• LecturehallPosterior Tibial Tendon Dysfunction
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Male Speaker: Our next speaker is somebody I know rather well. He is my partner. He actually will admit that I try to train him at Graduate Hospital where he did a residency and a fellowship. He has done amazing surgical work. He’s an intellect. He’s an educator. He is a professor at the Temple University School of Podiatric Medicine. It’s called an adjunct professor. He’s on the staff there. He’s a staff at Penn Presby’s in the wound care center and the director, board certified foot and ankle reconstructive surgeon. And it’s a pleasure to be able to see somebody that you have trained, matured, nurtured and have surpassed what the original professor might have been able to do or did do.

    So with that, I’m going to invite Dr. Michael Troiano to talk about Posterior Tibial Dysfunction.

    Michael Troiano: Very kind words. I appreciate that. Certainly not surpassed however. So this is primarily a resident lecture that really should have been given at the beginning of the summer, late spring because this is when you begin to see a lot of posterior tibial tendon dysfunction.

    I can remember as a resident, we were just starting to see more and more PTTD develop. Some, you know, we kind of hypothesized that it was because of the ever advancing in weight population, but I’ll tell you, for everybody that I think would have posterior tibial tendon dysfunction, that’s, you know, 5-foot-4 and 280 pounds, there’s somebody that walks in that’s 150 pounds and 5-foot-9 and they have it. So I don’t know that we have a full understanding with rhyme or reason what caused this PTTD, but I can tell you, when you have it, it is a mess to treat.


    Disclosures. I’m a Stryker Consultant. This is a Stryker-sponsored lecture, but it has nothing to do with Stryker.

    So in order to understand PTTD, we have to understand what the posterior tibial tendon does. First of all, it stabilizes the medial longitudinal arch. Why that’s important is because it makes that arch a rigid lever, all right, to propel the person as they’re beginning to walk. Now, as we know, when someone has equinus contracture in some capacity, the Achilles tendon, which is the biggest supinator in the body, turns quickly into the biggest pronator on the body. So the biggest supinator then becomes the posterior tibial tendon which is working antagonistically against the Achilles.

    So we have two plantar flexors in the ankle. One, the Achilles, one, the posterior tibial tendon, but they’re working, again, on a different plane, one to evert and one to supinate. And of course, ten out of ten times, the smaller posterior tibial tendons going to lose against the larger Achilles tendon.

    PT also abducts and supinates the forefoot during stance, so it allows a pistoning to take place and braces the foot against the ground as the foot resupinates. And then, of course, it locks the transverse tarsal joint.

    So if you look at the phase of activity of gait and you look at the gait cycle in general, that would mean that swing phase, PT is not really working. But that’s 65% of stance phase of gait, posterior tibial tendon is working and functioning very, very hard, number 1, to hold up this 200-pound body, and number 2, against often times the equinus which is in -- excuse me, the equinus of the Achilles which is working against it. So it’s coming under duress. It’s a muscle that’s used constantly in gait and it’s one that’s very prone to injury.


    For residents in the room, you’ll be asked time and time and time again on boards and final examinations, in training examinations what have you -- which of the following bones does the posterior tibial tendon not insert on? It inserts on every bone except for the talus. It’s just about in the midfoot structure. Has a vast, vast insertion. So you’re looking at mediocuneiform, first metatarsal, intermediate lateral cuneiform, you got a little branch of the cuboid, fifth metatarsal. Everything basically except for the talus is what it inserts on.

    So PTTD, which is pathognomonic for adult-acquired flatfoot deformity, right? The adult-acquired flatfoot deformity is most commonly caused by PTTD. Often develops in middle age and more commonly in women. Why women? Perhaps, you know, men are more likely to wear more supportive shoes, work boots, you know, sneakers at work, that type of thing, whereas a business professional woman is obviously more in a high heel and a flat perhaps. There are risk factors. Again, risk factors, not causative agents; obesity, diabetes, age, hypertension, and certain negative inflammatory diseases.

    Differential diagnosis. So many times do I see somebody with a classic posterior tibial tendon dysfunction. You have to look at the root cause. As Dr. Bromley identified earlier, we have to really solve the root cause. So this where your physical examination is extremely king. You want to look at that subtalar joint. Is there a catch or a hitch? You want to look at the x-rays. Has the TN joint adapted? Is there arthritic change that would make you think that there might be a calcaneonavicular bar, talonavicular coalition, what have you?

    There has to be, you know, some -- a younger person with posterior tibial tendon dysfunction, again, because it’s kind of -- it can be post-traumatically induced, but usually, the younger person is going to respond a whole lot faster than an older person such that if someone has a nagging PTTD and they’re a youngster, or a teenager, or adolescent, what have you, you really have to keep in the back of your mind tarsal tunnel.


    Get into that history. Mom, do you see, you know, perineal spasming? Is the patient complaining that they have cramping in the outside of their calf at night time? All signs of coalition.

    Then of course, acute posterior tibial tendon rupture is a differential diagnosis. In other words, I see a lot of industrial injuries, people stepping off of forklifts and hit, you know, in warehouses and things like that and PTTD, acute rupture, can occur as well. Often times, healing, elongated position, and then showing itself as PTTD, but of course, posterior tibial tendon ruptures are in the back of our mind.

    And then of course, chronic Lisfranc’s injuries. So many times, Lisfranc’s injuries that will have seen are treated poorly or missed and then what happens is the Lisfranc’s joint begins to widen and adapt. The person begins to live with it and they kind of arthrose and then it puts extra strain on the PT tendon. So if, you know, the underlying cause of the PTTD is the chronic Lisfranc’s injury.

    Pathophysiology, again, it’s generally a chronic degenerative process with progressive loss of function that results in muscle imbalance with peroneus brevis, right? Peroneus brevis is the biggest pronator. That’s not the Achilles, pathologic Achilles. So peroneus brevis and posterior tibial tendon are antagonists, but are in-phase antagonists. They’re working together. Excuse me. But out-of-phase antagonists. They’re working against each other as opposed to peroneus longus and the posterior tibial tendon that are working together.

    You’ll see progressive attenuation of the spring ligament allowing the talus to plantar flex and adduct as well as an unstable midtarsal joint. So this collapsing pes planovalgus deformity is often times going to be associated with PTTD and vice-versa. The PTTD is going to be associated with that collapsing pes planovalgus deformity.

    Ultimately, if this is allowed to continue, the attenuation of the deltoid ligament leads to ankle valgus and then that gives us the fourth classification which we’re going to get into the classifications right now.


    So stage 1 is just inflammation or tendonitis of the posterior tibial tendon. This is a classification system that was developed in the late ‘80s. It actually has been augmented very nicely. Johnson and Strom identified the classification system is largely now based on MRI findings. So it kind of -- life becomes action and that you can now actually see. It’s not just a clinical diagnosis. We can actually see the MRI finding.

    So stage 1 PTTD, inflammation, tendonitis. This is a person that’s largely going to have a rectus foot type, right? So treatment is often times just rest, but we’ll get into addressing the Achilles as well.

    Stage 2 is 90% of the PTTDs we’re going to see. Because by the time someone gets to stage 3 or 4, they know they’re in a bad way. Stage 2 is where we can kind of intervene and do something about it. It’s an acquired flexible pes valgus deformity. The key word being flexible.

    Stage 3 is rigid, all right? By the time someone has a rigid deformity, they’re well into their 50s or 60s, barring again a coalition and there’s a progressive development of hindfoot arthritis.

    And then, stage 4 is the one that Mark Myerson added which is ankle valgus. Meaning that deltoid just peers out, it just tuckers out, and everything collapses down medially, and then the ankle needs to be addressed.

    So non-operative treatment can be used in all the stages. All right. So this is something, you know, if we see our 70-year-old, 80-year-old multiple comorbidities, surgery is not something that’s absolutely required in this person. However, the conservative options are not great. Short of casting, or CAM walker immobilization recognized that, again as Dr. Bromley said if you don’t solve the root problem, which is the bony alignment, the posterior tibial tendon is just going to collapse back down again.


    So the person will heal, they’ll feel great, they’ll go back to activity and boom, they’re right back in your office six months later. So this leads conservative treatment of a MAFO, a molded ankle-foot orthosis and an Arizona Brace. Those are really your best choices conservatively.

    Immobilization, walking boot, things like that are going to work best in stage 1, but in reality, remember, the equinus of the Achilles tendon is largely what’s creating that collapse of the arch, right? So the equinus of the Achilles tendon takes that calcaneal inclination angle of about 20 degrees which it was supposed to be and it listed up closer to zero to parallel. And when it does so, it dumps the talus off and the talus screws itself down into abduction and plantar flexion and when that happens, posterior tibial tendon comes under duress, right?

    You take your Blix curve which is where that tendon is supposed to be strongest at 120% of its length, right? And then you bring it out 150% of its length, it begins to lose mechanical advantage and begins to tear. So I like to think of posterior tibial tendon Dysfunction as a suspension bridge, right? You have the arc of the bridge holding up the structure and then you have the tendons, which are the cables of the bridge interplaned with the arc of the bridge.

    So stage one, you can immobilize but physical therapy is absolutely paramount after. So many times I’ll see people and they’ll come in for a second opinion or what have you. They’ll say, yeah, I have PTTD. My doctor put me in a CAM walker, I felt great then afterwards the pain came back. Did you go to physical therapy? No. Did you try an insert? No. It’s not enough to solve -- you know, put out the fire, you have to then take the extra step and solve the problem. Patients are recalcitrant to those as we know because it doesn’t hurt so much anymore after immobilization of four to six weeks, right? They just want to get back to activity. Nobody wants to go to physical therapy, $30 copayment, three times a week, what have you.

    But they really have to understand that this is not just a tendonitis akin to I was out playing tennis and I have some elbow tendonitis.


    And now that I took it easy with tennis, I’m going to get better because again, in phasic activity, gait, the posterior tibial tendon is under duress, well, about 70% of the time of gait. Intervention, immobilization, orthosis, NSAIDs, physical therapy, stage one rarely requires opens synovectomy or tenoscopy.

    So on an MRI again, Johnson and Strom, one, you’re going to see -- obviously, this is the posterior tibial tendon, this is the sagittal. I mean this is the sterview or fact set. And here we see the posterior tibial tendon, usually it’s not this thick in stage one, a rim of fluid surrounding it and there could be some inter substance degeneration and tearing. Again, this is actually kind of a nice picture. Obviously, not a weight-bearing MRI but if we’re to draw this line right down the middle, everything on this side are supinators and everything on this side are pronators and you can see where does Achilles sit, into pronation. So the biggest supinator or neutral plantar flexor of the body now becomes the nemesis to the posterior tibial tendon because it’s sitting laterally and really driving that equines force into a plantar flexion position.

    This is stage one to stage two, synovectomy posterior tibial tendon dysfunction stage one Johnson and Strom to two. Here we can see the very normal FTL and then here we can see the posterior tibial tendon which is thickened, frayed and filled with synovitis. Stage two again, this is the stage that we’re most often times going to have to intercede surgically with. The presentation shows the presence of a flexible deformity including the loss in immediate longitudinal arch, hind foot valgus, forefoot abduction but there’s a functional loss, including the inability to perform a heel raise, whether the single or double, a patient should be able to perform a heel raise with minimal pain.

    The patient will also often time complain of fatigue, activity related hind foot and arch pain, and the intervention is going to be depending on the severity of the deformity.


    There is significant controversy regarding the surgical treatment of stage two PTTD and I’m sure we could have a full day discussion right here about the best way to treat it. There are people who do extra articular osteotomy, flatfoot reconstructions, what have you. People who favor fusions surgically. I’ll tell you, I am of the camp that if someone’s much older than 30 or 40 years old, unless they’re in great physical shape, you know, those joints have accommodated for 40, 50 years and I don’t think that it’s reasonable to perform a flatfoot reconstruction, align the joints and think that those joints have accommodated to their new or their older position and also you’ve realigned them and everything’s going to be hunky dory. I think that those joint services have largely accommodated and fusion are probably preferred as you get in to someone over mid-30s, 40s, what have you. Again, unless they’re light person and in great shape.

    Partial tears of the tendon without definite evidence of bony or cartilaginous adaption with evidence of DJD, the stage two PTDD. Again, that DJD is what obviates or in my opinion, makes unnecessary extracurricular procedures past the age of 30 or 40. Once I start to see that accommodation, I’m thinking fusion much more than extra articulatar procedures.

    And then the foot will still demonstrate flexibility. This is the key to stage two. There’s demonstrated flexibility such that you may be able to get away with a single joint fusion. You might be able to get away with the tendon transfer, you may be able to get away with extra articular procedures but once there’s no flexibility, now you’re looking more fusion of multiple joints. So here we see hind foot valgus, forefoot abduction, again remember the posterior tibial tendon really holds this foot out of abduction into adduction.


    It holds up the medial arch, it stops this Achilles tendon from moving laterally and becoming a suit -- a plantar flexor and, you know, here you can see it’s totally bode, you’re losing your mechanical advantage to the posterior tibial tendon. It’s coming under duress and strain with every step. You see, again, a loss of longitudinal arch, here you can see the talus actually sitting on the ground, talonavicular joint which is coming to contact with the floor.

    And again, I don’t care what shape this person is, 80-year-old, 90-year-old, posterior tibial tendon should allow this person to get on tippy-toes at least pain free. So even if they can’t do a full toe raise, there should be no pain. If someone has no pain on put -- on two -- excuse me, on double heel raise or single heel raise, they probably do not have posterior tibial tendon dysfunction unless it’s a chronic condition and has been chronically ruptured and that ship has kind of sailed and they’ve learned to function without it. Pathognomonically, classically, people will have pain on a single heel raise or double heel raise.

    X-ray examination, we’re going to start to see talonavicular head uncovering. We see our calcaneal cuboid break and then here we can see our midfoot opening up into of inverted position. We can really unmask the midfoot joints. Meary’s angle begins to drop. Again, we can see some accommodation occurring here. The talus is literally pointing towards the floor, first metatarsals up in the air. This is a classic stage two getting into stage PTTD x-ray. So joint-sparing procedures, we’re going to go through some of them quickly. You have the lateral column lengthening. Obviously, these are all extra articular, cotton osteotomy, gastroc recession if physical therapy hasn’t worked, the mobilization hasn’t worked, FTL transfer, I don’t love FTL transfers for PTTD as an only procedure, their augmentative certainly but to think that the posterior tibial tendon is bad, so you’re going to augment it with another tendon and everything’s going to be fine, I think is not -- I think that that’s an amiss thought.


    And then of course, spring ligament reconstruction. There’s new techniques to reconstruct the spring ligament which were working. And all of these incisional planning is a hockey stick. Basically is the medial malleolus insertion of a posterior tibial tendon on a navicular. Groove director down, the tendon lays right under the medial malleolus. And this is what a partial tear looks like. The tendon is like a rope, so the rope can fray, the rope can rupture or you can get these inter-substance long tears which you see in the right picture here. It’s kind of striated tears.

    So no -- excuse me. Synovitis of the tendon sheath, so here we can see a little tether of the tendon being held. We can see this inflammation and redness. Sometimes, we need to peel away the medial malleolus or the bony structures because they’ll be this chondromalacia, this catching spot on the posterior tibial tendon which will further degenerate it. If you see this, curate it out a little bit, take a drill and just drill through just like you would in osteochondral defect to get some bleeding, some fibrocartilage to fill up that chondromalacia and offer a gliding surface. We’ve used amniotic membrane to restore gliding surfaces. I’ve taken wax, bone wax, you know, provided somebody doesn’t have a bee allergy and kind of like wipe that in there, get it in to stick so that the tendon glides. But the problem is, by and large, if you have a tear, then the immobilization needs to occur, and while immobilization occurs the tendon binds itself back up. So there needs to be some sort of compromise between non-weight bearing range of motion exercises that don’t tax the retinacula repair and don’t allow the tendons to sublux, but that offer range of motion exercises so the tendon doesn’t stick itself back down. Of course the neurovascular bundles is very much in concert with the posterior tibial tendon.

    I right away tell patients, you know, numbness is going to be the first thing on the consent.


    It’s often times just a little branch that communicates across with the top of the foot and in order to do an adequate repair, oftentimes that little branch needs to be sacrificed to do it and, you know, to do your work. So numbness is likely a sequelae of this procedure. Here’s the tendon sheath, you want to make sure that the tendon sheath is repaired. Otherwise again, the tendon will sublux out and realistically where’s the blood supply come from? The tendon sheath. So you want to re oppose it so that the tendon can heal nicely and the retinaculum as well.

    After the tendon is freed up, you can wrap it with acellular dermal matrix to augment the repair. Again, you can use amniotic membrane if the tendon is thin, if there’s concern about gliding mechanism and then we just go ahead and baseball stitch the tendon back together. A running lock at the end of it, you can see the tendon is in shape with acellular dermal matrix wrapped around it. And the idea is the acellular dermal matrix will turn into the tendon. You don’t want to use acellular dermal matrix or a thick piece at least if the tendon is normal anatomic size. If it is abnormal anatomic size, meaning that it’s thin, acellular dermal matrix is great. It will bring it back to a normal size. If it’s thick to begin with, you have to get at least score out the pieces that are degenerated before you wrap it or don’t wrap it all because nothing worse than a thick posterior tibial tendon that subluxes out of the groove or taxes your retinacula repair.

    Speaking of, there’s your final retinacula repair and you can see that the tendon is housed nicely in there and not going to go anywhere. So here’s the post -- here’s the MRI of a graft thickened tendon. You can see, this certainly wants to sublux out and that’s why we need to be cognizant about the size of our posterior tibial tendon.

    Okay. So we’re going to change lines, arthroereisis. Arthroereisis is something that’s not advocated by Johnsons and Strom, but I think it’s quickly becoming common place with PTTD stage 2.


    The problem is, most adults cannot tolerate an arthroereisis plug. Arthroereisis realigns peritalar subluxation, performs -- prevents deforming forces, influence in the healing of the tendon. So even if you can put the arthroereisis in for a little bit in a posterior tibial tendon and heals itself, and then it has to come out later, okay, because the patient can't tolerate it, it oftentimes will cause enough scar in the subtalar joint to make a difference.

    So if you get that internal brace, that internal cast, if you will, of about a year, that’s one of the cases where the posterior tibial tendon will heal itself nicely, and you can then control that foot without extra articular procedures that are lengthy or, you know, that are going to keep them in a cast for a long, long time because you have this internal cast.

    Again, arthroereisis is not indicated for advance PTTD and not indicated for associated DJD. This is going to be a person who’s in their early 30s, 40s, 50s. Again, that you don’t want to do the articular procedures, you don’t want to do effusions with, you know, their activity level is not crazy to the point where it would be worth it to do a subtalar fusion or a TN fusion, but at the same time they’re in extreme pain, you want to buy them a year to, kind of, scar up and then you plan on taking the plug out. Except for the fact there is new technology where some of these plugs are becoming absorbable, so you don’t have to take them out. You put them in, the plug sits, it does its job, and then it dissolves over time so it doesn’t hurt the person. Because honestly, if you’ve ever put an arthroereisis plug in an adult, they’re fine for about 3 months to 6 months but by that year to 2-year point, boy, they’re miserable and they need to come out.

    So, this is a calcaneal stance position that you are striving for on the -- a neutral position on the right, calcaneal stance position on the -- excuse me, neutral position on the right, calcaneal stance position on the left.


    Here, you can see the talus is adducting. You have a largely frontal plane deformity here. And then once we have their -- build up their arch, this is a neutral position. So when someone puts a plug in, the idea is to give them enough to pronate down, to in between neutral position and calcaneal stance position without getting to this calcaneal stance position and looking like the top-right picture here.

    Subtalar joint positioning, again, this is -- you want to -- this is a child on the bottom but Kite’s angle needs to be restored. Here you can see in a pronated foot in the left-hand picture here, and on the right-hand picture here a normal foot. Kite’s angle should be in that 20 to 30 degree range, not 30 to 40 as we see on the left.

    So, this is one of my favorite pictures because until I saw this, I really did not understand arthroereisis plugs. And a lot of my students at Temple will say, “I don’t get it. How do you put it in a plug laterally and it doesn’t stop -- it does -- it stops eversion from occurring?” Well, the way that it stops, is the calcaneus here obviously, wants to, kind of, come towards the screen and drop down immediately. And when it does, it’s jammed here on this side by that plug. So it doesn’t allow this to happen. The sinus tarsi doesn’t become obliterated because the calcaneus cannot pronate out of -- out of neutral into eversion. It can’t sit there because it’s blocked by the plug.

    Also, what it stops is it stops the talus moving anteriorly on the calcaneus, or the calcaneus moving posteriorly on the talus. So here we can see a rectus foot type, and a pronated foot type, and then here we see the plug promoting that pronated foot type. It’s stopping eversion, the calcaneus, if you have the plug sitting in position, and it’s also stopping anterior location of the talus or poster location of the calcaneus to collapse that subtalar joint.

    Blood supply. When you’re doing your plugs, you have to be cognizant. The posterior tibial artery has a primary branch to the sinus tarsi.


    You don’t want to nick that if possible. And then of course, this is a nice ligament disposition. This is right where you want to split the sinus tarsi ligaments and right in here is where your plug is going to sit.

    Again, for residents in the room, it’s a small incision curvilinear. You want to look out for the superficial peroneal nerve here. And then once you set your sinus tarsi plug, you want to take a C-arm to make sure that you’re in the sinus tarsi. This is exactly where you want the plug to be placed. This is the posterior facet of the subtalar joint. You want a half a centimeter to a centimeter tops from the edge of the calcaneus and this is where the plug sits. This is what you do not want to happen whereby the plug is extravasating outwards. You want it buried nice in here, not too far across, but again, a half a centimeter to a centimeter from the edge of the lateral calcaneus.

    Range of motion. Again, this is not to block all motion. This is to allow normal pronation. So you want the person to be able to pronate. I usually look at the talonavicular joint when the scissor is in there and I say, “All right. If they had, you know, 100% motion, I’ll give them about 30% so that they still need to pronate.” And if you don’t, if the person is very uncomfortable right away and the plug needs to come out. So here, you can see pre-operatively. On the left here, we see the TN joint dropping and then we see the plug here and we see, excuse me, and we see the plug here with the TN joint realigned.

    Again, a child pre and post-op. Here, you can see the TN joint drooping down. That’s been outlined and the next one is lifted back up. So the plug really does make a difference and, again, will take a lot of the strain off of the posterior tibial tendon so that it can heal itself and strengthen back up, kind of take some of the slack off of it. Here’s the K-wire a guy is sitting in the canal here.

    Post-operative management.


    Again, short leg cast, immobilization. You’re not looking for long, long period in the cast. You’re looking at two or three weeks until the incisions heal. Weight-bearing and then CAM booted about three weeks to six weeks. And then, range of motion exercises during that period of time. And then, sneaker with an orthotic after that. Your cache should be eversion and plantar flexion to really allow those ligaments and the posterior tibial tendon to heal adequately and then, of course, the CAM walker. And here, you can see the arthrodesis plugs sitting in the sinus tarsi or the canal, TN joint well-aligned, and on the A-P, we can see about half a centimeter to a centimeter off the edge of the calcaneus, and that widened midfoot is now restored. It’s all overlapping again. CC break is restored and the talonavicular joint is well-covered again.

    Complications. Obviously, two biggest ones are nerve entrapment and the fact that they need to come out. Now, flexor digitorum longus tendon transfer. Contraindication, STJ or forefoot varus. Rigidly. You want to use it in conjunction with the medial calcaneal slide osteotomy, harvest the FDL at the knot of Henry, and attach the talonavicular through a drill hole. This is a landmark paper by Mark Myerson who has shown treatment of stage 2 PTTD with flexor digitorum longus tendon transfer and calcaneal osteotomy. I’ll call your attention to the conclusions. The surgical correction of stage 2 PTTD with medial translation calcaneal osteotomy, flexor digitorum longus tendon transfer to the talonavicular, you’ll have excellent results with minimal complications. This is a study over about five years with 129 patients and all of their vast scores improved to high 80s and low 90s.

    This is a new technology provided by Arthrex. There’s other companies are coming out with this. This is refinement of the spring ligament. So again, I think this is a good adjunct to the procedure just like the FDL transfer.


    Not a sole procedure that you should be trying, but it certainly takes up for the spring ligament, deltoid ligament, and recreate the two, taking the straining off of the posterior tibial tendon.

    Lateral column lengthening. The indication is stage 2 disease with greater than 30% head uncovering. Contraindications. No significant transverse plane component. You don’t want to do this in some -- unless somebody has that CC adduction. This is obviously the Evans osteotomy. It takes place about a centimeter to a centimeter and a half from the joint. The PI Institute would advocate a half cut through the calcaneus, most orthopedists. And now, a lot of podiatrists are advocating going straight across. The idea is you put in the wedged graft and it turns, it pushes the calcaneocuboid joint, basically, really realigns the TN joint medially here and the biggest concern that you have is pressure necrosis at the CC joint if the graft is too big. So here, you can see the graft in good position alignment and the CC joint is well aligned, nice and straight.

    There’s been studies about autograft, allograft, you know, titanium graft, what have you. Answer is that doesn’t matter what you use as long as you lengthen that lateral column not too much but adequately to make a difference. And if you over lengthen it, you’ll get CC joint arthritis which is a problem. You also don’t want to over length it to the point where your grafts sits in the subtalar joint because people are miserable with that. If anything, air on the side of a smaller graft with a shorter graft.

    Medial cuneiform, cotton osteotomy, this was described way back in 1936 by Cotton. Cotton felt as though there’s a tripod to the foot, here, here and here is where you’re bearing your weight and his idea was to take a plantarflexory -- excuse me. Was to insert a plantarflexory wedge in the medial cuneiform to restore Meary’s angle. Not at Meary’s angle, but distantly closer to the first metatarsal in the cuneiform.


    Posterior muscle group lengthening, you can do your TAL, you can do your Vulpius, Strayer, anything if this person has failed conservative therapy, equinus stretching and things like that to get length on the Achilles.

    Stage 3, rigid deformity, now we’re getting into fusion procedures. Again, conservatively, we’re looking at MAFOs and Arizona Braces for nonsurgical candidates. Surgical treatments show -- are addressed to the arthritis and that surgical treatment is oftentimes fusion procedures. This if any time in an elderly patient is when the tendon is going to rupture, here, you can see a visible defect. You can tell that that posterior tibial tendon is no longer intact. You’re going to order your tenography, your x-ray, your MRI, your ultrasound.

    Here on MRI, you can see the graft is ruptured. Indications for surgery is subjective. Knee pain. This is a big one. I always counsel my patients, “Are you having knee pain?” Because certainly, you can prop their arch back up with your fusion procedure and fix some of their knee pain. Not as a goal but you want to monitor that knee pain beforehand so that you could -- you know, if they still have the knee pain afterwards, they’re aware that this may or may not help.

    Here, we see the tendon retracted completely ruptured, you’re going to measure the defect and then again, considering your length-tendon ratio, Blix curve, you know, suture up the tendon in, restore it, you can actually dock the graft tendon on both sides and you have a nice restored tendon. This is actually a tendon ruptured that I just did a couple weeks ago, with a graft in place, I twisted the graft because it was kind of thin to give it some more bulk and the repair.

    So when you have this foot, you’re looking at nothing but fusion surgery, here’s a triple arthrodesis. Again, you’re going to restore the calcaneal inclination angle, stop the dropping of the talus.


    Restore the TN fusion and repair the tendon at the same time. So there’s your triple.

    And then finally stage 4, which is Myerson’s edition. This is where the deltoid ligament is under complete duress. You’re going to look at your triple but also your pantalar fusion and/or your intramedullary nod -- rod. The idea is to stop the valgus from occurring because at this point, the deltoid ligament is so insufficient that there’s no repairing it with soft tissue and bony structures.

    So in conclusion, PTTD is complex multiplane deformity. Early stage often responds to conservative treatment, these patients have to go into physical therapy in stage 1 or 2 to get rid of the equinus. And they have to understand this is a cross that they’re going to bear for the rest of their lives, because if they stopped the equinus stretching, the PTTD is coming right back.

    Late stage requires joint destructive arthrodesis and then finally to kind of keep your eyes on something, instead of the arthrodesis, the advancing technology is showing that you can now start to do some rearfoot procedures, whether it’d be a Koutsogiannis fusion procedure what have you. And then instead of fusing the ankle, you can put the ankle implant into a little varus to account for the valgus and actually do a total ankle replacement instead of the fusion of the ankle. So something to consider going forward as technology begins to advance in TARs.

    Thank you very much for your time, I appreciate it.

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