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Good evening everyone. I hope uh you can hear me and you can see me. Uh Welcome to the 14th episode of Masters Techniques webinar. My name is Manish B. I'm a consultant uh at University Hospitals of Leicester. Uh On behalf of the Education Committee of BOFA, I would like to welcome you all on board. Uh This very popular Master Technique series. Uh We organize it about once every three months and uh we usually have two speakers and we pick up a topic which of is, is of interest to most of the foot and ankle surgeons. So tonight's uh topic we have chosen is um flat foot, not just flat foot but progressive collapsing, flat foot deformity. It's an interesting topic and it's something which we all debate about what causes it, um how to treat it, how to classify it. And in this evening session, our two guest speakers will help us to understand the basics of the uh pathophysiology and the treatment. So our first speaker is Mister Chandra Paula. He's a consultant for an ankle surgeon at Q hospital. Um He has done a fellowship just before me um when I started in Cambridge. So he was a previous fellow and I saw lots of letters of Chara at Edinburg Hospital. Uh Chandra has an immense interest in the spring ligament and the pathogenesis of uh flat foot. And he's going to share today his view, his understanding uh and we'll learn from Chandra. So Chandra, please uh start sharing your presentation once you're ready. Thank you. Hold on. Yeah, sorry. Just going. No problems. So, while Chandra is doing that, oh, he's done it now. I was going to Yeah, after Chandra, uh we have our second guest speaker and then after that, we'll do a discussion session. So all the questions please put in the Q and A. OK. Over to you Chandra Manish. Thank you very much for that uh introduction and I suppose it's uh I'm very grateful to be on this sort of platform. Um Today, I've been asked to talk about the importance of spring ligament in PCF D. The title of my talk is Axis and Ligaments. Um when I looked at this subject and I put PCF D into PUBMED, what it did was return 1600 articles and no one person can have complete knowledge over this subject. And uh I certainly didn't read 1600 papers for this talk. So the focus of my talk is going to be on the Spring Lignan and essential sequential ligament failure, the subtalar axis and ground reaction forces and a test that spring ment lacks to that. I think we can test for and the principal sort of rationale for treatment. I still believe PCF D is still a primarily a disease of ligament and it's ligament laxity that leads to the joint deformity and joint degeneration and stiffness. And it's that ligament laxity that leads to the tendon overload, uh dysfunction, synovitis and rupture of those tendons. But in order to progress, we need to dispel existing dogma. And there's several ways we can do this using rheumatological evidence, we can use E MG evidence. But one of the best ways of doing this is to actually look at stage two disease. What was stated was that the tendon lengthened and led to a dynamic instability of the arch. But if you take a tendon and lengthen it, what you're effectively doing is introducing slack into that system. And if you put enough slack in that system, that's like detaching it. And we do that when we do our t post tendon transverse. And if you look at the long term outcome of patients who have had tibialis, posterior tendon transverse for both drop feet and pes cavus, what we're finding time and time again is that the foot doesn't necessarily go into planus despite 8 to 10 years follow up on some of these patients. So if the lack of tip post doesn't induce planus, what's keeping the arch up? And Wang did a study where he was able to use string gauge poten to measure foot length and arch height. And what he found was when sectioning the long and short plantar ligaments, the plantar fascia and the spring ligament. 63% of arch stability was still maintained. But out of that 37% loss of arch stability, only 14% was due to the spring ligament. So, if only 14% of arch stability is due to spring ligament, can it be important? Well, we know that the spring ligament is a very resilient structure. And the Japanese were able to show using ultrasound on transverse sections. Spring ligament had very little strain that developed, but it does develop strain. And when you load the spring ligament, it's an elastic structure that develops strain. And when you unload it, it then goes back to its original position. But Rey was able to show that in the absence of plant fascia, the spring ligament undergoes plastic deformation. So the plant fascia is hugely protective of the spring ligament. In the absence of it, it will go into plastic deformation and permanent strain. And Cyce were able to show that cyclical loading is very important as well. So they were able to take feet and statically load them. Even if you statically load these feet 3000 cycles, you do not incr induce a Planovalgus model. But when you section spring on the plan fascia, you generated some elements of Planovalgus. But it was with that cyclical load into 3000 cyclic loads. What they're able to do is identify a radiographic evidence of a Planovalgus model. So it's not just the fact that the sprinkling sections to induce visible planus, you really need to cyclically load it to induce that first grades fail. And, but can the spring lid alone cause problems, er sectioning alone cause problems? And I think this is one of the most crucial studies done by Jennings. And what he was able to do was use positional potentiometric to look at peri talar rotational changes that occurred when you section the spring ligament. And what he was able to find was when he sectioned the spring ligament, he was able to induce non visible peritalar rotational changes without visible evidence of Planovalgus model. And he correctly concluded that the spring ligament did function as a linchpin to support that mid large. And we were able to show in a study where we looked at patients who had prenatal external rotation, uh stage 12 injuries and uh and supination exter rotation, ligamentous stage four injuries, ie patients who had complete deltoid rupture. What we found was that the deltoid firms up ie they had a negative et draw test, but the spring ligament was still loose, either had a lot of tail end abduction laxity. And this is crucial because for the first time in vivo, we know when 0.0 is when the injury occurred. And what we found was that the first ray destabilizes in patients who have been loading it greater than six months. And patients that hadn't been loading it for greater than six months still had a stable first ray. And in 75% of patients, patients had a reactive T PA. So the spring li is crucial in sort of protecting that first race. So if we know when the spring ligan fails, could we test the be testing for it early? And the answer is yes. But so it really, it doesn't matter whether it's the plantar fresh that becomes weak or the spring ligament becomes lax pressure on that spring ligament with these extrinsic pressures will ultimately result in talar navicular subluxation which will then generate an altered subtalar axis, opposing internal foot moments and increased reactivity of muscles. In particular, the tip post is the one we go for and why does Tipo react? Well, I think it's really important to appreciate the subtalar axis and the subtalar axis closely follows that central path of the uh mid talar body and the mid talar neck. And it's closely linked to Taylor's position. It's offset from the floor by about 42 degrees. But in pronation, the subtalar axis inter rotates and plant flexes and in super, it exits and dorsiflexor, but it's not fixed and it's dynamic throughout the gate. It varies between people sexes, the morphology of the subtalar joint. So, and it's very clinically hard to judge. And there are tests for it, but I'm not gonna go into it in this uh particular lecture. But in mid stance, the subtalar axis roughly points towards the hallux and in terminal stances, the tibia exter rotates the talar section rotates and locks the forefoot. You generate a net inversion moment through the ground reaction force that acts through your stable first grade. And roughly 60% of the force goes through that stable first rate generating that net inversion moment. But with sprinkling and laxity, what you're doing is decreasing the arc of uh external rotation at the forefoot, diminishing that ground reaction inversion force. And with destabilization of the first grade, you're transferring the load to the second me metatarsal further diminishing that inversion ground reaction force and with significant spring laxity, you end up generating an E version ground reaction force which tip posts just simply can't act against. And if you look at the anatomy of F DL, which runs a far more straight line course, the strongest fibers to post start far laterally and insert as far lateral as the fifth metatarsal base sometimes. And in er terminal stance, subtalar axis externally rotated and much of tibialis posterior acts medial to the subtalar axis. And therefore, you generate a net inversion moment particularly at the navicular. But with that diminished er er external rotation of that subtalar axis, much of the anatomy of tip post now allows lies lateral to that subtalar axis and you're diminishing that net inversion, ground reaction force that develops at the navicular and the end result of this is the muscles have to do more work and it's not just tip poster Agrian was able to show that there was increased activity in soleus. And in order to compensate for first stra the abduct hallucis and flexor is also increasing in its activity. So a lot of muscles are trying to compensate for this er functional er loss. So when does tendon reactivity occur, cos the reality is if the tendons are not active, they cannot be overloading. So we've got to look at where peak overload occurs. And if you look at maximum voluntary contraction during the gait cycle, both soleus and tid post maximally contract at about 48% of gait cycle in mid stance where we examine the foot soleus and TPO are only acting at about 20 30% of their activity. They cannot be overloaded. It's that this 48% we're gonna be generating this overload when the tendons are active, not inactive. And what's happening at this point, what we're seeing is that the foot is in terminal stance, the contralateral foot's off the ground, the entire weight's going through that uh foot ready for forward motion. And the subtalar axis is now parallel to the floor maximally er localized to, to absorb that ground reaction vector around that subtalar axis. So it's in a perfect position to take that inversion moment perfectly designed. So at peak tip post activity, the contralat foot's off the ground where a toe off the sub ax is parallel to the ground. And at this point, the fore foot is fixed to the ground. The foot can't invert because tip post, although acts as a net inverter, the foot cannot come off the ground at that point, it's actually fixed to the ground. So what really happens? It's se it's primary action is to externally rotate that tibia in, in doing so you're excellently rotating the talus and doing so, you're excellently rotating that subtalar axis and therefore you're generating that net inversion moment which then drives that linkage to the heel and along with the tender achilles inverts that heel and that's all well aligned. And this is the diagram I'm taking from a sister paper. But that middle foot also shows that soleus which constitutes about 62% of the transverse muscle bulk actually rotates internally to insert on the meter side of that calcaneum. And therefore, when you get midfoot spring and laxity, you're generating a 4 ft oppose opposing moment to that soleus. And eventually that center of pressure line will uh transfer far laterally. And along with failure of the middle column will cause the lateral column to destabilize. And I feel when the lateral column destabilizes, you're in a, a more advanced stage of PCF D than, than just when the middle column destabilize the zone of instability is now spreading to the lateral column to the ankle. But when the spring ligament fails, it's very difficult to detect. It's not a painful condition. And one of the reasons might be this. So we did a study where we looked at the force required to generate a hill lift. And when you uh use the plant's fascia sectioning as a baseline, we need, we did a certain amount of force to generate a heel lift. We then sectioned the spring ligament destabilized the first ray and then sectioned the lateral plantar ligaments. And what we found universally in virtually every cadaver is when you section that spring ligament, the force required to generate a heel lift actually decrease uh spring ligament in isolation doesn't necessarily cause tendon reactivity because you're not actually overloading them. It's when you destabilize that first ray, you get a massive upswing and a statistically significant increase in force required. And um although we didn't test to post, it's, it may be that the spring is actually a silent er er situation wasting for that first rate of valve causing that reactivity. We did this using caves and a custom made jig. I'm not gonna go into that. So the spring ligament laxity allows medial talar head subluxation and talus internal rotation and where does that occur and occurs, two points occurs congruently early in er stance where the whole talus and the tibia internally rotate and occurs incongruent where the talus internally rotate successively within the ankle mortis itself and that's actually underappreciated. It's very important to note that when you are going into toe off, uh particularly in accelerative gaits, you can have 10 times your body weight or force generated going through that stable first range congruency of that tavi axis allows that huge axial force to be transmitted to the tibia to then generate a forward propulsive thrust. But without that er congruence, what were happening, what we're seeing is that weight uh that force transverse transfer to the middle column. And that's not important in itself. But when you transfer that force to the middle column, what you're doing with that to navicular subluxation is generating a secondary vector which is torque. Now, you're putting a rotational pressure with cyclical loading on that talus. And when you look at that axial plain sequence, what's happening at the talus within the mortis, you have four principal constraints. You have that spring ligament preventing that talar head from swinging immediately. You have ATFL pulling it back into place. You have the constraint from the bony congruence and deep Tso. And the problem is PFD, two of these constraints have got, you've lost your spring ligament and you've lost your bony constraint, which can constitute up to 30%. Now, the talus is really principally dependent on AFL and deep deltoid and it has no muscular attachment. So there's no dynamic instability, er dynamic stability that's conferred ATF R acts in tension. Therefore, deep deltoid will always fail in shit. And therefore you get this deep deltoid failure far before Johnson Strum's er stage four classification where you get that valgus tilt and you get this anteromedial instability of the ankle that is detectable very commonly. And this Taylor inter rotation, there's been more and more papers coming out on it and it's almost very difficult to appreciate radiologically and it's often underdressed in surgery. But this is the key paper by Kim et al. And uh they were able to take patients who had PCF D and look at patients in the sort of adult population and they had this inclusion exclusion criteria. But in reality, they looked at P PCF D was classified as patients having a 10 on coverage angle of growth and about 20 degrees. And they divided, they were able to select 79 patients and divide these into two groups, moderate abduction and severe abduction group. And the severe abduction group had a talar coverage angle of greater than 40 degrees. And then they had a control arm of patients who had uh no evidence of PCF D and using selective to tomograms that they were able to overlay. They were able to look at this angle which is the transmetatarsal talus angle and with internal rotation, this angle critically decreases, they looked at other angles as well. But this was a principal angle and they were also able to look at the angle subtended by the medial border of the lateral malleolus and the lateral border of the talus. And any increase in this angle represented an increase in uh in some rotation of the talus. They also looked for degenerative changes within the er middle malleolus. But the key measure, key measure was this trans malleolus talus axis. And what they found was a statistically significant decrease in that angle in patients with PCF D. So that talus is rotated even in moderate abduction patients. And when you look at the other angle, which is the angle subtended by the media border of the lateral malleolus and the lateral border of the talus. What they found there was a statistically significant increase uh between control of moderates and moderates and severe. Again, proving that uh the talus is internally rotating and probably very early on and under appreciated. And in all their patients, they found an increase in media arthritis and there's that pressure on deep deltoid cos it's failing in sheer and, but I don't believe it's the whole story. And when you go back to sort of Kim's paper, and you uh we realize with cyclical loading, you're applying internal rotation torque and you lose two of those constraints. Um does deep deltoid always fail. And the answer is no. And what we found was that with atrial e laxity, deep deltoid doesn't fail. So when you clinically test for deep deltoid failure, that's with a heel, external rotation test and an anteromedial draw test they're quite solid on that middle side and they have uh significant antra lateral instability. And when you go back to Kim's paper, this is the key diagram and you look at the controls and you look at that lateral side in the control group, you see a certain degree of anterior position of the talus compared to the lateral malleolus. And in the moderate abduction group, it's roughly the same. But in the severe abduction group, you can see there's a significant anterior translation and that's in picture c of that talus on the lateral malleolus. And if you look at the middle side, in C, it's congruent. But in B the medial side is incongruent and the talus has almost shifted posteriorly. So there are different patterns and that's that key anterior translation. And what we did was we took uh cadavers to test this and we took six control feet and six paired feet. And with these paired feet, we're able to induce planus by section and sprinkling with superficial deltoid plants fashion first destabilize the first gray and we randomized those pair feet to ATFL, sectioned or ATFL intact and cyclically loaded them to 2000 cycles. And this is the thing I want to share with you. So if you take these feet and you take the control feet with cyclical loading, you are seeing a very small increase in strain in deep deltoid as measured by anterior meal separation. And um what we found was in the er group that had planus induced with the ATFL intact, that deep deltoid strain rate massively increases. And that's why you see the sheer failure of deep deltoid. But in patients where we cut and sectioned ATFL, the deep deltoid strain rate almost comes back to the control level. So with spring ligament laxity, the lack of ATL is hugely protective of that deep deltoid, it almost brings it back to original levels. So a of lac laxity does protect against deep deltoid. And what we found was that patients with planus uh with uh AFL intact deep deltoid strain was about 3.5 micrometers per cycle. And the reason for this is we believe that the talus rotation hinges on ATFL which acts in tension and is favorable in deep deltoid bells and shear compared to when is absent where the hinge is on deep delta. And a the talus is able to translate out. And the relative strain that's developed is 0.6 micrometers per cycle, which is almost the same as the control. So if we, I know that spring ligament is important, can we test for it? And I just wanna share this video quickly. It's about 30 seconds and it's the left foot that you just wanna observe. And I don't think there's too many toe signs, but he's able to his comfort go single STRS leg leg raising on the right. It's a bit more hesitancy on the left. But when you take the heel off the ground and you control the heel for pronation, ie put the heel into neutral or varus and prevent heel external rotation. What you see is this massive abduction swing and that is what we call the neutral heel later push test where you neutralize the pronatal forces and you can test for that abduction and the problem with testing for it when we went through, it was, uh, when you look at the anatomy, there's almost 26 different papers uh looking at the anatomy of Delta Spring. And part of the problem is is there's different names for the same ligaments, some ligaments are emitted. There's variability of sizes of bands that are described. But the key paper I think uh you should be alluded to is by Kentaro Amaar. And what he did was was able to reflect the capsule super deltoid and Spring as a single structure and looked at the, looked at it from the inside. It's actually a single reflectable interconnected structure with no different bands. And those extrinsic outside bands are just represented representation of forces that develop in that. So when you look at superficial deltoid spring anatomy, it acts across this, this big joint ligament actually acts across three joints, the tibiotalar joint, subtalar joint and the ta navicular joint. And it's a trapezoidal structure in the majority of people. And if you looked at a world without supra deltoid spring, what would we see we'd see that the tibiotalar joint is still constrained medially by the deep anterior and posterior ligaments. The subtalar joint is, is still constrained by several ligaments. But it's that talar navicular axis that has no medial constraint. So if you wanna examine for spring ligament laxity, the best place to do it is to look at the talar navicular axis. And we were able to um I'm not gonna go through this in detail but selectively section loaded, unloaded tendons in retrograde and prograde fashion. And it's only when you divide the spring ligament, you get this massive abductions er swing when you control the subtalar axis and the tibiotalar axis. And therefore, we came up with this saying, applying a small force with the hind foot and neutral, generating a 1.5 centimeter translation at the hallux really is attributable to spring ligament failure. And you can compare different feet and notice subjective firm and non frm endpoints. And I'm glad to say there's increasing amounts of validation studies that are coming out and sliva was able to show it has a good interclass, uh coefficient of growth and 0.8. And the basis of the test is when you er control for pronation, you're using the first metatarsal and the 10 vi axis by taking a small strain that develops in spring ligament, you're able to use that er metatarsal tenovir axis to amplify that strain to generate a large degree of shift at the hallux and that's what we're looking at a visual interpretation of strain that develops media at that tenovir axis. And this we feel can only occur due to Deb function of that spring ligament. And therefore, you have to introduce the concept of this stage, naught disease of ligament failure, I believe. And when you look at the plantar grade foot and you look at Jennings study who show that spring ligament failure does cause those per rotations but no visible deformity. That's exactly what's happening in the, when the foot is on the ground, that middle spring ligament has failed, but there's no visible deformity. But when you take it off the ground, you get that massive abduction swing as the talus swings through that, that poorly er, that poorly defined that poorly defined spring ligament and the first straight ground reaction force will always put the foot back into neutral, but in the absence of spring ligament and as the first rate fails, the foot progresses into this planus and then TPO comes in to try to counteract it. So why address the spring ligament? Well, it's the primary i it's the internal, primary restraint to foot pronation externally. Uh We look at the first gray as a primary restraint, but internally, the spring ligament also acts as a primary strain and it allows that realignment of the subtalar a access to a more anatomical position. And you've got to remember bony fusions and osteotomies are not a substitute for spring ligament reconstruction as a spring ligament reconstruction is not a substitute for real lining your bones. And there's no specific guidelines. The option has really come down to nonanatomic anatomic spring Delta spring allografts, orthograph and synthetics. Are there any, is there any evidence that one is better over another? And I'd allude you to this paper by Gavin Hayes Malloy. And what they were able to do was look at a retrospective level three evidence review of patients who had had a, a uh synthetic reconstruction with an internal brace compared to a hamstring allograft. They weren't like the light reconstructions. But what they found was that radiographically, the synthetics did better compared to the hamstrings and clinically, they did better and the patient reco about reported scores. And that's despite that circle at the top, right, showing that the synthetics had far less medial displacement osteotomies that had functional better outcome with the synthetics. And again, it's not proof but it's heading in that sort of direction. And um if you look at er, the allographs, there's multiple options out there. Uh you can use a tendon allografts and this is one by Brodell, he reconstructed spring and Delta spring and this is one by er Robinson where they used the er stump tip post to reconstruct that spring ligament. But really people have moved onto synthetics and the advantage of this is it restores sling function allows that derotation on that reduction of that Talus and it avoids talus tunnels, screws and washes and precarious placements of these. And we're able to try to look at er, which one of the reconstruction is the most important and there's several out there. But this one, we looked at what we did crucially, I think was looked at whether a simple repair was better than a reconstruction. And which part of this, this uh well defined reconstruction, one was the most important. And by sectioning these and applying an abduction force, what we found was that reconstruction was always better than a repair. And uh even if you think a repair is good, what you're trying to do is put back failed tissues onto itself. And what we found was that by sectioning that dorsal ligament, we found that the plantar ligament was still able to er preserve abduction er plane laxity. But when you sectioned the plantar ligament with the dorsal intact, the dorsal limb had no effective uh resistance, but there's multiple options. And what you're trying to do is resolve this vast ligament into a single linear construct, which is really impossible to do and uh it can help aspects of it, but you're not gonna solve all of it. And the ideal reconstruction is put 20 different reconstructs covering the whole span of that ligament. But these are some of the common constructs to come off the medial malleolus and to go off the top. But we know this shouldn't be your primary option. Because in mid stance, when the Teli is maximally internal rotated, these fibers are slack. So that can't be your primary option. When you come off the medial malleolus, uh at fixed bone points, you have two options. You can either come off the median malleolus or the substantiate and you come down to the inferior part of the navicular and they're both good options and that's commonly used as an adjunct. And uh we know that the problem with using this limb where you come off the mo of Malleolus is if deep deltoid has failed in she and your tension in that, you're gonna translate that er Talus posteriorly and allow some abduction laxity to happen. And in fact, your deep function that spring l it has to act across two joints and that limb is actually perpendicular to the plane of the tone navi axis and therefore resolved will have very little function in the axis you want. And therefore, and we know that limb has very little benefit. So your money shot if you're gonna use one limb is that I can only tell you what I do. I use a two plants construct. If it's big enough, I do a four plants construct a double up. Some people do put it down into the medial can form, II have reservations about doing this. And the reason is is that there's a lot of studies now showing particularly in finite element modeling that if you decrease the er n caniform er motion, you massively increase strain across the spring ligament. And uh therefore, I think reconstruct is better than repair. Augmented reconstruction is better in the plant room is the most important. And the problem we're trying to compare these is that you have so many compounders, but research is gonna come out showing what is the best. So it's not if, when you look at stage naught one and two, and these are ligament ligamentous staging and it's nothing to do with the PCF D staging. Um It's important to restore tripod stability but redirect that subtalar axis. But I'm just gonna quickly go back and I've almost finished. Uh If you, if you basically er redirect your, if you introduce stability in your first grade, it doesn't matter if your uh spring ligament is lax and your uh subset of AX is internally rotated, you're still gonna generate an eer vector. What you need to do is, and that's it. If you plant flex it, it's still gonna act against you. What you need to do is reconstitute that spring ligament to reconstitute the subtalar axis and therefore generate an net inversion, ground reaction force. And the calcon osteotomy is important and uh doing a heel shift, you get several benefits. But again, you're improving your ground reaction. Er your inversion pull around the subtalar axis from my last slide. Deep deltoid instability is very hard to control. And you've gotta remember anterior constructs are not gonna stop that internal rotation and in the future should be be reconstructing AFL. I think we probably should and should be preserving to post. Yes, because it's an external rotator of the tibia unlike F DL and it acts to excellent rotate that. So in conclusion, spring like laxity, I believe is a route to development of PCF D. There's patterns of internal rotation failure of the talus that are emerging, restoring that subset of axis is critical to foot, foot function after restoring the tripod stability and it should be part of modern treatment plans. I'm gonna get you out on this and this is a quote from John Lennon and I believe this is true, the more I see, the less I seem to know for sure. Thank you. Thank you very much um uh Chandra for a very uh interesting talk and uh I'm sure there will be questions we'll follow. So let me now introduce um to our second speaker. So Chandra, if you can uns Yeah. Uh So our second speaker is the first um we have got on master Techniques from USA over the phone, but obviously uh online. Uh And thank you so much um uh CAA to be with us and I know it's a time difference. So you had to cut down your commitments and, and to be with us. Um doctor, he is um an associate professor at Duke University. He's also the president of the Weight Bearing International uh city uh Society. He's editor in chief uh of foot and ankle clinics and he has several research interests. But I think the one which is close to his heart, he has done a lot of work on progressive, collapsing flat foot. And he's one of the pioneers for the new classification, which he's going to share with us. So says up all over to you. Oh, thank you. Can, can you guys see my screen there? Yeah. OK, good. Well, first, uh II appreciate the invitation. It's uh it's a great pleasure and a great honor to be here. So, uh thank you. Uh The organizing come in both us for the, for the invitation. I do have conflicts uh with uh every talk of PCF D because of my relationship with uh with uh curve be and, and other companies with Weight Bearing CT. Uh and uh it's always great to be with my British friends. I just did a, a uh a road trip with my family uh through the north part of the UK. And here are some pictures were recently with um uh British friends, including the British Mafia and a OFA s on the top left there as you guys can see. Uh But always a, a great pleasure. Sorry to interrupt. Your sls are not moving. Oh, really? Oh, let's do it again. Yeah, that's good. OK, let's stop and do it again. So I was showing some stuff and you guys couldn't see it. Let's do it again. Uh And you guys see now. Yeah. Is it, let me see if it's moving? Is it moving? Yes. OK. I apologize for that. Uh Here's the pictures. Uh So this is the, the, the British mafia and a ofa s familiar faces for you guys there. So it's always a great pleasure uh to, to meet you guys and, and to visit. Um So again, I appreciate the invitation. So I think you guys asked me to talk a little bit about the uh the classification. And uh I II gave a similar talk at a, a this last meeting. So tell a very brief uh a little story behind the consensus meeting that happened in 2019 just before COVID hit um with some uh uh experts on the field though, I was uh one of my fellowship in the USI, I had the, the play here, the honor to train under Doctor Delan and Doctor Ellis. There are uh two of the most published authors on the subject. Uh And uh you know, II always had my passion for flat foot. I had some work uh even before arriving there during my research time here in the US. And then uh it was a, a great opportunity for me to learn from them and to come up with some ideas. And one of the ideas that we had was that based on some information. Uh and I think this is uh one of uh probably the most important slide of the talk. Um And uh uh part of the concepts that were introduced or uh I would say expanded, I don't wanna say introduced but expanded with weight bearing ct regarding bone alignment. And we just had a great talk uh about uh spring ligament as a possible, you know, initial factor for PC FDI think is highly controversial. I can't disagree with a lot of what was said there, but I, I'm not sure that uh we can narrow down to one single stretcher unfortunately, for us as surgeons. Uh but I think the concept peral subluxation is very important. It, it it goes, it swings the pendulum back to the to the bone alignment a little bit more. Uh but this comes as a peritoneal subluxation is basically the foot uh subluxing under the talus uh in PCF D with uh uh a malalignment of the subtalar joint where you could be born with a more inclined valgus, subtalar joint that we are seeing here on the, on the poster facet. Uh the presence of subtalar joint subluxation that you can assess by looking into the posterior facet here or the middle facet here, facet subluxation, poster facet subluxation, as well as indirect signs of of peritoneal subluxation. Uh most importantly, sign of starts impingement. That is basically the later process hitting the Calcaneus and the Calcaneus hitting the Fila are uh important concepts that we thought uh needed to be introduced in the uh the literature. Uh And it were, they were not really utilized in the classification. So we started thinking about it. We exchanged emails, we did a full review of the literature and it was tough, very hard to make decisions on that regard of uh of, of how who to invite for in person meeting. So we sent invitations out. Uh We actually sent a full questionnaire uh ahead of the time to talk about things. And because the, the lectures about the classification, we ask it the experts that we invited, do we think the classification is outdated? And then should we discuss a new classification system? And it was 100% agreement that that was the case. And then the the meeting finally happened in November 2019. A lot of people ask me, how do if did I feel during the meeting? That was me there, right. Uh No one uh close to the other people that were in the meeting. Uh We all make, we all had talks about specific subjects. Uh and, and these are just some uh pictures from the day of the consensus there. It was a, it was a great meeting and one of the things that we discussed was about the classification system. So we came up with this after discussing all the topics. So we discussed pretty much every single topic uh in two days there. So a total of 16 hours of recorded meeting. And uh we came up with this proposal and we voted uh to uh once we were done with the meeting for uh agreement between the, the experts and we, we had 100% agreement to get that out. Uh A lot of uh uh man came out in Fen International. A year later, October 2020 including the one where we recommended this change in the nomenclature. Uh And the reason for that is multiple. Uh So we didn't want the adults there and we didn't want the acquired because a lot of patients, they had flat feet their entire life, they just started becoming symptomatic when they're adults. Uh And they all, of course, it can happen during uh uh late childhood or, or uh adolescent teenager times and early adulthood. Uh flat foot is, you know, we think it's un it underestimates the problem. The arch collapse is just one of the many deformity patterns or uh uh deformities that we see in a, in a, in a P PCF D. And as uh we had in the prior lecture, like the poster T to 10 is just the tip of the eye spe. So we came with this progressive collapsing foot deformity. Again, it's OK to have a flat foot. It's not OK to have a flat foot that is getting worse. That's that could be progression, collapsing foot deform. So basically, it would be the pathologic flat foot. And if you look into the classification, the only thing that really changed first, we didn't like the idea that the prior classification systems like stage 1234 gave an idea that you would have to go for one to get to two and then to get to three and then four, this sequence doesn't really happen in patients. Uh And we thought that basically the only two stages that would be sequential would be a flexible deformity, becoming rigid, deformity, uh chronically. Uh So you would have to be flexible first to be rigid unless you have something else like a tarsal collision or something that would explain a rigid flat foot to begin with. And then we, we did not reinvent the wheel. If you really look into the classes that we call deformity classes, it's basically uh getting everything that was already in the other classification system and things that are important for, for providers to look into. Uh And uh uh adding that as classes of the former, the only new thing was per sub, that would be the class D there. And then we wanted people to be able to look into the, the feet, look into the patient and be able to describe what they see based on the presence of these deformity patterns. So the idea of the class classification was always, you look at the patient and you tell me what you see and then I will be able to understand what you're talking about. So basically, if you see hind foot valgus, you would put a letter A here. If you see midfoot of 4 ft a deduction, it's controversial. Some people prefer four footed deduction. Some, some people prefer midfoot deduction. So we put midfoot forefoot, so we didn't get into too much discussion on that. Uh But if you see midfoot 4 ft a deduction, you would put a, a letter B there. If you see collapse of the longitudinal arch that was previously described as uh media colony ST 4 ft Vries, when you correct the, the hind foot super controversial. I think the class D is class C is the most controversial one in my opinion, but medial column collapse or arch collapse would be class C, then you put a letter C there. If you see peritoneal subluxation, that is not easy to see with X ray, you can have uh indirect signs of it, but you would put up a letter D there. And if you see a valgus deformity of the ankle, they would put a class E there. So you basically could combine those letters and every single deformity class can be one or two flexible or rigid. Uh And we're gonna play with the classification a little bit. We did look into uh uh uh the uh the reliability or the uh of the classification inter and inter observer reliability. We published this in food and in international a couple of years ago. Uh And we describe the frequency of the classes. So class a most frequent followed by class C. Uh That would be the collapse. Class B would be the 3rd 1 76% of a reduction. Class D uh less frequent also because people are not very uh uh I would say gouged and, and, and, and used to look into that kind of deformity and class Z as expected, the ankle deformity less common. Uh in the combination, we found that uh A 1 B1 C, one or one ABC with valgus abduction and collapse was the most common one followed by AC that is valgus and collapse and then followed by one, A BD Valgus abduction collapse and per of blood. But again, the idea of this classification was never to be super high reliability. Uh The idea was if you tell me you have a one ABC doesn't matter where you are in the world, you would be able to understand what that person has in front of them. And when we looked into the interobserver reliability as expected, class D uh was the lea the the lowest numbers because, you know, you, you can't really see what you're not used to see. Uh So class D still creates uh a lot of a contro uh controversial discussion and class C, as I said, I think it's tough, uh particularly if you think about dynamic positioning of the fourth, we want to correct the, the hind foot that's also controversial and debatable. And so that was the second lowest uh reliability that we found. But overall the inter observer reliability for the full classification was 0.85 and the inter observers 0.56 that is not a very good reliability. But again, that was expected when we uh when we came up with the classification. So people ask me, uh and II would be glad to discuss in the end here is like, is the new classification PCF D classification the size of? Of course, I'm biased and I would say yes, it is. It, and the reason for that is it allows any provider to describe what they see. Yes, what you see might be different than what I see. But if you tell me what you see, I would be able to imagine what you have in front of you and that's the reliability part. Uh uh And that the deformities can happen concomitantly and they don't have to be sequential. Uh And that was a big mistake of the uh Johnson Strum Myerson and Myerson modified by Bloom and other classifications in the literature. Uh So it helps you to think into what are the deformity patterns that you have present in that specific patient and it helps you to think about how you would correct those. So, but if you want a cookbook, that's not gonna be it there. It's almost impossible to have a cookbook or a classification that will give you exactly what you have to do for each patient. Why? Basically because surgeons approaching the ph is completely differently. Uh And it's just too comfortable with the form for a cookbook to work. Well, so it gives you an idea but it's not gonna give you uh the exact treatment that you have that you wanna have. So that would never exist, doesn't matter how much research we do on this. Uh And I do want to acknowledge some stuff cause we're gonna go into some cases to play around with a classification. Uh And you know, I want to keep in mind that we do live in a two D world, right? And that includes ourselves, the surgeons. So when we see this hind foot valgus, we wanna do a, a needle displacement calcaneal osteotomy. It doesn't matter what uh what else. Uh You see, you just say I'm gonna shift this hill and then you see this, you see a reduction of the midfoot or 4 ft or TV and coverage and you already think I'm gonna do a lot of column lengthening there or spring ligament reconstruction to correct that or both. Uh We always think plane by plane and then you see collapse like this and you say I'm gonna do a cotton or I'm gonna do a Lapidus and I'm gonna bring that first ray down. So we always try to compartmentalize things in different boxes in different planes. However, we forget that the foot is a three dimensional structure uh with uh uh 28 bones and, and, and uh uh multiple joints. So when you change the position of any part of the tripod, the entire foot is gonna readapt to that position. So when you move your heel, you're not just changing hindfoot, valgus, you're changing the entire thing. When you bring your first weight down As we teach for cable ves like a 4 ft driven hindfoot. Ves, you bring your first weight down, you're gonna generate uh va in the hind foot. So yes, we live in the two in the two D world, but we have to transition into 3D if you really want to understand PCF D. So let's use cases to, to, to, to play with it. So I'm gonna go relatively quick for the cases. Uh It's not the idea to uh go to the, to the bottom of the, of, of my choices here. So you guys can criticize. But this was a 33 year old female. Again, a very young patient with complained on the left foot. Uh She always had some flattening of the Lunar arch but she started getting worse in the last couple of years. She had a pop, she felt a pop while doing some martial arch a couple of months before she came to see me. You see the hind foot valgus that is asymmetric. You see a very unstable first ray. You can actually see the first tarsometatarsal joint popping uh in and out there. Uh You can do any measurements that you like to do. I put some measurements here th first, OK, inclination talar avicular curva. Thus, first in the axial plane, you can look into your ankle joint. Uh There's not, there's no uh visual valves there. You can look into your hind foot alignment angle. You can see I measured 32 degrees and 28 of hindfoot moment arm. Uh What is going on in the subtalar joint? What is going on in the subfibular area? You can't read t with the hind foot alignment angle. Unfortunately, so I did an MRI you see that the, the, the poster tibial tendon in this young patient was not good. There was a lot of uh uh in uh inflammation around it. Uh If you kept going distally, you saw that it was actually ruptured. So probably that was the pop that she felt there's some degeneration of the interosseous ligament there. You can see a very horizontal cervical ligament. And then when you look at those signs of peritoneal subluxation that we discussed that I showed you guys in the beginning, she had a 25 degrees angulation of the poster facet on the midpoint of the subtalar joint. She had signs of a of posterior facet subluxation. She had sinus starts impingement. She had me facet subluxation. And uh even though the heel was not heating. Remember, weight bearing CT is weight bearing, but it's still static. It's not dynamic. So maybe she was hitting this Calcaneus on the fi when she was walking, we won't be able to be sure. Here again, sinus starts impingement. You can see a little bit of translation of the first metatarsal joint. Maybe you can make argument for a little bit of gapping on the plantar side of the first E MTI measure my middle facets f luxation 59%. I love the 4 ft arch angle for collapse. Uh We can talk about that. Uh later, 4.44 0.2 degrees and normal is in between 15 to 25. So significantly collapsed and I use foot and ankle set a lot. She had look where the center of the ankle joint is, look where the bisecting line of the tripod is. So that gives a foot and ankle set of 11. I do uh my fancy distance and coverage maps that we publish on. So basically looking into three dimensionally. So 41% of the sinus stary was covered, that means the normal goes up to 5%. So it was a lot of sinus stars, impingement, sinus stars coverage. She had 55% coverage of the middle facet, 78% coverage of the poster facet. And um um pretty much it completely dislocated that, that that number is wrong there. So I apologize. Uh uh completely dislocation of the facet. So if we play with the classification, do you see Valgus? So I would II think you all would agree that there's Valgus there. So yes, and it was flexible. So that's a one. Do we see mid foot a reduction? Uh II would say yes, we measured and yes, it was flexible. So that B1, do you see collapse of the one you do now, arch media colon collapse? Yes. And it was flexible. I'm telling you it was flexible when I, when I me uh assess. So that's ac one, do we see peritoneal subluxations? You had multiple signs of peritoneal subluxation. That is, yes, it's flexible. D one, the valve is the form of the ankle. No. So there's no E so it's a A 1 B1, C 1 B1 or ABCD. So what to do with this patient? Should we let it go? Should we continue to treat conservatively? Should we do surgery if we're doing surgery? What are we gonna do? Um So basically, like I said, the deformity classes can give you an idea of what to do. So if you say that there was valves there, you can think about uh automatically you think about a medial displacement called canal osteotomy. But remember an F DL tendon transfer a lateral column lengthening a first ray procedure, either a cotton or lappy cotton, bringing the first ray down and a subtalar joint fusion could correct kind of foot valves as well. So it's not just the medial displacement called Canio osteotomy. Uh Do you see them before the deduction? We said yes. So automatically you think about lateral column lengthening. However, again, F DL tendon transfer sprain delta ligament reconstruction, a first ray procedure, they all are gonna change uh a deduction as well, not just the lateral column lengthening uh collapse. We said there was collapse. So you can do Colton automatically come to your mind. But a La Coton an NC fusion, of course, a ta joint fusion that we wouldn't think here. Uh Hopefully. Um Also there's some literature now for an F GFA tendon transfer to the first Meath. So you mentioned J and Kane, he published on that uh could also change uh uh uh the collapse of the longitudinal arch. And what about peritoneal subluxation? We said that it is present every single procedure that you do will influence your peritoneal subluxation. So there's no one single procedure that will change it and the other ones would not. So, peritoneal subluxation is the influence for every by everything that we do. Of course, if we had uh more frequently, maybe for example, reconstruction, the interosseous ligament uh for sure. Spring and delta reconstruction changes uh uh peritoneal subluxation. Also, there's a lot of attention now for uh cervical ligament reconstruction. Those would also change uh peritoneal subluxation. So, uh what I did for this patient was a gastric name, recession, a medial displacement called can osteotomy of 11 millimeters. I did a lap Coton with a 10 millimeter wedge. I did an F DL tendon transfer. I did spring deltic uh reconstruction. I did bone marrow aspirate. Not gonna go into the details here, but this is the final x-ray for her intraoperatively and this is the video of her from before surgery to uh 12 weeks weight bearing ct. So you can see the foot derotating and the peritoneal sub being corrected. And again, remember I did not do a lot of column lengthening. So look at the uh correction of the tail avicular coverage without a lateral column lengthening. So again, you don't need a later column lying to correct uh a deduction. Uh A as brilliantly demonstrated in the prior lecture as well. This is the patient with 18 months showing that she uh maintained correction uh and uh and was doing was doing good. I'll go very quickly for the second case. Uh completely different. Uh 76 year old female. Uh with uh with this x-ray, you can see a lot of abduction of the avicular joint. The ankle is spared. There's some arthritis in the ankle, there's collapsed. There's sinus starts impingement. Uh Here is the clinical picture from the weight bearing CT where you can see the avi duction, the hindfoot, valgus. I measure her foot and ankle set. Look where the center of the ankle is. Look where the bing line of the tripod, the collapse. The amount of peritoneal subluxation completely dislocated, hidden on the fibula. And there were classified, there is hi Valgus. It was rigid. So that's a two. There is a deduction. Yes, it was flexible in my opinion. So that's B1, it was collapsed or doing the arch. There was uh uh yes, and it was flexible. So I put ac one, there was peritoneal subluxation that was rigid. So I put D2 and there was nothing in the ankle. So that would be a A 2 B1 C 1 D2 or one BC two AD. And then I did a Subtalar joint fusion. I did uh A B uh lus uh um uh bra longus tendon transfer. I did a Lappin. I did uh um an F DL tendon transfer to protect my subtalar joint. Uh I'm sorry, my, the avicular joint and I did a spring deltoid ligament augmentation and this is the patient uh x-rays uh demonstrating the correction and the weight bearing ct postoperatively showing the amount of correction that we were able to get. You see that now, the talus, the center of the ankle and the center of the tripod are exactly on the same line. You see the middle of facet uh corrected with the, with the subtalar joint fusion. And this is the patient with six months demonstrating uh preserved correction there. Uh So again, it is decisive. However, don't wait for a cookbook. Uh because I don't think any authors or or, or group of experts will be able to give you guys a cookbook. This is just too complex, too two dimensional for us to be able uh to uh to nail it down to an exact treatment option. Uh We do have some extra meetings happening and we have some other people that join the team. Uh And then we are, we're working on some updates on the classification uh and some next steps for treatment and that should be coming to the lead future very soon again. Thank you so much for having me. And uh it's a great pleasure to be here. Brilliant, really, really interesting talks tonight. Um Lots of, you know, unconventional thinking outside box sort of uh approach. Um So let's start uh the discussion. So first question says that you gave the talk, can I ask you and this is to, to understand uh what, what I uh you know, so the new classification A B and C as far as I can see, you can see it clinically. You don't need any investigation. Whereas for D you need a CT or a standing CT. Is that right? Yeah, great, great question. I mean, uh not, not necessarily, yes. If you have a weight bearing CT, it's easier for you to gauge that and to measure it. Um But, but you can, you, you have indirect signs of per subluxation. Uh and uh the HSS group, I think, I think maybe J and K was also the first alter for that one. But uh they also pub they published on um uh the form that can be seen in the x that indirectly correlated with peritoneal subluxation. Uh So you can see it on the x-ray. Uh I would say, for example, sinus starts impingement is a sign of peritoneal subluxation. So the presence of sinus starts impingement could be uh the interpretation of peritoneal subluxation right away. Uh As I think, Sh uh Chandra showed uh if you really think about it, there's no way that the, the subtalar joint is subluxing with the tail, avicular joint staying in position. So they, they happen uh concomitantly. So uh I, and I believe if I remember correctly that it just has papers show that the TV coverage is the one that predicts the best the presence of, of peritoneal subluxation in the weight bearing ct uh as one would expect. So, uh the, the, the answer to the question is yes and no. OK. Fair enough. Um Chandra. Uh So what causes spring ligament dysfunction? So we can't hear you. Are you muted? Can't hear you, Chandra. No, I think. Yeah. Nice speaking. Hello. Yeah, I can, we can hear you now. Not sure what you can hear me now. Yes. Yeah. Perfect. Yeah. So uh it's a really good question. It's very important actually because we're, we're sort of finding out more and more about different ways the spring ligament fails and Um So when you look at the spring ligament, it's supported superiorly by superficial deltoid. So you have significant amount of fibers of tibial spring ligament that insert onto it. So when you look at patients and we've looked at patients who've had supination, abduction injuries to their ankles. So these are patients who've had no pronator forces, but the foot fractures, the middle malleolus and supination auction stage two injuries in inversion. So when you look at these patients and we've only had a few of them and we've looked at these, what we found was that even if you restore the media malleolus in some of these patients, when you compare talar and navicular abduction on the injured side, compared to the contralateral side, we're finding a lot more laxity at the sort of tacular articulation. And therefore, when you're talking about the spring ligament, you can't talk about it in isolation. And the mechanism of that injury causing that increased 10 navicular abduction must be from the fact that superficial deltoid and capsule has ripped off that medial malleolus and therefore, has decreased the tension on that spring ligament and therefore allowed that talar navicular subluxation to occur. And therefore, we've now got to think of spring ligament laxity in two terms, one intrinsic spring ligament fiber laxity. And the second is when superficial deltoid fails, you also get springing laxity within itself. Ok. So I think, yeah, there's two points. And then if you're looking at sort of within the spring ligament itself. It's, it's just multiple factors. It could be age collagen degradation, just sort of repetitive use, hyperlaxity that might be preexistent BM I et cetera that intrinsically cause laxity in that spring ligament or significant tears. And we've sort of, you know, we've got to pay in the review and we're trying to classify that as type one and type two. Type one. Springland laxity is where it's defunction secondary to superficial deltoid and type two's intrinsic pathologies within the Spring L itself because they may be able to be treated differently one by sort of pulling the uh superficial deltoid back in place and the other by tightening spring ligament. Thank you. There are quite a lot of questions coming from the audience. So the first question which I would like to ask both of you can answer, how do you decide how much medial Calcaneal shift to do uh in view that there is a large normal variation in the lateral moment. So Chandra, you can answer first perhaps. Yeah. So uh the answer is so when you look at Calcaneal Anatomy, if you look at the sort of average diameter of the calcaneum of, you know, this is from sort of anatomical studies, what you're finding is the average diameter is about three centimeters in total. So you can get a pretty good shift. And if you know, uh so Mark Myoson typically described it, I think as one centimeter but then you can go more and uh, you really wanna get that calcaneum back under, er, that sort of ankle joint and you wanna decrease that sort of valgus ground reaction back to uh heel contact. So the maximum I feel you can go is probably somewhere between sort of 1 to 1.5 centimeters. I think beyond that, you're gonna lose contact area uh to actually get enough healing to happen. So, yeah, says it. Yeah. Yeah. II II agree with, II mean, you know, II, II do uh weight bearing CTS and I think I saw uh sorry to jump into another question there, but I do weight bearing CT for all my P CFD cases before. Uh Yeah, I know I'm blessed to have that available and I know it's, it's not available uh everywhere uh or randomly available. But II use the foot and ankle set uh and other measurements to plan my surgery. Um The food and AO that actually gives you exactly uh the, the, the amount of displacement that you would need uh to correct the entire deformity through an MD C. Uh Of course, that's not possible. Sometimes it tells you that you have to displace the heel by 2.5 centimeters. That is impossible. Uh But that gives you kind of a gauge of how much you would have to shift. Uh But if you don't have that, I think there's enough data in the literature. Um Again, coming from HSS where basically what you're trying to do is to have a neutral heel uh intraoperatively where your so he is aligned with the leg and you can elevate your leg and look at it. And, and then what that showed uh using x-rays is that when you have a neutral cinical heel, um you have radiographically slight virus like a, a little bit of virus. And uh and doctor Ellis has shown it before that when you have very mild virus uh in the hand foot moment arm, that's those are the patients that did better when they looked into a patient reported outcome. So I think that's a, that's a good idea for you to shift as much as you think you need. Put a provisional wire. Look at it if you did too much, go back if you need a little bit more, try to push more. So I think you can still do that clinically. Um And uh and be very precise. Thank you. Thank you. Another question is about um when do you, is, is age a criteria to say whether we are going to do deformity correction without fusion? And you start thinking about fusion or is it all physiological age is not a criteria? Look at the joint health. That's a question from one of the audience so that you can go first. Yeah. Um Well, you know, I'm not here to be uh to ignore the age, right and say Yeah, I don't, I don't even consider the age. It would, it would, I would be lying but it, it, it's not part of my first uh five algorithm uh bullet points. You know, I think if you have a good joint that is not arthritic and the majority of the joints are not arthritic, people make a big confusion. That's another big difference between the prior classification system and the PCF D classification system. If you, if you, if you look into the Myers and Blumen classification, they talk about sinus starts impingement, describing that as sclerosis on the sinus tarsi as a sign of rigidity. And that's not true in my opinion, because it's a rotational problem. You can have sinus tarsi impingement, it could be bad sinus starts impingement and you do a joint preserving correction and the sinus tarsi impingement will be gone and you spare that joint uh and patients do fine. Um So the age uh if they have a good joint, if they're flexible clinically, if they have uh a good inversion strength, uh or if they have uh possibility of repairing the inversion strength with an FDL tendon transfer or an allograft reconstruction. Those things are more important for me than the age itself. Uh But there are some patients that come to you and they are one and done type of people. They are seventies, they just retired or retired five years ago, they want to enjoy life and they say I want the solution that will give me 10 years and after that, I'm ready to go. Uh And then in that scenario, you have to respect what the patient wants. Uh But the number itself is not primordial for me. Do you want to add anything? Yeah. And I completely sort of concur with that. Uh when you see these MRI scans, when you do see some edema laterally, it's not a uh contraindication for me to, to do or not do a flat foot reconstruction. Because again, as, as I said, that impingement, that edema you see laterally doesn't mean that the ankle is degenerate. So from my side, um again, age is not a, a thing per se, but it's everything, it's the physiology of the patient has the patient medically well, is he an active patient? Is he able to rehab afterwards? Is he able to stay in APA P afterwards? So, I think um and other tissue is gonna be able to take that reconstruction. So if you've got a very sort of osteoporotic bone, you're gonna struggle to get your bony anchors into, um you're gonna struggle to get sort of good fixation. So it's not age, it's, it's really their physiological age, not their chronological age that you're really looking into in the safe physiological age is way ahead of their chronological age. I certainly would consider it. Thank you. Uh Chandra, uh you might have answered it in your talk, but there is a question about um that you nicely explained the basic signs of flexible flat foot. Does this knowledge change your operative plan of type two flat foot? Uh When would you augment FDL transfer with some kind of spring ligament plication? Yeah. So the answer is, is sorry, sorry. Yeah, sorry. It's made me think a lot more about the way I do things and way that things are probably going to go in the future in terms of sort of soft tissue management. Because what I think PCF D is, is really a Perry Taylor problem. It's that Taylor swinging round and um we may not be able to see it early. And therefore, I still think that deformity is a secondary consequence um of that soft tissue instability that's happening and you might see that soft instability very early. But in a stage two flat foot, uh I always do a middle heel shift. I always now do a spring ligament reconstruction because in that terminal stance, you've got to be able to ext rotate that tibia. And there's only three ways you can get tenar congruency. And one is if you're considering a lateral lengthening, it's not an operation I like due to multiple reasons, you can do it through a 10 of arthrodesis, but you're gonna stiffen that foot. Although you maintain congruent, see it see expense of that joint. And the best way of doing that is by doing the spring ligament reconstruction. I always do a uh a minimum two plan a construct. But if the ST is big, then I will go for a four planter construct with 4.7 swivel lock in that at that place. Do I always pass F DL? And the answer is yes. And I think um the F DL is still gonna provide some inversion power because I excise to post in virtually all but patients. So when I assess these feet, there are multiple zones of instability. One is deep deltoid laxity that the tip post acts around. One is spring lant laxity that the tip post acts around. One is medial column instability that the tip post acts on. And one is the lateral column as well, cos tpase fibers insert far laterally. And if any of these in my mind are unstable, the tipa is gonna react and therefore, if you're not gonna control these, er I get rid of tip post. So patients who have isolated spring lant lax in the flexible flat foot where the er middle column is is very stable. The last column is stable, then I will not excise TPO to an F DL transfer. But in the others, I always do. I hope that's clear. Uh But yeah, if there's, if the zone of instability has spread away from the middle column into the tibiotalar joint into the lateral column, I will do a tip past transfer. Thank you, Chandra. Uh Well, I think I think I mean, we would need a, we, we need another day here discussing with Chandler would be awesome. I think he's doing a amazing job. But I think that's, I mean, I think this is the area that we, we, we disagree the most. Uh, um, is, I agree, um, I agree with, with, with some points of what, what he's making. Uh, I'm, I'm, I'm ii think it would be great and very, uh, not, I don't wanna say easy. Uh I think the part that we agree is that the soft tissue, I is the main driver of things. Uh I agree on that on that regard, but explaining entire the entire PCF D on soft tissue only. Uh I think it would be too simple, but I don't think there's anything simple on this. I think it's like it's a multifactorial disorder. That's why I have so many different deformity components. So, you know, develops in different ways in different patients. Uh And I II am biased towards the bony malalignment. Uh And so I think, you know, we maybe we never know what's the chicken, what is the egg? Uh And then we also disagree on the spring ligament reconstruction. Actually, my data uh from patients, not from the, the great beautiful cadaver studies that he did and the biomechanics. Uh but Doctor Delan also experienced with his spring deltoid reconstruction is that in our opinion, the most important one to be reconstructed is actually the Tibial Spring, uh, a part of the, of the Deltoid. Uh, I rarely do a formal spring ligament reconstruction when I see Deltoid spring. Uh, I, I'm basically doing me amount to a, uh, I rarely put an anchor on the su and my opinion without having the beautiful data that she has is the one that, uh, uh, that influences my correction the least. So, it's the one that I do the least as well. Um But again, there's no right or the cool part of all this that there's no right or wrong, right. And I agree, I can't agree. Uh La uh I can't agree more with John Lennon and what Chandra put in his talk, the more we studied this, the less we know and just to throw even more contro uh controversial uh aspects on the discussion here. I actually think that the reason why the literature was so successful with the early publications from Myerson and Lucian about MDC O and, and, and F DL tend to transfer solving problems is because uh the spring ligament, sorry, the, the F DL kind of works as a spring ligament reconstruction, particularly if you're thinking about the deltoid spring, right? Because it's the exactly same trajectory of the deltoid spring ligament. Uh And then when you, when you do that loop under the tables, you're kind of reconstructing that part. So I think the F DL tendon transfer is more important for static reasons than for dynamic reasons of inverting the foot. So that's why I think F DL transfer are so successful. So for example, when I do an F DL tendon transfer, uh I don't do the Tibial Spring because I think my, my, my F DL is already doing that for me. I would do only a tibia Avik in that scenario would go from the tibia up uh into the NAVI but from top down and not from bottom up. But again, we would need, we would need a full weekend here, Chandra to, to talk about this. Uh But again, very beautiful work. And uh OK, now I II mean there are a few questions. So, but in the, you know, interest of time, I was waiting for this question, I knew you will come and there is one somebody who asked this question. So both, both of you, you can have your say, what is your opinion on the role of arthrosis screw? Who do you want to go first? Yeah. OK. Um OK. Look, first thing to say is I don't use it in my practice. And the second thing to say is I think it has different roles in different populations. Say in the pediatric population, it has a completely different role to the adult population. So when you look at the pediatric population, if you think of a patient with congenital hip dysplasia and you direct within the 1st 18 months of that hip being sublux into the ace table, you cause that cry radiate cartilage to grow normally. So it's very important to redirect that. And I think it's the same in the pediatric group. If you take your acetabulum pedis and you redirect the talus into the to of it axis and put the middle facet back over the susar talus. What you're gonna do is make that grow better. And there's some evidence and indirect evidence from Oxford that actually published this, I think where that actually showed that patients with sort of uh flat feet in the early adolescent group actually have a smaller middle facet that develops uh compared to people that develop PCF D later. So the pediatric population that the early adolescent population that develop a flexible fat feet, I think is totally different to the adult population that have been normal for years and then develop it because the morphology of their joints has uh completely formed normally. So therefore, if you're talking about that group of population that's skeletally now mature and you're putting an arthro rais screw. The first thing to say is that is not a substitute for doing everything else. The second thing to say is I don't think it's an implant that can be used in isolation. I know there are reports out saying they've had single surgeon series that have had phenomenal results by just an arthro a screw, but it's not something that I would recommend or is it within my practice So I have to say I've never used it. When would I use it? I'm unsure. I think if, if the soft tissues are terrible, uh You've done all your bony realignment, you've reefed everything and that sort of talus is still swinging out and you're getting that lateral sort of impingement. There may be a role of putting one in just to control that while the soft tissues are healing. But the problems I have with it is how long do you put it in? What size do you put in? It has a high complication rate in terms of repeat surgery, pain, et cetera. And when do you take it out? And I don't think there's any guidelines on that. So, yeah, that's my opinion piece. Yeah. Thank you. Yeah. Well, I agree. I agree with him. Uh You know, I uh I was trained in Brazil uh with the idea that arteries screw was a disaster and I should never get even close to one. But after studying peritoneal subluxation and looking into subtalar joint subluxation, uh y and seeing the results of some particularly European alters are showing with the arteries, he does, you know, get my attention. And if there's one thing that the arteries screw probably does is correct per subluxation. Um So I'm entertaining the possibility of studying it on in the lab and before I even jump into something, uh but II couldn't agree more with Shandra with everything that he mentioned about, you know, for me, it would be great if I could do a 10 minute surgery instead of a three hour surgery that would make my life much easier. And, uh, my, my, my practice much more profitable. But again, we go back into the discussion of, there's nothing easy and simple with PCF D. So it would be too simple to think that you would put a screw there and solve all the problems. I'll leave you there. Thank you very much. Um I mean, look, there has been a lot of um questions from the audience and I'm sorry, I can't take all the questions because um we are late here. Um So I, I'm going to close the session off. But uh thank you once again, both to Cesar and Chandra for uh your time, your effort. And really you have um given a lot of food for thought. Um You know, uh uh we, we, we don't know all the answers as you say, but we probably start thinking about it in a different way from now on. At least I will um everyone have a good evening and thank you once again for attending Master Techniques and uh we'll see you for our next uh number 15 Master Techniques. Sometime in February, we'll uh announce the date and speakers um keep in touch and uh have a have a good night. Bye-bye.