suturing it with an anchor to the fifth metatarsal with some soft tissue reinforcement. This is a patient who had tenodesis. This is a seven-year follow-up. She also had a dorsiflexion osteotomy at first met for a mild cable varus deformity. And this is what it looks like. All right, now, so she's everting her foot. You see that she's firing her extensors a little bit too, but she's clearly moving her foot in the aversion through the peroneus longest. Now, longest tears are much less common. And like the brevis tears, they occur primarily where the maximum mechanical stress is applied to the tendon. For the brevis, it's where it turns at the lateral malleolus. For the peroneus longest, then, it occurs at the cuboid tunnel where it makes the most acute turn to then traverse diagonally across the plantar surface of the foot. The second most common, which is not common, is a tear at the perineal tubercle of calcaneus if that calcaneus has enlargement, irregularity of the bone, or the inferior retinaculum has been damaged. This is a paper that Chris Stockton, a former fellow, and I did just looking at perineus longest tendons and their association with abnormalities of the os perineum. It's obvious that this is a tendon tear you can diagnose on radiographs if they have an os perineum because retraction of the os perineum proximally means they must have a longest tear. It never retracts more proximally than the inferior retinaculum because that widened portion of the distal longest won't go through the inferior retinaculum, which is very tight. But here you see a fractured os perineum, which has migrated, and here you see the signal inside of a perineus longest. Here is, there is increased signal in this portion of it, and here you see scar, but that's not really normal tendon in any way. This is another example of a patient who, or this is an example of a patient who had a longest tear, and you can see that the longest has lost its normal tension. This is what the radiograph looked like, or the fluoro and intra-op. This is what the specimen looked like, and this is the attenuated area where the chronic tear occurred, and the os perineum is in pieces as shown by a fluoro of the specimen at the time of surgery. Here's another example of a longest tear, in this case associated with osteoarthritic changes of the os perineum against the cuboid. This is an osteophytic ridge, and here you see the arthritic changes in the os perineum. The most difficult are tears of the perineus brevis and longest. I can't prove to you yet, but think that the incidence and severity of, well, I can prove to you that the measures of calovirus are more severe in two out of the three things we measured on standing radiographs in combined tears, and I showed you that data very quickly earlier. But these are frequently patients who've been previously operated. This is a, quote, repair of both the perineus longus and brevis, which have grossly scarred and stretched and are not functional. This is what the specimen looked like. Here's another patient who had similar story in which she developed a monotendin where the two tendons are really not recognizable, and it's just a giant, massive scar. Here you see the distal fibers of the brevis, so the abnormality has extended up to the muscotendinous junction of the brevis, although not quite to the longest. There's nothing recognizable here, it's scarred here at the lateral mal. This was a case in which I did a long flexor tendon transfer, I think this is FHL, and used it to, when I was in early series, I was trying to see how to treat concomitant tears. And in this case, the longus is brought down, threaded through the lateral malleus through a drill tunnel, sutured back on itself. Now the reason that I don't do flexor tendon transfers anymore are two. Number one, FDL and FHL do not have the strength to function as a substitute for the perineal tendons. Rather, they can be used as an interposition graft the same way you can use the FDL for a posterior tib. You can never really fix a posterior tib with an FDL transfer, just using it as an interposition to try to reestablish attachment to the proximal muscotendinous unit of the posterior tib. And this shows why also I've now gone to Allograft, because the muscotendinous junction of the flexors is far too distal in most of the severe combined tears, which extend above the lateral malleus, and there's nothing to sew into. So even in this case, I added an Allograft and sutured it to the FDL or FHL. And after that, I realized that probably wasn't necessary. For example, this patient with double tears, excised them, placed an Allograft, sutured it to the brevis stump, reconstructed the retinaculum with the pancervis tightening technique, and then sutured into the proximal part of the muscles with no flexor transfer. This is the fellow I showed you at the beginning of the talk, who has a sort of subtle caboveris. It's not the worst you've ever seen, nor the best. And he had very bad-looking tendons after his previous surgery, and it's just anatomically indistinguishable. In this case, I used an Allograft, and the order of correct reconstruction I used is to fix it distally. I put this with a biotene adhesive screw to the fifth metatarsal, then sutured it to itself, then reinforced it to the local tissues. These are the branches of the serral nerve, which I tried to preserve. I brought it proximally, and here, stretched on the proximal stumps, the brevis does not look very good, the longest better, and it takes three people to do it. Somebody to pull distally on the stumps, someone to pull proximally on the Allograft, which I pre-stretched on an ACL-type stretcher, and then someone to sew it together. And here, we've got enough length on the Allograft to double it up, to sort of reinforce, but only down to a point that it will not get stuck in the retinacular reconstruction. This is what he looks like after his radiograph, if they did a dorsiflexion osteotomy and a calcaneal osteotomy. Let's see if this is the one. So here, we saw him in clinic last week, and this is his strength of eversion. Now the best way to, well, the only way to isolate perineal function is to have the patient with the ankle in plantar flexion, and then have them evert across the midline of the limb. That's the only test of perineal function that isolates the perineals and produces a puri version. It's also the best way to have the patient rehab the perineal reconstruction. So in summary, to me, the most important is recognition. The eye sees what the mind knows. When we see cabal varus or perineal tendon tears, we should think of the other. And the various techniques for reconstruction are in a review article in FAO a couple years ago. Thanks. All right. Thanks, Jim. I'm going to try to share my screen. I am running on a power outage, so we'll see what happens. I've never done this from a phone before. Tell you what, that's not going to work. Lucas, can you just go ahead and share your screen with my slides? Here we go. So I'm just going to do the old-fashioned next slide. So go ahead, next slide. Move on forward there, Lucas, and you can hit slideshow to make them big, if you don't mind. So while he's getting started, I'm just going to talk on a different, a little bit different topic. We're going to shift a little bit. I'm hoping to speak on, yeah, if you can just hit the button that says slideshow on Google Slides. So I'm sorry, I'm working off a little bit of alternate technology right now because we have no power. So I'm going to speak on upper motor neuron pathology, because we always talk about CAVUS all the time in terms of CMT and in terms of idiopathic CAVUS. What we almost never talk about is what we often see, which is patients that have had cerebrovascular actins and a brain injury. There's a couple of interesting things that we can move forward with that. Next slide, please, Lucas, while you're finding the button. So this is a little piece of phenomenology that's way back in the 1920s, and I got to thinking at one point, why do we have equinovirus? It turns out there has been a little piece of work that's been done on that. There we go. If you can just, yeah, that's better. It's been done on that back in the day. There are a couple of neurologists, yeah, go forward to that same slide, that went down to Panama, next slide, please, Lucas, and actually decerebrated a sloth. Now that's a fascinating thing to do, because what happens when you decerebrate a sloth? This is the only mammal that spends its life upside down. They posture into flexion, as opposed to knee extension and hip extension and ankle plantarflexion. They posture into a completely different spot. Next slide, please, Lucas, and you can actually still hang a decerebrate sloth as if they're hanging from a stick. They can hang from a tree. Next slide. And so what that's basically telling you is phenomenologically, we get equinocavivirus because the brainstem is predisposed to use antigravity muscles to maintain tone in antigravity muscles. That's not a perfect biologic reason, but it tells you that the brainstem action, left unopposed, is giving you an extension posture in the ankle and essentially using the antigravity muscles. Next slide, please. So next one, I'll keep going. Now this is the homunculus, the dreaded, you can stay there, the dreaded sign of the medical student and the areas that supply the lower extremity are deep within the sagittal sulcus. That turns out to be the areas that's supplied by the anterior cerebral artery, which is a less common stroke pattern, but a fairly common pattern of cerebral vascular accident. Middle cerebral artery strokes are actually the most common. That's where you get aphasia and upper extremity. Most of the ones that we see when we're seeing issues have to do with anterior cerebral artery. Next slide. And important thing to remember about strokes from our point of view, 80% are thrombotic, 12% are hemorrhagic, the rest are anoxic. Next slide. But that impacts our discussions of timing. Now CVAs involving the brainstem also cause severe deformities. Next. The dynamics of acquired spasticity will impact when you choose to operate on somebody who's had an upper motor neuron syndrome. So remember they get a period of spinal shock, the initial flaccid paralysis and hypotonia. It fairly rapidly comes back within days to weeks. And you remember this probably from your ICU days in med school. And then there's a very slow return towards normal. And where we want to operate, if we need to, is after we've stopped looking at a moving target. And that length of time depends. If it's a pure cerebrovascular accident, a pure stroke, it's usually about six months. But if it's spinal cord injury, it's 18 months or longer. If it's anoxic, unfortunately they almost don't get back much of anything. And if it's traumatic brain injury, it's about 18 months or longer. So basically your typical stroke, your typical cerebrovascular accident, six months, spinal cord injury or traumatic brain injury, you need to wait almost two years before you can reliably operate on that patient with some understanding that you're not working on a moving target. Next slide. The indications for surgery in a patient who's had, and my power's back on. The indications for surgery in a patient who's had a traumatic brain injury or other issue has been pro for ambulation and positioning and transfers. Next slide. The ambulation potential after CBA is 25 percent will achieve normal ambulation. Seventy-five percent will achieve some level of ambulation. These are in patients who are unable to walk at the time of the stroke. Next. And the prerequisites for gait. This is important because you will sometimes see patients who are brought in by their family with a stroked out foot, with a capoveris foot, and they'll be in a wheelchair. And it is important to understand and counsel the patient that they have to have other things beyond the foot that are going to work if they have to, if they want to be able to walk. And one of them is voluntary hip flexion. You have to be able to move the leg forward in space. And that's critical. If you don't have voluntary hip flexion, or you have a hip flexion contracture, you need to have that addressed, or perhaps you can't do much for that patient. You have to have adequate standing balance and stability of the limb. Next slide. You have to have a plenary foot and ankle, you have to be able to extend the hip and knee and balance of the trunk. Next slide. A quinocavoveris deformity, as you typically see in a stroke patient, is brought on by spasticity of the anterior tibial tendon. Now, this is an important distinction when compared to all the other things we've been talking about tonight when we talk about either idiopathic cavus or we talk about CMT. They are not spastic conditions. But this is a spastic condition, and of course, this is the old-fashioned EMG you used to see on the boards or the OIDs in which they would show you an EMG. But what you're seeing is a tonically active anterior tibialis, and that is a typical pattern for a stroke patient. Next slide. So, let's go to the next one. This is a patient, I don't know if the video is going to play, but hit it and see if the video will. Sorry, it's not going to do it. There is a video here, but it's not going to go. So, this is a, nope, just stay there and we'll just try not playing the video. Let's keep going. Go back there. All right. So, that's a picture of a patient who's had a stroke. You can see that tonically active spastic anterior tibialis. Let's move to the next one here. And so, anterior tibialis transfer is primarily used in upper motor neuron disease. Next one. This is the classic stroke patient procedure. Now, notice it's in black and white. It's in black and white because I don't do a splat or a split anterior tibial tendon transfer, but the classic split anterior tib is to take half of the anterior tib and move it to the cuboid all the way. So, you're using it like a harness across the front of the foot, much like a bridal procedure which we're going to talk about in a second. Next slide. And so, this is what it looks like afterwards. Now, notice what's going on. That lateral limb is incredibly tight, and you don't see anything fired up on the medial side. Next slide. So, don't do this. It doesn't work as advertised. The splat is kind of a silly historical procedure that's still hanging around. Unfortunately, our pediatric colleagues still do it a fair amount. Next slide. There's been some work in the adult foot and ankle world, and this is from 2003 from JBJS. It's a cadaver model of tensioning errors in the split transfers, basically showing for both the anterior tib and posterior tib that anything that's not exactly perfect is going to basically lead to the transferred limb taking all of the load. So, when you do a splat, fundamentally, you are just transferring a tendon to the cuboid. You're not really leaving a functional tendon behind. Next slide. So, I looked at this myself in a patient in a model that we did, and we looked at whole tendon transfer to the third cuneiform, taking the entire anterior tibialis, much like Ponsetti used to do for recurrent clubfoot, and compared to the cuboid, not all the way to the cuboid. Even with a flexible foot, you're just barely moving it past the subticular axis, and you're not going to overcorrect it. You're not going to overload the first ray when you do this. So, the operative pearl here is to do the, I'm being told I froze, am I back here? It's good. Okay, good. So, the operative pearl here is that you can't overcorrect it by moving it to the third cuneiform. All right, next slide. Now, let's talk a little bit about posterior tibialis transfer. We've had some talk about this already. It's the best option for foot drop, if available. Typically, it's not used for spastic cases, and it's typically not spastic, except in cerebral palsy. But there are certain cases where a posterior tib transfer, like a drop foot, or very commonly for patients that I'm seeing today, patients who've had failed spine surgery. Next slide. This is from the JBJS Reviews article from 2008 on it, interosseous membrane transfer of the posterior tibialis. We've talked about this already, and I honestly think the point that Glenn made about harvesting an extra centimeter and a half of periosteum and getting full length is critical. It's also critical to use modern fixation. So, we've moved past suture buttons on the bottom of the foot, and to be honest, we've moved past the bridal procedure, in large part, because of the availability of good interference screws, which allow us to put it into the middle cuneiform or the third cuneiform. I typically use the third cuneiform. I think most of the people do. I'd be interested to hear at the end of the talk if other people use the middle cuneiform, as this review article said, but to be honest, it probably doesn't matter a whole lot. Next slide. The pole comes from the center of the leg. It's slightly everted, if you put it into the third cuneiform, and it can be done with or without a triple arthrodesis. Next slide. The bridal procedure is a historical procedure in my book. I don't do these anymore. The bridal is to take the non-functional peroneus longus and the non-functional anterior tibialis and bring it together. It refers to a horse's bridal, not Dr. Bridal, and that's an important point, but it looks like a horse's bridal in the front, and it was done historically. There's a nice paper by Roe Rodriguez from the 90s about doing these. It's fairly effective at patients with peroneal nerve palsy, at getting them out of braces, but in the modern era, where we can just plug the posterior tib in with an interference screw, I don't do the bridal procedure. There's a lot of slop in the bridal procedure, and I don't think it's necessary today. Next slide. And go on to the next one. Now, it's important to think a little bit historically when we're talking about tendon transfers, because there are other tendon transfers that work, and in fact, the first transfer of the posterior tibialis was described in 1933, and it was in JBJS, and then it was revisited in 1961. Now, if you do that, you can bring it circumferentially around the medial side of the tibia. It does work. You don't have to bring it through the interosseous membrane. This has occasional, very occasional circumstances where you might want to do this. If you've got a lot of HO in the interosseous membrane, and there's been trauma, or something that prevents you from doing it, don't forget you can do this. But if you do this, historically, they did a triple arthrodesis to control the foot because the axis of pull is not the same and you will still tend to invert. But it's something to remember historically as a little historical oddity. Next slide. Peroneus longus transfer. I'm gonna talk about two types of peroneus longus transfers. The first is for balancing. Glenn has talked about this already, but the longus to brevis is a classic transfer in CMT. Next slide. And typically, this is done for a four-foot cavus as we all know with depression of the first ray. Next slide. The motor weakness patterns in CMT involve the occasional sparing of the EHL and then often sparing of the peroneus longus, almost always sparing peroneus longus. Now, there's some thought as to why this might be. I've written a paper on this as a thought paper. Next slide. About why do we see these variable patterns in CMT? CMP is not a stocking glove distribution type of neuropathy. You don't see just the most distally innervated muscles. In fact, the anterior tibialis, which always goes out, is the first muscle innervated by the peroneals, by the peroneal nerves that comes around the fibular head. There's a small recurrent branch that goes right to the anterior tibialis and supplies the anterior tibialis. Why is the peroneus longus spared in some people? Why is the EHL, which is the most distal of the anterior compartment muscles in the leg, spared in some people? And so there is some thought. I've had some thought about this, published this in CORE. There is a similarity between the main form of CMT, CMT1A, which is a focal trisomy of the PMP22 gene, peripheral myelin protein 22. It so happens there's an analogous disease called hereditary neuropathy with liability of pressure palsy, which is a deletion of one copy of the PMP22 gene, which gives you drop foot. It was described in potato diggers who kneel all the time. So there may be something about some element of compression. And it turns out we did some dissections. There's a lot of variability in the branching patterns of the peroneal nerve around the fibular head that may explain why some patients with CMT get some of these unusual sparing characteristics of some fairly distally innervated peroneal muscles. Next slide. Regardless of the reason, you can use this to your advantage. And the classic one is peroneus longest to brevis when the longest is spared and the brevis is out. Next slide. And then next slide after that. So Glenn mentioned doing it down in the foot. That was the way I was taught by Roger Mann. I don't prefer to do that. I do this approximately, either with a pulvertaft, and sometimes I have done it side to side, but I agree with Glenn that a pulvertaft is stronger. Why do I do it up high? I do it up high because A, it doesn't matter functionally. And B, it keeps this little ball of scarred up pulvertaft weave out of the foot, out of the shoe, and out away from the serral nerve. So I don't have to make the same level of dissection around the serral nerve. And that's just an observational thing that I've found some patients have had some pain from pulvertaft transfers, peroneal to peroneal, in the foot and around the path of the serral nerve. And I don't see any reason to do it down there. So that's the argument I would make. Next slide. Now, peroneus longus transfer for a foot drop. Well, that's a surprise. Nobody expected to see that coming. And this has to do with the changing phenomenology of cavus foot and tendon issues that I'm seeing in my practice. I will tell you that outside of CMT, the patterns of cavus foot and the patterns of tendon imbalance that I am seeing have changed dramatically over the last 20 years. And it really has to do with what I would consider to be an epidemic of spine surgery in this country, because what we're seeing is failed spine surgery. So peroneus longus transfer for a foot drop is actually a resurrection of an old CP operation, but it has some benefits. Next slide. And now the classic old way was polio. That's my father in the middle with his crutches, not his x-rays, but he had polio. Affected my life very deeply because I grew up next to a patient suffering from it with classic distal motor sparing. Next patient, next slide. And of course, polio affected the anterior horn cells at certain levels, but because it didn't affect the long tracks left distal sparing. Nowadays, we're seeing nerve root issues from failed spine surgery. Next slide. And we are seeing commonly situations in which we have distal sparing of the peroneals and proximal failure of motor groups. Next slide. So I am seeing more and more of these. Lucas, are you able to play that video? I doubt it. No, I don't think so. Yeah, let's skip. So I was gonna show you a beautiful picture of a peroneus longus transfer in a failed spine surgery patient that was brought around the outside and was able to regain dorsiflexion. The patient did have mild cavus, but well, you're gonna have to trust me on this one tonight. Now, the EHL to the foot is another classic transfer operation done in CMT polio failed spine surgery. Next slide. And the classic is for EHL sparing with over pull of the toes as seen in CMT and as used to be seen in polio. Next slide. The classic transfer was a Jones procedure, which was an IP fusion with transfer of the EHL to the metatarsal neck. Next slide. Now, what I commonly do nowadays, there's not a lot of reason to do a Jones procedure because actually if I have a forefoot cavus, typically I'm gonna buy myself a little bit of insurance and do a dorsiflexion osteotomy of the first ray. So usually if I'm going to bring the Jones procedure into play and bring the EHL, I'll transfer the EHL directly to the midfoot and commonly do it in conjunction with a posterior tip or something else. Next slide. And I think it's important to remember, it's rare that you can truly reestablish dorsiflexion of the hind foot through a Jones procedure and an EHL transfer alone. The cross-sectional area and the penation of the EHL typically is just not adequate to provide enough force and quite enough oomph from an EHL alone. Much like Jim was talking about, the FDL is a pretty wimpy muscle. So is the EHL in and of itself. And so I consider the Jones procedure and the EHL transfer to the midfoot or to the first ray as an adjunct. It's just not adequate in and of itself. We're running late on time. Lucas, let's move ahead. I'm gonna do one case and take a couple of questions because we're already at 1030. Go ahead to the one that says a transfer too far. Just clip forward. We'll go past these rapid fire questions. I'm sorry about that. But I wanna try to get one case. There you go. So go to the next one. So I wanted to get in a little bit of the stroke foot and hemiplegia. So this is a 31-year-old male with hemiplegia after an AVM and an intracranial hemorrhage that he suffered unfortunately at 28. He's now three years out. He shows up with five plus anterior tibialis, spastic, strong as hell. He's had Botox, but it's not working. Still, despite the five plus anterior tibialis as is common, the hind foot is overpowering because of his brainstem activity. And he has a 30 degree Aquinas contracture. He has, he does not have posterior tib. It's non-functional. But his anterior tibialis is inverting his foot. His Silver Shield test is negative. He has the true Achilles contracture. His perineals are totally out. He has a five out of five gastroc and he has a 15 degree knee flexion contracture, which is not limiting. You can still walk with a 15 degree knee flexion contracture. He's able to stand and pivot and he has fixed plateaus of one through five. Next slide. So that I showed his picture before. I was gonna show you a video, but it's not gonna work. But this is his spastic anterior tibialis. Next slide. So just to cut to the chase since it's 1034, these are his x-rays. Next slide. I did a triple. I did a triple because his anterior tibialis, because his posterior tib was non-functional, his perineals are non-functional and this guy needs stability. But I made two choices. And I'm curious to hear what the panelists think about this. The first one is that I moved the anterior tibialis to the third cuneiform. Now we've heard Jim talk about already of the importance of doing perineal work for pain relief when you're dealing with perineals and still doing hindfoot fusion. So the question I'd like to ask Jim and Bruce and Glenn, I chose to do an anterior tibialis transfer even in the setting of a triple arthrodesis because I have seen on a couple of occasions, patients when you do a triple arthrodesis with these really dramatic spasticity cases like you see in upper motor neuron disease, spin out through the ankle or develop ankle instability laterally or have later problems at the level of the ankle. If you have an anterior tibialis that's pulling like hell on the thing, despite the fact that you've stabilized the hindfoot through the triple. Do you agree with me or is this a transfer too far? Am I smoking dope and doing too much? I think you had to do that. Absolutely. I'm not sure you had to do the whole triple. Maybe you could have done a subtalar fusion and transferred the two bands of third lateral cuneiform, but absolutely you have to transfer it in my opinion. Jim and Bruce, are we right thinking that anterior tibial transfer is still a good idea in these really spastic cases? It's certainly a reasonable option. I'm curious what you did with the FDL. So I did a release of the FDL at the knot. I didn't put it in here, but I did do a release of the FDL at the knot of Henry because usually what happens, you have an Aquinas contracture and you bring them up and I tell the patient, look, I never know how tight your FDL is. Your FDL may be tighter than we expect. And it's very common in these particularly spastic Aquinas, you do the TAL and you come up and all the toes are down. And I tell them I may release it at the knot. That speaks to the other point with the claw toes. I have found over years that if I try to do hammer toes and put in pins and then pull the pins at six weeks in spastic cases or in something, any sort of upper motor neuron disease or a focal dystonia case, which we never talk about, that they just recur. And so my rule now that I teach my fellows and myself is if you've got a upper motor neuron disease case with claw toes, just put screws in the toes and leave them there and plan to leave them there forever. Anybody else have experience or anecdotal thoughts about that? The FDL can torture you if you don't straighten those toes and make it permanent. It can get everything else right and they're still walking on the tips of their toes. So I think putting the screws in and releasing it's fine. I brought up the question because you can use it to help with dorsiflexion. It's nowhere near the strength of the tibialis anterior but it can be an augment. Yeah. It was a longstanding problem. Did you release everything immediately and divide dysfunctional post-tip and take it away? The interesting thing is he was reasonably supple despite the fact that his posterior tip was relatively flaccid. These patterns are also different. That's what makes the spinal cord injuries and the traumatic brain injuries and the bleeds and also the failed spine surgery so interesting is that the patterns are so remarkably different. So I didn't have to in this case, but I have done it. And I have done, the other thing that nobody talked about tonight because y'all weren't talking about spasticity is fractional lengthenings of the posterior tip which is a procedure that our pediatric colleagues do but we don't talk about much and I do them. I still struggle to find the right indication but there are some of these spastic cases I will do a functionally a strayer of the posterior tip. You just have to do it high enough. You just have to do it high enough in the legs. Oh, it has to be in the muscle. It has to be about two or three centimeters above the platon at least to get up into that spot. But there are cases that are appropriate for that, I think. We have to shut down, Greg. Jim, there's one question that you were gonna answer. I was following the questions. What happens when there's no function in the perineal musculature? It just, there's no perineal function. You're muted, Jim. And you're left with, what do you do? Do you do a subtalar fusion? Roger may need to say that. I include, we include, we know a bad perineal. We include the lower leg on the MR in order to rule out fatty atrophy of the perineal muscles. And if they're non-viable, then you have to do a fusion but you may still need some form of bracing. So you wouldn't do an FHL transfer in that case? Doesn't have the power. I wanted to say that I like the way you reason this stuff, Greg, and I found in some of the spastic hammer toes, it's insufficient to release it proximally. And that if I release them at the PIP joint in addition or instead, then the pins work better. I think the FH, the FDL is still tight even though it's not maybe connected to the muscle anymore. It's contracted enough that makes a difference. Yeah, I agree. And I don't hesitate to pop them in both places. I've just been burned on too many hammer toe procedures that come back as mallet toes. And I've seen a few of those come back a few years later. I've seen a lot. It's 1040. I know we have a lot of questions in the chat. I'm sorry for everybody that we ran over. Lucas, do we need to shut down or can we do one or two chat questions? You have about five more minutes. Greg, we were talking earlier. I just have one question for the group. We can go really quickly. Transfer, let's say of the posterior tibial tendon, how tight do you make it? I hear everyone say, oh, everyone goes, we make it maximally tight. And if you look at the literature, these people often complain in the literature of lack of plantar flexion. I'm not talking about my patients that has an Achilles lengthening. I'm talking about it being overtightened, but maybe you can't overtighten it. Maybe the sarcomeres stretch. Let's just go down the line. Jim? They stretch. Tight as you can make it as tight as you can. I'm pretty much for brute, yeah. Bruce? I don't really overtighten it. I dorsiflex the foot and put it in with enough tension to hold the foot slightly above dorsal neutral. Agree. So you respect Blick's Curve type issues. So let's do the chat questions. Greg, what's your answer? Just tell me your answer to the question, Greg. That's what you're making. I'm saying that the muscle will add sarcomeres. And so it does Blick's Curve shifts, but it can't shorten. So it can only, muscle can only lengthen and it can add sarcomeres. Chat questions. I had one about heel fat pad shift. That was a long time ago. Have you ever seen the heel fat pad shift? I had answered that. I had answered that by text. Okay, sorry. I didn't see that. All right. Can you repeat it for everyone else? Let's move along to another one. It wasn't, it's a bit esoteric. Brostrom procedure in CMT and capoveris. In general, how often do you do brostroms in CMT? Do you have to do it or is it necessary? Jim? If they're loose. But it only works if you straighten the deformity. Yeah. Bruce, do you see it a lot? I very rarely add a brostrom. At our consensus meeting, most people said most that they frequently do a brostrom. I rarely have to do a brostrom in a CMT patient. They're just not high functioning enough to stretch it out. But interestingly, and that if you see it, I'll often see isolated calcaneal fibroligament laxity. It's odd. It's not an anterior problem, but that's- My answer is about capoveris. There's a lot of capoveris that is in CMT. So there are cases that have capoveris. Absolutely. You have to correct the capoveris and then do a brostrom if you need it. But not often. Let's take the corollary to that. Are you willing to do a total ankle in a patient with CMT after you've corrected them? That's a great question. I'll leave it to the group. That was my case, actually, which we won't get to. But if it was somebody who has arthritis in their ankle, I corrected their capoveris and they have a lax ankle with arthritis. And if you can do everything, what would you do to the total ankle to correct the ankle? My only comment on that is CMT people do not have normal sensibility, right? So I will correct the ankle and leave it even if there's arthritic changes, unless it's just so severe you can't get the ankle reduced. But if I can reduce an ankle, even if it has moderate arthritis, I'll leave it alone in a CMT patient. Bruce. Not a big series. I would be hard pressed to do an ankle arthroplasty in someone with CMT unless it was very mild. A fusion not only takes the pain away, but creates stability. I would definitely try to push the patient toward arthrodesis. So I'll speak to it. I've done it twice, but they were in patients who already had significant hindfoot contracture and arthritic change. So very late stage CMT. After rebalancing, I did go ahead and do it because otherwise they were gonna have a functional pan tailor. Do you all really find patients who have pain from their ankle arthritis? They may be unstable, as Bruce said, but how often do you really find patients with pain? I see a CMT who needs it. It needs a fusion or a replacement. No ankle pathology. I think what we're gonna do is try to answer the other questions in the text. If my fellow panelists could help with that, but I think we have to wrap up. We've gone 15 minutes over. So I wanna thank everybody and why don't we jump on the text. I apologize for my technical issues here. As you see, I finally got power back. So we made it through. Thanks everybody. Thanks, Lucas and Irvin and everyone helps to organize this. I really appreciate it and hope this was useful. Thank you very much. Thank you all. Night everyone.

perineal tendon tears

cavovarus deformity

treatment

biomechanics

perineal tendons

surgical techniques

tendon transfers

subtalar fusions

classification

repair

ligament instability

varus hindfoot deformities

optimal function