• LecturehallThe Use of Orthotics and Heel Stabilizers for the Management of Pediatric and Adolescent Flatfoot Deformity
  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Male Speaker: I am going to share some of my basic thoughts with you on pediatric flatfoot and orthotic options, and I always felt that the pediatric population is a special group of people. Why?

    They’re pleasant. They don’t have all of the problems in life that most adults bring in with them, and they’re receptive to just, “Hi, how are you?” a handshake, a smile, and depending upon how old the kids are, your practice has to be kind of prepared for what goes on with youngsters. And I’ve treated kids from two to three weeks old with clubfoot deformities that I had to correct, both surgically or from manipulation and serial casting, to torsional deformities that are severe, that have required osteotomies of the tibiofibular unit, to obviously minor things such as warts, ingrown toenails, et cetera.

    You need to be prepared for a disruptive component in the practice, a kid that’s crying, a kid that’s sniffling, a kid’s got a runny nose, a kid’s in diapers or they’re not in diapers. So we’re now in a situation.

    It’s not that diabetic patient that’s sitting there with a Charcot foot, it’s this little baby ready to be assaulted by me, the doctor, and they already know that they go to the pediatrician who has this white coat on, sticks a stick down their throat, something up their nose, something in their ear, and he gives them a shot in the ass.


    Now, that’s not a good scenario for the youngster who believes coming to my office and my practice the same thing is going to happen. So there’s barriers, there’s things that need to be broken down, and relationships established.

    I spend a lot of time in history taking of the parents, and as to knowledge about the youngsters, knowledge about the birth. Full term, problems in birth, were there any drug interactions or drug problems during birth, caesarean section.

    Questions that may be able to enlighten me as to what is the etiology of certain deformity, was it a breached birth? How many other children do you have? Do they have the same type of problem? And through the years, you begin to realize that this is a kind of practice that will lead to a future of many years of following a patient, and I’ve been in practice for 48 years.

    So I have treated enough adults through those years, who bring their children in, and the amazing thing is now even the children that becoming adults bring their children in, and it’s a very rewarding type of practice.

    The pediatric patient is very unique because they don’t complain of a lot of pain. They don’t have this arthritic joint, they don’t have significant pain in the hip, or a low back, or a knee, or a heel pain syndrome unless they have calcaneal apophysitis that we may see in 10-, 12-year-old patients.

    The biggest problem that we see associated with flattening of the arch, which is probably one of the most common things that I see, is the fact that the parent brings the child in, they may be somewhat awkward in the way they walk, they may shy away from activity such as running or jumping, they may wear down their shoes terribly, they may complain of pains in the calf at night, growing pains as it’s been called.


    Now I never realized, I thought that growing is going to cause calf pain, not that you can’t get a cramp in your calf, but more times than not, it’s interesting that if you deal with the etiology of growing pains, more times than not, you realize associated with flatfoot syndrome, overactive muscle, overuse syndromes.

    Now, will they outgrow this condition? Yes. And now when they become an adult or a young adolescent, and they’re more active, what happens? It’s no longer growing pains, they stop growing. Now you’re calling shin splints. It’s the same phenomena.

    And I’ve also looked at the fact and felt that here we have a moldable, adaptive foot type, that we are able to make something for and possibly avoid the need for surgery in the future. When you look at hallux abducto valgus and bunion deformities, they didn’t develop at birth, they weren’t present at birth, I said this earlier today. They develop over time.

    If you have a severe deforming force such as primary equinus or equinus, that causes severe hyperpronation, it unlocks the entire foot and we eventually begin to develop hypermobility of the ray. You’re going to develop hallux limitus rigidus, you’re going to develop hallux adbucto valgus. You’re not going to necessarily see an arthritic great toe joint, but you will see juvenile hallux abducto valgus.


    And it’s usually pretty severe. The etiology of that is in the structure of the foot. Now, what happens when more times than not when a mother or father goes to the pediatrician and tells them, “My youngster’s got a flatfoot,” what do you think the pediatrician says? “Don’t worry, they’re going to outgrow it.” But if they all outgrow it, how do we see so many adults and adolescents with flatfeet? Obviously, they didn’t outgrow it. Now, you can have adult acquired flatfoot. That’s a different phenomenon. But the youngster who has a flatfoot does not outgrow it.

    So what are my goals when I’m looking at a flatfoot in this child? And I’m talking about weight-bearing kids, probably around the age of three, right through adolescence. What are our goals? What are we trying to accomplish? One, maintain stability of the foot. Two, allow a normal development. I want that foot to develop around a normal position. Neutralize deforming forces. Orthotics can neutralize deforming forces. Allow for the normal motion to take place, support deformity.

    Martin Ruth talked about single plane osseous deformities, rearfoot varus, tibia varum, genu varum, single plane osseous deformities, forefoot varus. And what did he say? Support that deformity. Take an orthotic and post it, that’s what post-it’s are doing. Hold the foot up in the position and eliminate a necessity for compensation.


    Because compensation leads to symptomatology. Kind of basic principle when you think about it. And you want to control that in three planes. And therein lies one of the biggest problems we’ve had.

    Essentials for triplane control with orthotics involves neutral position casting. I am old school. I use casts on all of my patients that I’m making custom orthotics for. I never have a patient step on a fallen box, they get too much soft tissue deformation. I can’t control the position properly.

    I don’t like the scanners. They can be effective, but more times than not, I want to feel that foot in my hand, reposition the subtalar joint, position the midtarsal complex, lock the forefoot on the rearfoot. That I can do with neutral position casting. And I can shape that arch of that foot in the contour of this cast by the two things that I have to work with, and that’s my two hands.

    I do like an offset calcaneal position in varus, and I’ll show you what I mean by that. I like long phalanges going down to the first and fifth metatarsal necks. And I allow for normal lateral and medial column function. Recognize the lateral column of the foot is stable. The medial column of the foot has always been considered the dynamic part.

    So how can we make one orthotic, one simple shell that’s going to allow for the dynamic component and a stable component? So is there something that we can do to incorporate both control?

    And then rearfoot posting.


    What are we trying to prevent? Remember I mentioned earlier, talar escape. With peritalar subluxation, the talus escapes right out of the cup of the navicular. So we have ligamentous integrity, which is compromised. One at the subtalar complex and then two, on that basket called the spring ligament, which supports the head of the talus plantarly. So those ligaments become compromised as well.

    So we want to maintain the integrity of the talonavicular joint, support the medial column, support the position of the lateral column, maintain the TC relationship. Prevent hypermobility to the first ray. And then improve posture, which can occur.

    The kid has knocked knee. Obviously, you’re going to see a significant genu valgum -- a coxa vara genu valgum. The foot comes to the ground in a certain position, you have a problem. That is an everted position of the foot at heel strike. That is virtually impossible to bring that foot back into a normal position for heel strike.

    Recognizing that heel strike, the foot is supposed to be inverted by a couple degrees. Instead, we’re now placed in a position of valgum because of the structural position of the leg. You superimpose body weight on top of it, you superimpose internal rotation from the leg on top of that position, and you’ve lost it.

    Orthotics can be therapeutic and diagnostic. Therapeutic, obviously, if they control symptoms, everybody’s happy.

    Prevent deformity. Over time, we can prevent deformity.


    Identify uncontrollable forces. The patient that can’t tolerate a good orthotic is telling you that there’s deforming forces that I cannot control with an insert, so they’re not going to wear it. It’s going to hurt. They’re taking it out. Equinus is one of those.

    And then, of course, determine the need for surgical intervention. Growing pains, awkward gait, calcaneal apophysitis. Calcaneal apophysitis is a symptom that we see around puberty. The apophysis is present. It has not closed. It actually is a self-limiting disease in a sense, because once the apophysis does close, the heel pain goes away. But it’s reflective of something going on. And I look at the apophysis as a traction compression environment.

    Achilles comes down and search into the posterior aspect of the calcaneus, the apophysis component. The planar fascia attaches to the apophysis posteriorly, and then moves forward into the foot. So you have soft tissues being pulled in one direction and the other, compressing and closing a traction problem at the apophysis. Let alone the fact the hyperpronated foot with apophysitis is a poor functioning foot and does not absorb shock well. So you’re adding another element into it, but it’s actually a condition that responds extremely well to orthotic management control.

    Arch pain, I’ve talked about or mentioned. Some youngsters do develop arch pain. Note, of course, that your orthotic can be used to maintain the position you might have achieved if you have to operate on the patient.


    So it was diagnostic, it’s therapeutic, and it’s not something that’s a waste of money in the parents’ eyes, because if I eventually have to operate on your youngster, I’m going to use that same orthotic to act as an external brace or support while the process of healing takes place, following the surgical procedure. And certainly, prevention of recurrence or deformity.

    So take a look at this little flat foot. And here’s a kid probably about three years old, maybe four. And can you see the signs already that are being exhibited by the pronation component? The calcaneus seems to be transposed somewhat, away from the position under the leg. This is the support component, under here. Once you start to shift the weight, we have a problem in the rearfoot. The internal rotation of the leg is going to exaggerate that with every step that is taken.

    The forefoot abducts. That’s that transverse plane dominant component. That’s the oblique axis to the midtarsal joint. So you get transverse plane transposition. The foot goes laterally, the arch drops down. That’s oblique midtarsal function. Sagittal plane, transverse plane, they are the dominant planes.

    And then these patients usually develop a supinatus of the forefoot. That’s the third component. It’s a different axis. That’s actually the longitudinal axis to the midtarsal joint.

    So this foot is now collapsing, and what do we do? Do you allow it to continue to do so? The question that is often asked, and no wonder I asked is, is this a fat flat foot, versus the flat fat foot?


    Some kids are pudgy the first few years of life, so there’s a fair amount of adipose tissue in the arch, the heel of the foot, and it looks like it’s flat. And as that foot matures, the osseous structures become more dominant, soft tissue restarts to recede somewhat, and now you’re going to be able to identify or appreciate the structural component. Certainly, an X-ray is going to provide us some additional information that we have to look at.

    I showed you this before. Here’s an example of what happens as the youngster matures, we’re seeing the signs of internal deviation -- let’s go back here a minute, sorry -- of the tibia coming down, arch is dropping down, tuberosity in navicular and talar head is prominent. The arch is dropping to the ground, first ray comes up, which is hypermobility, we’re seeing at an early age. And we know hypermobility is going to lead to instability, and with the forefoot abducting, we will eventually increase the direction of the hallux in a lateral direction, because of the pull of the adductor. HAV, hypermobility of the ray, to the intermetatarsal goes out, we are in the early stages of the development of either a hallux limitus rigidus over time or hallux abducto valgus.

    Look at it from the back, look how much this foot is showing collapse in this area, as I’m going through the midstance phase gait. All the force is going through the medial part of the foot, and the foot is shooting out laterally. And here we are showing the hallux.


    As the line of progression goes forward, and the foot goes lateral, the hallux receives additional force, pushing it in a lateral direction. And of course, you see how the arch is not coming back into a supinative position. The calcaneus is in an abnormal position, and you have the hallmarks of a pretty significant flatfoot. So we see complete loss of the longitudinal arch, sagittal plane, transverse plane, as I’ve told you. Helbing’s sign, that’s the everted calcaneus, it’s really abducted more than everted, and then, of course, forefoot supinatus that we see.

    Again, the symptoms, where the pain might be, do not only look at the foot. We are foot and ankle specialist who really treat the lower extremities. So I watch these kids walk, I watch patients walk constantly. I want to see what’s going on with that foot. I want to know the angle of gait, I want to know the influence of frontal plane deformity. I want to see the position of the knee.

    All of these factors come in to play. How clumsy, how awkward they are. When the heel comes off the ground, as the rear foot supinate, does the calcaneus invert? Is the tibialis posterior functioning the way it should? Or is it in a compromise position because the axis is altered by the hyperpronation?

    So we look at x-rays and we see the effects of this hyperpronation syndrome. I showed you before the obliteration, sinus tarsi, the talus coming down, same line often broken anteriorly, and the superimposition of all metatarsals, that’s my supinatus component. That’s what happens with severe hyperpronation syndrome.


    And with the supinatus, the medial column is coming up, and when you go into the final propulsive phase, you’re going to jam the great toe joint.

    So let’s look at the goals. What’s a good surgery approach?

    I want to control three planes, sagittal, transverse, and frontal. Where I differ with Merton Root, who was a dear friend of mine, by the way, I learned a lot from Mert, is he thought because we have triplanar motion at the subtalar and midtarsal joints, those joints can only move in three planes, so if you are able to control one of those three, you’re going to control the other two. It doesn’t work in a pediatric population.

    So if we take a look at this little diagram, we could see very nicely how the entire foot wants to move away from the ball and socket talonavicular articulation. So many, many years ago, as I thought about trying to control and reposition the foot, I realized I’ve got to actually swing this entire foot back in front of the talus. The talus functions in gait as a leg bone, so an extension of the tibia, it’s locked in the ankle mortise. So there’s no way I’m going to bring that back by itself without trying to bring the leg back. I can’t do that so easily.

    So what if I can reposition forefoot on rearfoot and then prevent this from happening? A regular orthotic is not going to be able to do that. The ball and socket joint is that dominant. When we look at in a transection, you could see in the neutral position to slightly supinated versus the pronated position.


    So the talus, plantar flexes and adducts, the calcaneus is moving away, here’s my spring ligament underneath, I’ve got no basket of support. And the interosseous talocalcaneal ligament is somewhat compromised. That’s what I was talking before about that component of laxity within the joint or peritalar subluxation. Is that severe?

    One must be very suspect when you see a foot that looks this flat and this everted. Is it the foot itself or must we be looking somewhere else?

    I already mentioned genu valgum or tibia valgum. What about ankle valgum? So when I take X-rays of my patients, especially in this age group, I’m taking a dorsal plantar and lateral view. I’m also taking ankle views to be sure that I don’t have a deformity in the ankle complex, which makes it that much more difficult to do anything at the level of the foot to treat.

    Now here’s a good example. Mother, child. And you start to see, here’s that nice HAV, and we’re starting to see the pronation effect. Look at this, as this is starting to drift somewhat, and this foot pronating more.

    Limb length discrepancy, by the way, is another problem area. When you have a limb length discrepancy, unilateral bunions, the biggest cause that I’ve seen through the years, pronation on the long side, limb length discrepancy, and it doesn’t have to be more than a quarter eight, to a quarter of an inch. The body tries to compensate for it, supinate one side, pronate the other side. So the bunions are always on the pronated side. It doesn’t take rocket science to realize the association of pronation and HAV deformity.


    So here, take a look at this foot. Here’s a juvenile hallux abducto valgus. Look at this, talus is outside, moving away from the talus. This even has a little bit of a gorilla form navicular. So it’s still somewhat in the cup but it’s actually misleading, it’s probably out about here.

    The forefoot goes lateral, pulls the hallux with it. Why? The adductor transverse an oblique head, pull the sesamoid and the base of the proximal phalanx. They go with the foot. This is a ball and socket joint. First MPJ, I’d consider a ball and socket joint in a younger patient.

    So it can easily move. We know there’s a rotational component. We know that there’s a transverse component and there’s a sagittal plane component. That’s ball and socket. So anything pulling this way, the only thing holding anything relatively straight are your ligaments. And what happens to ligaments when they’re being pulled? They stretch.

    And then the intermetatarsal angle increases because of retrograde force, because of the hypermobility of the ray. And one looks at that and says,”Well, what caused the bunion?” What caused this to happen? It’s the mechanics.

    I mentioned earlier, you can go in and correct all of this and realign it. I’m not going to do a lapidus on a kid that age, with an epiphyseal plate still open. I am angled maybe about 14 degrees, maybe 13. Not a candidate for a lapidus, but if I were to correct that surgically and I don’t do anything for the hyperpronation, guaranteed recurrence of deformity.

    So let’s take a look at some thoughts beyond what I’ve already stated. Look at the severe hyperpronation in this foot. Tibialis posterior is the strongest supinated foot but cannot supinate a pronated foot.


    The TP and the peroneus brevis are stabilizers of the subtalar and midtarsal joints. They both attach onto tuberosities, one at the base of the fifth, one at the tuberosity in navicular. They have great mechanical advantage on both sides as long as the foot is held neutral or positioned to maintain alignment. Once one side goes more than the other, you tug, that’s it. The posterior tibia loses its ability to resupinate, to stabilize, and the peroneus brevis gains mechanical advantage.

    How many people use this type of typical orthotic? That was a root type of orthotic. Rearfoot post, forefoot post, no phalanges. What do you think that foot is going to do on this? It’s going to slide right off. You put it in a brand new shoe, it’ll hold some stability for a while, but the foot slides right off. That’s not the answer.

    Whitman plates, Roberts plates, so they were phalanges put up to try to deal with the calcaneal position. Prevent the calcaneus from everting or even possibly adducting. These are good ice scrapers. I still get these occasionally with patients.

    Let’s look at this device that I developed probably 25 years ago. I coined it the DSIS, dynamic stabilizing innersole system. It has a deep PLC, it’s got a five degree offset in the cupula. So when that foot goes in, it’s inverted by five degrees. Long lateral and medial phalanges, high phalanges, and independent medialateral column function.

    So what I’m doing is taking that foot, putting it in position, having it in various position heel strike.


    I’m putting phalanges that are going to protect the sides of that foot. The foot is not going to be able to abduct because I’ve got a long lateral and a long medial phalange that come up high. That’s what it looks like in a prescription device. And the central part being cut out is to allow medial and lateral column function. This is a controlling type of insert that will not allow the foot to shift off, abduct, evert or go into a position of supinatus. And it’s made from this little guy, as I mentioned to you before, I like neutral position casting.

    Here’s a great example of a plate. Look at this plate. It’s got a big rear foot cup. It’s got a big post on the rear foot, probably about 6-7 degrees. Here’s a phalange holding the calcaneal position somewhat, but look where the forefoot goes. Poop. Gone. As soon as that foot moves away from contact phase, starts entering mid-stance, you’ve lost the game. The foot pronates right off of that type of insert.

    That’s when I realize you’ve got to go all the way down to the necks of the first and fifth metatarsal, and that’s what this looks like, how it cups the foot, maintains the position of the calcaneus. Here it is in the arch, all the way onto the neck of the first metatarsal. Here’s a good example showing the position. Here’s the foot before the DSIS is put in, and here it is with it.

    And we’re actually even seeing changes in the IM angle. And obviously, the talocalneal angle are divergent, and the position of the forefoot on the rear foot, looking at the cuboid as well as the talonavicular articulation.


    Now, I’ve reestablished a position.

    Next question is can the patient tolerate it? As I’ve mentioned before to you, if primary equinus or equinus is a deforming force, all of this beautiful but they won’t tolerate it. So those are the patients that I’m going to have to go in and do a TAL or a gastroc. So I am of the belief that motion is life. We want to be able to maintain normal motion and eliminate abnormal. These types of inserts in my opinion have very little ability to work on the pediatric flatfoot.

    Not bad. I was just over by 30 seconds. I thank you for your time.

    TAPE ENDS [0:30:50]