CME Surgery

Posterior Tibial Tendon Dysfunction Stage II: Arthroeresis and Panel Discussion

Harold Schoenhaus, DPM

Harold Schoenhaus, DPM provides a brief overview of stage II posterior tibial tendon dysfunction (PTTD). Dr Schoenhaus reviews diagnosis, conservative management, and surgical treatment. Dr Schoenhaus' presentation is followed by a panel discussion about the current care of PTTD.

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Goals and Objectives
  1. Understand the etiology of PTTD
  2. Pathology associated with PTTD
  3. Understand comprehensive approach to PTTD
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  • CPME (Credits: 0.75)

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    Release Date: 03/16/2018 Expiration Date: 12/31/2018

  • Author
  • Harold Schoenhaus, DPM

    Surgical Editor for PRESENT e-Learning
    Penn-Presbyterian Medical Center
    Philadelphia, PA

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  • Lecture Transcript
  • Harold Schoenhaus: I’m going to start off with a talk on posterior tibial dysfunction. It’s really set up as a kind of a panel. After I provide some basic information of what PTTD is and what I’ve done over the years for it, stage II primarily, then we’re going to open it up to Drs. LaPorta and Kalish as well as the audience to provide information discussion. We have a 40-minute session. I hope this works the way I anticipate it. We can start with the presentation. Posterior tibial dysfunction and I’ll call it stage II in the arthroereisis I identify because that’s an approach that I’ve taken through the years in the absence of degenerative joint disease. Ken Johnson, many years ago, who was the editor of Foot and Ankle, I introduced the concept of this syndrome. It’s obviously an adult flatfoot with pain along the course of the posterior tibial tendon. Learning objectives, understand the etiology of PTTD, the pathology, and understanding comprehensive approach. Disclaimer, consulting to right medical, bacterin, Amniox and they should have Propan there as well. In stage II, what do we see? Partial tears of the tendon without definitive evidence of bony or cartilaginous adaptation or evidence of DJD of the subtalar or midtarsal complex. The foot still demonstrates flexibility with the ability to reposition the associated subluxations. You can have a complete rupture of the tendon. But as time goes on, if that rupture continues, you’ll get the associated DJD. Clinical sign, here is a good example of a patient that did have a rupture of a tendon, the absence that delve, if you will, on the medial side going from the medial malleolus down to the tuberosity and navicular. When the patient stands, we see the complete collapse of the longitudinal arch. It’s interesting you can see the recruitment on the weightbearing side of the tibialis anterior. The tibialis anterior just exaggerates the forefoot supinatus that develops with this severe flatfoot deformity. One of the diagnostic tests to demonstrate pretty close to a complete rupture or significant pain is the ability or inability of the patient to get up on their toes without inverting the rearfoot. The normal foot, as you see on the right, inverts at the calcaneal level. The patient with PTTD you see the significant swelling on the medial side, inability to invert the calcaneus. You can use sonography, x-ray and MRI. I think MRI is helpful in evaluating extent of tear, not necessarily whether it is torn or not. I’m more interested in what’s going on within the tendon sheath and also the extent of tear that we might see. Here’s example of what MRI is able to do for us. Here’s an example of the fluid that one sees within the sheath. We become familiar with reading our own MRIs. I never rely on just the x-ray tech or the CT tech or MRI tech to tell me what’s there. From a conservative standpoint, treatment of this disease or disorder, strapping, padding, NSAIDs, physical therapy, casting, orthotics, and surgery, and also use CAM walkers by the way. Indications for surgery, painful flatfoot, medial arch, ankle pain, and knee pain. These patients have significant postural symptoms extending up into the knee with an associated genu valgum. The patient that’s going to need surgery has a minimal response to conservative management. These patients are uncomfortable and unhappy campers. The intraoperative findings, rupture of the tendon, degeneration, partial tear, proliferative synovitis of the sheath, and a condition that I have coined, posterior malleolar chrondromalacia, which is the groove behind the medial malleolus which is lined with hyaline cartilage. You will actually see breakdown in that area which can cause irritation to the tendon with the associated synovitis and fluid. Incisional planning is going to be based upon the extent of deformity and what the MRI has identified for you.


    Is it down to the insertion and how far up the medial malleolus you need to go. The tendon sits in the first compartment of the laciniate ligament. Rather easy one to find usually. Obviously, don’t be misled and go down to the third compartment where you have a neurovascular bundle. Here’s examples of what tendon looks like with PTTD. Be sure to roll the tendon over when you’re looking at it clinically. Sometimes the tears and the defects are on undersurface of the tendon. Here is a good example of the associated synovitis that you see. There’s the groove. You can see a little defect right in the groove where there is breakdown. Tendon can be completely stenosed and bound down secondary to other types of trauma. The tendon sheath should be maintained if possible. But if there is a significant synovitis and hypertrophy, I will excise a portion of that and create a new sheath and I’ll show you what we do. Here’s an example of freeing up the tendon. If the tendon is torn, you need to make a decision. If it’s early on, can you repair it? It’s rare that you’re going to do an end-to-end anastomosis so we may use a graft or acellular dermis to act as an interpositional graft and it must be done under tension. In order for that tendon to, in any way, work again, you got to consider the length-tension ratio once you have reanatomosed the tendon. What I usually do in those is I tie it end-to-end with a graft in place lying on top of the medial malleolus and then pop it into the groove behind. In my earlier days, I used a lot of tendon, bank tendon if I had to repair it, now I use all acellular dermis which can be rather strong and it differentiates right into tendon or the sheath. Longitudinal tears, I like to open it up. I take a curette, clean out any material that seems to be abnormal. There are times I will resect abnormal or the section of the tendon that is torn. Then the decision is to be made is what are you going to do with the remaining portion of tendon or defect? Here’s an example of wrapping acellular dermis right around the tendon itself. It’s going to act as a nice protective barrier and/or interpositional graft. In the longitudinal tears, I will actually take a section of acellular dermis, lie it right within the tendon defect and so the tendon around it. Here we are with the acellular dermis. It’s like a jacket rolled around or you created a burrito. If you don’t have any sheath left to go over by the ligament itself, we can use acellular dermis to repair that as well. Now recognizing that this is a severe hypermobile flatfoot and you’re going to see a fair amount of transverse plane domination and flattening, the fact that you’ve simply gone into repair the tendon, in my opinion, is not going to be enough to realign the subluxation, control the hyperpronation and enable that patient to ambulate again. There are times that I use an arthroereisis which will act as a beautiful plug within the lateral aspect to the sinus tarsi. If I have to do a tendo-Achilles lengthening, I will do that as well to eliminate additional deforming forces. The arthroereisis is to realign the peritalar subluxation, prevent the forming forces influencing healing of the tendon, allow for a functional adaptation of the tendon that you repaired, and you’re continuing control of the hyperpronation syndrome. If you want to use a good functional orthotic, you need an orthotic with a deep heel sit and long phalanges that go down to the first and fifth metatarsal neck so that you stop the dominant transverse plane subluxation that is taking place in these patients. The arthroereisis, hopefully, will minimize the need for bracing, because patients don’t necessarily like to be in that type of brace or orthotic. It’s certainly not intended for advanced PTTD with associated DJD of the subtalar-midtarsal complex. I’m sure you’re all familiar with what arthroereisis is all about.


    This is taking a subtalar joint that has pronated dramatically and recognizing that as we move in the transverse plane, the foot, meaning the forefoot components slides directly away from the talonavicular joint. You see significant transverse dominant change. We want to reposition it to hopefully come back to somewhat of a neutral position. Not supinate it and get away from this pronated position. In an essence, this is what arthroereisis has and always is and always will be. You’re taking the talus, propping it back up on the calcaneus, moving it from the pronated position to a more supinated or neutral one and then placing something within the canal. I have placed everything possible in that canal through the years from silicone plugs that I’ve carved myself, to back plugs, to any of the metals, and of late, because adults don’t tolerate plugs very well of the metallic type, I’ve even taken acellular dermis and rolled it up. It becomes a very tight unit and place it in. It’s almost like a Tootsie Roll going into the sinus tarsi. It will differentiate into a fibrous tissue within the canal. It will block the subtalar motion, and the adult seem to tolerate it much better. But I have used many different materials and you’ll know that there are many companies that have arthroereisis. You pick the one that you think is going to be best for you. In essence, you’re taking that foot with its pronatory component and propping it right up. Never overcorrect with lateral arthroereisis. You’re bringing the foot to neutral. I even like to see some pronation. Don’t overcorrect these deformities. But it’s dramatic how you can move a foot from significantly pronated, eliminate the deforming force with a TAL, deal with the disease at the posterior tibial tendon. Interestingly, the posterior tibial tendon from a phasic activity standpoint is a stance phase muscle that works in conjunction with the peroneus brevis and they provide stability of the subtalar and midtarsal complex. Don’t expect the tibialis posterior to supinate the foot per se during gait. That’s not its function. It’s to stabilize the direction of supination. You’re trying to realign the foot so that the PB and the TP can work in conjunction once again. Obviously, we, as surgeons like the simple approach to anything we do. As far as I’m concerned, if you can’t find the sinus tarsi, you’re missing the forest through the trees. But you can use cannulated approaches to find the actual canal itself. Postoperative management, after the surgery is performed, I put them in a short leg cast depending upon what adjunctive procedures I might do such as the TAL. They may be in a cast or anywhere from three to six weeks followed by a CAM walker. Physical therapy is helpful to reestablish strength of the tibialis posterior tendon. I can’t stress enough, it has to be placed under tension when you do repair of this tendon complex. Then orthotic management control to help with what you’ve done. Complications, obviously infection, restricted range of motion, dehiscence, nerve entrapment, scarring, re-rupture and tear. At this point, I’ve introduced the topic where we’ve talked somewhat about how to approach the tendon, use of orthobiologic materials, arthroereisis. At this point, I would like to turn it over to my panelists, Dr. LaPorta, Dr. Kalish to either pick apart what they’ve seen, discuss what they’ve done that I might not have done and what their approach is and what their success has been.

    Stanley Kalish: Very nice, Harold. I don’t disagree with anything you said. I think if I were to simply look at the cases of tibialis posterior, of tendinopathy and rupture, and all the various stages that occur, it would be simply that in a younger person, I’m trying to repair the tendon and try to biomechanically stabilize the foot.


    I don’t particularly have a high incidence of use of arthroereisis in those patients but if I was at that point where I was deciding between a fusion versus an arthroereisis, I would probably be leaning toward the arthroereisis in the younger person. Again, the definition of youth is totally subjective. If I had a patient that perhaps was obese and I didn’t think arthroereisis was going to hold up with him, then I would do a fusion. On acute tendon ruptures, and I’ve seen a few this year, I have repaired them primarily and have used graft jacket or something of that nature to try to accentuate it. I follow a little bit of Sanchez’s article on the use of PDGF and platelet-derived growth factors, insulin factors, hepatocyte factors and all those factors that you should be using concomitantly in his study of about 13 Achilles tendon ruptures. The results were similar to what I found, encouraging but not definitive that they made such a great big difference. But I think it’s such an innocuous procedure to add to the acute tendon procedure, whether you do a primary repair, accentuated with biologics. I like to add PDGF mixture. As far as fusions, triple arthrodesis and operations like that through endstage, as you’ve said, arthritic situations. I like to see what Guido thinks.

    Guido LaPorta: Just a couple of comments. Harold knows I’m a big arthroereisis fan. But I use it a little bit differently in this deformity. I usually use an arthroereisis as an internal brace to help whatever else I’ve done, especially if I’ve done a tendon transfer or a repair. I think you’re fooling yourself if you think six weeks down the road, that tendon is where it’s going to go. It probably takes the better part of the year for that to happen. An internal support is usually a pretty good idea. I found the two occasions you showed very interesting because me, personally, would have done an arthroereisis in one of them and not in the other. One of the things I’ve found over the years is that a very important angle that most of us don’t look at, I certainly didn’t until about 12, 15 years ago, is the lateral talocalcaneal angle. All of us have been taught to look at the DP view and look at the talocalcaneal angle but I looked at the lateral one. What I found, on the lateral talocalcaneal angle, even in some of the more severely pronated feet is that that angle is normal. The concept of propping the talus back up on the calcaneus actually doesn’t make much sense in that particular foot because it’s already where it should be, in the sagittal plane. Whereas in the second case, there was definitely an abnormal lateral talocalcaneal angle. The talus was plantarflexed more than the calcaneus was. That makes perfect sense to do an arthroereisis-type procedure and in that particular case. Another x-ray that I think we should all be doing is a hindfoot alignment view. I, by no means, am saying that someone with the experience that Dr. Schoenhaus has can’t look at a foot and be pretty close, if not dead on, with the positioning of the heel. But I would challenge you to look at hindfoot alignment views, a 45-degree x-ray taken from posterior aimed at the subtalar joint with the patient standing on the x-ray beam. I would bet that half the patients that you measure in valgus clinically aren’t, that they are either vertical, and in some cases, a couple of degrees of varus. The reason I think I think that happens is that the posterior tib is firing continuously to try and decelerate the pronation that’s occurring within that foot and that’s what wears it out.


    Therefore, I think arthroereisis in a foot that has a heel vertical, or a heel couple degrees of varus probably won’t work as well as you would like. It’ll correct the deformity but it’s very difficult for the patient to walk when they’re locked, if you will, in varus. You remember that Dr. Schoenhaus said, don’t overcorrect these deformities. Leave a little bit of valgus. I think he is doing the exact same thing I’m saying by allowing that foot to pronate some. Couple other comments. The MRI at best is about 40% correlative with what you actually find in the tendon. MRI is a good test to tell you something is wrong with the tendon. It’s not a good test to tell you what’s wrong with the tendon. I’ve had abnormal MRIs where I’ve gone in and found a perfectly normal tendon. I’ve had normal MRIs where I’ve gone in and found longitudinal splits. But it does give you a good picture of a chronically inflamed tendon so that you know that something is happening there. Harold, I really like what you did with the tendon, with the burrito procedure. I think that’s a great idea. When you tubularize these tendons, take out all the garbage, you’re sometimes left with like a fusilli in there. There’s not much going on. What I’ll usually do is I’ll split that tendon. In my particular case, I usually lay in something like an Ortolan substance, something that’s got a lot of beef to it and I’ll bury it in the tendon and incorporate that in my repair. But the acellular dermis is also a very good idea, especially to prevent scarring around the tendon because half the job is repairing the tendon, the other half is getting it to function. In some cases, the acellular dermis is a very good choice. Orthotics, if you’re using them as the primary form of treatment, in a stage II tibialis posterior dysfunction, I think you have to consider, at least, starting with a supra-malleolar device. I think that really, in most cases, is what would cause the tendon to be put at rest and actually give it a chance to have a healing process occur. After surgery, should it come to that, I agree with Harold that the orthotic must have a very deep heel seat, 20, 23-millimeter heel seat or heel cup. I like to do an overcorrect that I call it a total contact cast so that the orthotic is really supporting. I also tell the lab, by the way, keep your grubby hands off the positive. Do not fill in the arch. The reason I tell them that is that if they do that, what you’ll find is your patients are standing on an orthotic and there’s going to be half an inch between their arch and the device and they have to pronate to get to the device. Before the device does any good at all, they have to pronate to get to it. I tell the lab, don’t fool with the positive. Make the device exactly the way the positive looks. Now there’s also a question, I think, Harold. If you do a fusion, let’s say, or you do extraarticular osteotomies to stabilize a foot, do you really need to repair the posterior tib significantly? I think the answer is yes. The reason is not because of its foot function. The reason is that one of the other functions of the posterior tib is to decelerate rotation of the leg. As long as there are some subtalar joint motion available then I think repairing the posterior tib is in fact a must. I’ll stop there.


    Stanley Kalish: There was one a few years ago seem very popular with Bruce Werber in a lot of lectures on Topaz. We mentioned nothing about Topaz procedure. Occasionally, I still do it with the thought process that was left with me that it does increase vascularity. I was just interested in both of your opinions, whether you still think radiofrequency repair has a place in your tibialis posterior, tendonitis and ruptures, linear ruptures particularly.

    Harold Schoenhaus: I don’t use it.

    Stanley Kalish: Why?

    Harold Schoenhaus: With the advent of amniotic fluid, that’s another approach to consider, to repair or help repair the tendon where you’re going to inject into the tendon sheath amniotic fluid as opposed to Topaz which is it’s a former trauma. It was shown to have some benefit on the Achilles tendon for sure. But I think, in today’s world, I’d rather use something that has got stem cells and embryonic type to help repair and possibly even assist in regeneration of the tendon without much trauma, additional trauma. That’s just my thought on that.

    Guido LaPorta: I would agree with that, Harold. Topaz works by the way. I use Topaz for a number of years. And the concept, I think, is sound, basically irritate the tendon enough so that you jumpstart the inflammatory process and allow it to heal. But I also think and agree with Harold that you could get the same benefit by taking an 18 gauge needle and needling [indecipherable] [26:43] and injecting some stem cell as you’re doing that. I think that’s probably the way I think it should be done this time also.

    Harold Schoenhaus: Let me ask the panel or anybody in the audience, what about flexor tendon transfer? You go in and you find a TP that’s really beyond what you think is repairable or even going to be functional. Should we take the long flexor tendon and root it through the navicular. It’s just as a stabilizer.

    Guido LaPorta: I do that a lot. I don’t reroute it to the navicular. I reroute it to the cuneiform. Hansen calls that an augmented Kidner procedure. It’s not a Kidner but I think trying to put that tendon into the navicular can be tenuous, especially if you have a good-sized flexor. I think it works much better when it’s rerouted to the cuneiform. I also think you can augment that procedure by doing a peroneal stop on the lateral side. You can pull up on the longus and pull down on the brevis and increase the mechanical advantage of the longus. Again, we always used to say the peroneus longus and tibialis posterior work synergistically and when one of them is out, the other one doesn’t work too well. I think you should give consideration to spring ligament augmentation. Now, the problem with spring ligament augmentation is that whenever I saw it presented from the podium, nobody did a spring ligament augmentation, they did a talonavicular joint capsulorrhaphy but they were nowhere near the spring ligament. Am I allowed to mention names?

    Harold Schoenhaus: Sure. Why not?

    Guido LaPorta: Okay. If you look at and consider the use of an internal brace from Arthrex, you can do a spring ligament augmentation that is incredibly effective and allows you to do much less with the surrounding tissues so you can get greater stability with less dissection when using techniques such as that. I think those are all important augment techniques. I think as Harold mentioned in his talk, when you have a stage II tibialis posterior dysfunction, you usually need to do osseous and soft tissue and you usually need to do medial and lateral column. You better make sure that you’ve neutralized the posterior muscle group because the equinus will tear apart anything that you do in the foot.

    Harold Schoenhaus: What about in isolated TN fusion as opposed to the other joints? What’s your findings on that?


    I certainly have done a number of isolated TN fusions which knocks out probably 85 to 90% of subtalar motion and provide significant stability. I’ve watched my patients over the years with this one isolated fusion who have done rather well, again, being sure that you don’t supinate the foot in position when you do it. It seems to have a long lasting effect. I don’t see the associated arthritic change at the subtalar or CC joint and it’s a powerful procedure.

    Guido LaPorta: It is. Are you going to talk or you just?

    Stanley Kalish: No. I was just agreeing with it.

    Guido LaPorta: Alright. It is. Craig Camasta did a great article on the TN fusion for these particular cases. It’s a pretty simple procedure to do. It’s powerful. It’ll knockout 80% of the motion in the hindfoot. The only thing I would caution you is that if you’re considering doing that, make sure the heel is positioned where you want it. As Harold mentioned, don’t oversupinate the foot. The only way you can judge that is by where the heel is. We always judge our fusion position by bringing in the C-arm and getting an axial view of the heel and relating it to the tibia. We want to make sure that heel is not in varus when we fuse the TN joint. It’s a pretty effective procedure.

    Stanley Kalish: Do you think that these augmentation procedures, these advancement procedures, whether they’re to the navicular or the cuneiform, aren’t they essentially just a fibrotic type of a block that act like a talonavicular fusion? Do you actually think you’d get that much function after you do that?

    Guido LaPorta: No, I don’t think you get that much function. I personally don’t. I think it’s an internal brace. The only time I consider it is when I have made a visual inspection of the tendon, posterior tib, and say, nothing I do to this tendon is going to make it as strong as I want to, so I’ll have to augment it.

    Harold Schoenhaus: I think the suggestion that Guido pointed out about the spring ligament, that sucker is big. It’s powerful. It’s part of the basket of the talonavicular articulation. I look at that joint as an acetabulum and it’s a ball and socket joint. The bottom part of the support is certainly the spring ligament, which is sitting directly underneath that. Then your tibialis posterior kind of reinforces under that. It’s possible that in our soft tissue repairs, that that augmentation would be incredibly important to do. I have not gone in and really looked at that spring ligament, and said, that sucker should be reinforced. It’s got to be stretched out. There’s no way that’s coming back to be the support base that it was originally. The other thing Guido pointed out, which is something that we don’t think about often, is true function of muscle tendon complex. We always think of a muscle working from a point of origin to insertion. Muscle function is very much predicated on what’s the stable part. If the distal part is stable, its effect is going to be more proximal. During the gait cycle, the leg is moving, the foot is moving. You got to think in terms of that tendon, I’m sure you’re going to try to repair, so it again can function from its point of insertion back to origin with influence on the leg. Yeah, I’d like to hear some comments. We could put the lights up. We could get some comments from the participants.

    Stanley Kalish: Yeah, Harold, I have one question for you guys.

    Larry Harkless: I have a question here, Harkless.

    Harold Schoenhaus: Larry Harkless.

    Larry Harkless: Can I ask a couple of questions?

    Harold Schoenhaus: Who is that?

    Stanley Kalish: Who is it? Come up here.

    Harold Schoenhaus: Sure, Larry guy.

    Larry Harkless: Do you all believe that most of the problems that happens are primarily malalignment? Would you all agree with that concept, if you started the pelvis and go all the way down, that most probably developed because of malalignment?

    Harold Schoenhaus: You’re asking is the malalignment present that’s causing the disease?

    Larry Harkless: Yeah, or is it a primary disease in the tendon? We’ve just taken posterior tibial tendon. I’m thinking about everything in the lower extremity, because everything works as a smooth [indecipherable] [34:37] with gait. When there are malalignment problems, we don’t talk about this in all kinds of segments. Send some at the osteopathic medical school, and I have problems with my neck and all of that now and begin manipulated. They think all these malalignment stuff, and they said, everything in orthotics is malalignment. I think they’re probably little target because I’m so bow-legged, and I have skin problems in my knee and hip and all that, and I’m 63 years old. All these stuff wears off because of malalignment.


    I’m just asking, what do you all think because you all got gray hair like me.

    Stanley Kalish: I think it's definitely a mechanical issue. I guess there are very rare situations maybe in amyloidosis or some weird diseases, autoimmune diseases that directly affect the tendon sheath that I don't see that as the cause. I see this as a purely mechanical cause or see it as an endemic obesity-related disease, and I don't see it all as a primary disease of the tendon.

    Harold Schoenhaus: It’s interesting, Larry, you bringing this up because the etiology, I don't think we've ever truly identified, because you can have an obese patient and have unilateral PTTD. Is there some form of trauma? Do they have a genu valgum? They could have primary disease in the knee. What are the inciting causes that have led to extra pronation where the tendon has to work that much harder, and then you've got the obese component which is adding that much more stress to the area, and the tendons starts to break down. I think there is a mechanical component, whether it's associated with limb length discrepancies, malalignment syndromes that had been present since pediatric days and that they just continue to grow with adults, and then the valgum of the knee or the position of the ankle becomes that much more exaggerated, and then the tendon works that much harder and it breaks down. There's no reason why one tendon alone is going to be subjected to some abnormality, like a fibromyalgia patient that’s got an isolated posterior tibial tendon tear.

    Larry Harkless: Harold, you missed my talk yesterday, but I'll show one slide. I was talking about infection, but I'll show the slide that talked about heterogeneity.

    Harold Schoenhaus: Yes, I heard that sir.

    Larry Harkless: That’s like the autonomic nervous system as I get older and think about what I know and what I don't know, because with autonomic nerves, the system get turned and we don't know what happens, and why it happens, and all of that. So those are variabilities in medicine, and so heterogeneity is the variability, and no patient is the same. That's why sending surgery and just doing surgery, you got to look at the whole patient. I think that you all are saying that, but I just wanted to make that point to everybody. Go look up the word heterogeneity and look at the sources of it and go back to what Harold is saying in this whole process. I think I'm going to hush.

    Male Speaker: Good point, Larry.

    Guido LaPorta: Larry, that's an excellent point. I have a couple of talks on biomechanics coming up, and I'll show you an x-ray view. People think I'm nuts, but anytime I reconstruct a foot, I do standing hip to ankle x-rays for alignment purposes. I can also measure leg length off that, but I do them for alignment purposes, because I think it behooves you to determine is the unilateral flattened foot causing the malalignment, or is the malalignment producing the unilateral flattened foot? These patients come in different flavors. These patients can show up and they have a perfectly normal contralateral foot and a TPPD on the other side. Well, that might be a primary disease of the tendon. If that patient comes in and they've got bilateral hyperpronated or peritalar subluxation, then that might be a malalignment. I think you need to know that. I mean, the worst thing you could do is put a patient through a major reconstructive procedure like this and find out that there was something above the foot that was contributing to their deformity. Harold did tell you, you want to know if somebody has a leg length discrepancy, do an arthroereisis on the side that's pronated and watch them walk in with their shoulder tilted to the opposite side, because you didn't bother to measure the leg length preop. There's usually a reason why these things happen. That's a great point. Thanks for that question.

    Harold Schoenhaus: I'll go further with this. Patients who have degenerative joint disease of the knee unilaterally with the genu valgum and develop pronation problems in the foot, the foot breaks down. Then, they go in and get a knee replacement. I have two patients this week alone in my office, both of which have gone through an orthopod for a knee replacement because during valgum, their foot is as flat as can be. I said to the patients, did the orthopod look at your foot? Did the physician who is telling you they're going to put a knee in looked at the alignment of the foot? They said, absolutely not, didn't even think about it.


    From my perspective, working from the foundation back, you can go get a brand new knee. If your foot is flat as a pancake and nobody addresses it, you're going to create further problems within the knee with breakdown of the knee joint.

    Stanley Kalish: Hey Harold, I had a case just about four weeks ago. It was just the opposite, where the orthopod was getting ready to do a total knee and he said, “Let's stand and fix the foot first.”

    Harold Schoenhaus: Right.

    Stanley Kalish: I was kind of surprised.

    Harold Schoenhaus: We need to be educating the orthopod relative to that. One more time for one more question.

    Female Speaker: Actually, I was just going, I mean, the IHS, the Knee and Health service. A lot of my patients will come in and say "Oh, I have pain for some time,” and that's the most I can get. When I ask what kind of pain, they think I'm nuts because why wouldn't I know that already. One clear information that I almost always get is either a car accident. Large number of my patients don't wear seat belts right in the back of pick up trucks, so there's always some sort of hip or knee trauma. Horse fell on them on that one side, very frequently walked into a fire pit. I mean, burns, it's amazing, can cause these problems. Burns on the upper part of the lower extremity will change biomechanics.

    Harold Schoenhaus: Absolutely.

    Female Speaker: It's not evidence based, but it’s just experience.

    Harold Schoenhaus: Thank you. I appreciate this talk this morning. It actually met with my expectations that we would present the topic and hear from experts as to how we approach something of this magnitude. PTTD is alive and well and we're going to be treating it forever. I thank the panel and we will continue.