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Harold Schoenhaus: Now that youâve heard enough surgery, I think itâs time to focus a little bit on an area thatâs been near and dear to my heart called biomechanics. And for those of you who donât know who I am, Iâm Harold Schoenhaus. Iâve been teaching biomechanics or pathomechanics at the Temple School for 45 years. Busy practice, surgical practice, major reconstructive. And Iâve always felt, in order to get good results, long term, what differentiates our profession from any other dealing in foot and ankle is the understanding of biomechanics. And, at that point, you start to squirm in your chair and you say, âWell, Iâm a surgeon.â âIâm a podiatric surgical resident, give me the knife, let me cut, let me use these fancy screws, plates, external fixators, everything under the sun.â And you walk out of the OR, and youâd say, âGreat, high five, everybody; everything looks great.â Then you wonder why number of years later, we have problems, because of the underlying etiology that led to deformity still exists. And residents, unfortunately, you are in a bad position in a sense because you donât follow these patients long term. I mean, if youâre a first year resident or a second, and you spend time in a physicianâs office and see the pre-op, do the surgery or involved with it, and watch post-op for a year, year and a half, that would be real nice. Thatâs ideal in my mind. But thatâs a philosophical approach as to why biomechanics is not a dying art, not a dying science, itâs imperative that we consider all of these factors in evaluating a patient. The foot is extremely unique. Surgery, in my mind, is carpentry, very artistically done and all of these things that we see in the exhibit hall for fixation and enhancement of what we do is just for that purpose. Give me the best screw that I can have to utilize to change or alter position and maintain it. But after thatâs done and over and the healing is taking place, what happens? Now, Iâm not going to bore you too much on a topic like forefoot varus, why is this important? Iâve selected this topic because of different foot types or types of forefoot varus all based upon the ability of a foot to compensate. I have nothing to disclose in this talk, I am not paid by anybody for a discussion like this, but the goals and objectives are to open your eyes and your ears and a thought process of how important biomechanics is to my surgical outcome. And you heard great talks this morning. You talked about hallux valgus and bunion deformity, fabulous of what Kalish [Phonetic] has been able to do. But what led to that deformity to develop in the first place. And unless you do some type of more involved surgical approach like a Lapidus, which kind of deals with hypermobility of a first ray in a far more advanced direction, etiology is still there and what do we do about it as not only surgeons, but practitioners for many years to make a successful practice. So when you look at an inverted forefoot to rearfoot relationship, and Iâm sure youâre all doing biomechanical examinations on your patients before you operate on them, which Iâm being facetious because my own residents donât do it. And I say, âWhat was the cause of this?â Oh, I donât know, is you got an increased IM angle. Yes, we know that. Thatâs an X-ray finding. What led to that? Why are we going to do a closing base wedge, will it work? Why at Kalish, why a scarf, I donât care what the name is, as long as you have design in your head to say, âIâm going to take care of the deformity as well as the deforming force that led to the deformity.â Now, do we understand what that is? So, sure, you can do all these fancy measurements, identify the fact that when you strike the ground with a foot thatâs inverted, and if itâs forefoot varus, the rearfoot may be okay, but the forefoot still inverted to the supporting surface. And to compensate for that, if motion is available, the subtalar joint is going to pronate. And unfortunately, itâs going to have to advance to unlock a midtarsal joint to pronate.
And weâre going to see what the result of that is. If you donât have the ability to compensate fully, then youâre going to be into the uncompensated or partially compensated variety where your problems are going to be more lateral than medial. And an orthotic management control is going to be critically important. To compensate for an inverted forefoot to rearfoot relationship, what must the calcaneus and the subtalar joint do? It has to evert, and the only way you can evert is by pronating. And then compensated forefoot varus, which will focus on and fully compensated, itâs going to cause significant rearfoot pronation. And once you evert the subtalar joint through pronation, you unlock the midtarsal complex, because the subtalar joint controls midtarsal activity. And once you unlock the midtarsal joint, and you enter end of contact phase, go into midstance and propulsion in a pronated position, the oblique and transverse axes of the midtarsal joint are going to dominate and weâre going to see transverse plane position and motion of the forefoot. Weâre going to see sagittal plane depression, the arch drops, thatâs all oblique midtarsal activity. The longitudinal midtarsal joint supinates, itâs a supinator, so you can have severe hyperpronation due to forefoot varus, and then superimpose upon that forefoot, what we call, forefoot supinatus, which is a triplane soft tissue deformity. In kids, when we see that inverted position in the first ray up in the air and youâre going to go in and do extensive flatfoot reconstruction, what do you often do for that medial column? A cotton to drop down the first ray may not even be necessary if you reposition a foot and allow the mechanics to allow peroneus longus to de-rotate a medial column. Often on the OR table, we want everything to be perfect when we leave the OR, so that foot now has an arch, everything looks great, I might have done a displacement osteotomy of the calcaneus. We might have done a transpositional distal osteotomy of the calcaneus, so we could do a cut, we could do an advance, we do a cotton, and you walk out and you say, âWow, perfect.â Maybe too much surgery, and Iâm going to be talking, I think, on arthroereisis later today and show you what you can accomplish when less is more. So here, youâre looking at an everted or transposed calcaneus, the arch drops. Take a look at that, we see it in the younger patient, severe transverse plane domination, sagittal plane, the arch collapses, this patient goes into the pediatricianâs office and itâs concerned, the parent brings the patient and what are they told? âDonât worry, theyâre going to outgrow it.â Youâre not outgrowing this because of the deforming force and you see this X-ray with significant transposition. Look at the talonavicular joint, the TN joint is a ball-and-socket joint. It allows for a beautiful abduction, if you will, of forefoot on the rearfoot, exposure of the talar head, and you still can have good stability of the calcaneocuboid joint. So we see other effects of compensated forefoot varus with dropping of the longitudinal arch, anterior displacement of the cyma line, the V portion of the talus falls into the sulcus of the sinus tarsi and you have superimposition of all the metatarsals. When you see superimposition of metatarsals, pathognomonic of forefoot supinatus, but that is triplane soft tissue. You can reverse forefoot supinatus, love to be able to do it in the younger patient. So when you look at forefoot varus, if I canât compensate, I stay on the lateral side and you develop lesion subfour or five. If thereâs some compensation available, you develop the Tailorâs bunion. In fully compensated forefoot varus, all hell breaks loose in a forefoot.
We develop significant hallux abducto valgus deformity. We develop sub-met 2 keratomas. Very recalcitrant to treatment, but we can fix all of that, canât we? We can do osteotomies to the first ray, we can reposition the hallux, and we could do an osteotomy of the second metatarsal, that will take care of the keratoma. That may be what youâre going to do surgically, but you still havenât dealt with the etiology, which is this flattening component of the foot. So here, if you look at the video of the patient, this is just a still portion of that video, look even in the younger patient with hyperpronation syndrome, how you develop dropping of the arch, bulging of the arch medially, abduction of the forefoot, abductory twist, hypermobility of the first ray, even see dorsal prominence to the first metatarsal. Limitus hallux abducto valgus associated with hyperpronation syndromes, you canât let that youngster continue to hyperpronate. You canât expect that foot to spring back up. At two and three years of age, you may have a lot of fat in that foot that looks like a fat flatfoot as opposed to a flatfoot that has fat as well. A differentiation becomes critically important in your selection of a treatment program. So when you look at significant etiology of hyperpronation, you think of internal torques, you think of equinus, you think of compensated forefoot varus, flexible forefoot valgus, valgus of the rearfoot. We see that even in the younger age population. In the adult, posterior tibial dysfunction, severe flatfoot, when one looks at etiology of hallux abducto valgus, unless youâre dealing with a rheumatoid arthritic or some type of trauma or something youâve done iatrogenically like take out a tibial sesamoid and you develop an HAV, transverse plane hyperpronation, Iâm going to show you the importance of that, oblique midtarsal function, adductor pull, hallux sesamoid displacement, subtalar pronation, hypermobility of the first ray, functional or structural hallux, structural elevatus or hallux limitus. These are terms that you might have even forgotten about. After you study biomechanics in school and you get into residency, how many of these terms do you continue to use or look for? Hereâs a young patient hyperpronating, look at the talonavicular joint, fair amount of exposure of the talar head. The foot is moving in a lateral direction and look at your first toe. If you draw a line of the cuboid, long axis, and look at the base of the proximal phalanx, they are parallel. Showing that whatâs happening in the rearfoot is directly affecting whatâs going on at the distal portion of the forefoot, because the adductor is attached through the oblique and transverse head, and primarily transverse head to the lesser metatarsal region. So my lesser metatarsals follow the rest of the rearfoot and move in a transverse plane laterally, they pull the hallux and the sesamoid apparatus right away from the site. So here, we have long axis of cuboid, long axis of the proximal phalanx of the great toe. And we have hypermobility of the first ray. Hypermobility, by definition, is motion at a time when there should be no motion. You watch these patients walk, do a gait analysis, visual at least. And as soon as that heel comes off the ground, you see exaggerated hypermobility of the first ray. When I see that with significant HAV, my thought process goes to deal with the element of hypermobility occurring back here where we see that diastases, if you will, or diastases between the base of the first met, second met, medial cuneiform, second met base. That ligamentous structure lost a lot of its integrity. So here is the hypermobility component. Etiology, transverse plane dominant force associated with HAV and associated with hyperpronation syndrome.
Take a look at that little pencil I put on the lateral aspect of the foot and you could see the forefoot moving laterally. Calcaneus sometimes looks perpendicular, sometimes it looks everted. Oftentimes, itâs transposed. But the rearfoot has pronated to its maximum to open up the midtarsal joint, and there it is, thereâs your parallel that I showed you on Xâray of cuboid long axis to the hallux long axis. So, if I fix HAV, donât you think you need to get that forefoot, rearfoot position realigned, so I donât get recurrence of deformity? And certainly, youâre going to take all of these other elements into account. The actual position at which you see the patient, how bad is the bunion deformity, how bad is the IM angle. I wrote an article many years ago about 1990s talking about etiology of bunion that bump on the side, what is it? Transverse plane, hyperpronation, sesamoid displacement, bone production, increase in the angle, and hypermobility of the ray. Here it is. Hereâs that medial aspect of the great toe joint. Every time you do a bunion surgery and open up the joint, you have this tenacious structure on the medial side thatâs almost like thickening of the capsule and thatâs part of the tibial collateral ligament and tibial sesamoidal ligament. So one is going straight down from the medial head down to the sesamoid, the other is going from the medial head to the base of the proximal phalanx. So if everything is pulling in a lateral direction, hypermobility of the first ray is going to move the first ray medially, we are pulling on bone. And the bone on the medial side actually is similar to what you see in heel spur production. Proliferative bone, itâs an enthesopathy, which now leads to the formation of the bunion. Now, interesting, when you look at this structure, looking at the great toe joint from distal or proximal, you see that big groove. Tendency would be, where should I take this off if Iâm going to resect the medial eminence? Well, thatâs a simple shot right down the groove, except if you look inferiorly, thatâs where the tibial sesamoid is suppose to sit. So when I make these cuts, I come from dorsal and come on an angle to come out in this direction, almost leaving what looks like a shelf here, to allow for the sesamoid to be repositioned. The sub-met 2 keratoma designed and developed by the very nature of the fact of first rays out of the way, youâre putting all of your weight now on the second metatarsal head, youâre everting the forefoots, you get a rotational component. You usually develop a retrograde force on the second metatarsal from the second digit, because when you look at hammertoe formation, the etiology we see it in cavus feet, we see it in hypermobile flat feet because of intrinsic weakness, intrinsic inactivity, and inability to stabilize the second toe against the supporting surface, so now you get an additional retrograde force. So what are you going to do? Well, we better take care of the hammertoe, you may put an implant in the proximal joint, thatâs good part of a procedure maybe, and weâre going to do an osteotomy of the second metatarsal, do a Weil, shorten it. Okay, now youâve done what? Youâve moved the vector of force or when youâre in the propulsive phase pushing off instead of now being on the second met, what do you think is going to happen overtime? If you do nothing else with that patient, theyâll be happy for the first year and then theyâre going to start to develop that callus and a shift of a transfer lesion to the third metatarsal, donât worry, we could do a Weil on the third, then weâll get to the fourth and then you got a fifth, so that will start on the other foot, because the etiology is the hyperpronation.
And if youâre going to do a corrective forefoot reconstruction, you may have to do something in the rearfoot to deal with the hyperpronation if you canât control it surgically, or you canât control it with an orthotic. If I have a hypermobile first ray with a severe flat foot and Iâm not going to correct the flat foot, the patient may be 45 years old, 50 years old, they donât want flat foot reconstruction. You could take the adductor, which pulled that hallux and sesamoid laterally and transfer it right into the first metatarsal. So you close in the first metatarsal angle down and then hold it in position by the adductor, so the foot is going to continue to pronate in a transverse plane, itâll hold the first ray where it should be. You wonât develop a recurrence of HAV deformity. Thereâs a keratoma. Boy, those things are nasty little guys. Hereâs a good example, look at the second digit markedly hammered, hallux abducto valgus, deep keratoma. And these are old pictures showing that shearing force that can come with rotation of metatarsals. In digits, when we talk about the fact that you will develop hammer digit syndrome, I said hyperpronation and cavus. Hyperpronation, we look at intrinsic fatigue, loss of propulsive stability, secondary contractures of EDL, EDB, flexure contractures, HAV deformity, which pushes the second toe out of the way overtime, contractures of interosseous muscles, bony adaptation, capsular and ligament contracture. A lot of these things you may deal with surgically. Iâm not going to go into detail on all of that garbage. I mean, Iâm sure youâve done enough Weil osteotomies and interdigital dissections that you realize that thereâs a nice balance of intrinsic power between the lumbricals and the planter and dorsal interossei to try to stabilize the lesser digits against the ground. What controls their ability to do that? The position of the foot. And hereâs a good example when you look at a neutral foot versus a pronated foot, how the angular positions and pulling of tendons contribute to development of hammertoe stability or instability. Hereâs a beautiful shot. Look at the position, the foot on your right showing a normal foot with normal alignment of intrinsic and extrinsic muscles plantarly. And then on a pronated foot, and you see how everything has shifted including the flexor hallucis longus, which is now both strung plantarly helping to hold the great toe in an abducted position. We do a great correction, weâll correct the bunion deformity, realign the toe, so itâs straight and then wonder why the hallux doesnât dorsiflex very much. Of course, youâve increased the tension on the flexor hallucis longus tendon and muscle. And you could see hereâs the intrinsics, here is your transverse and oblique head of the adductor which can join right at the fibular sesamoid and then continue forward to insert it to the base of the proximal phalanx. So as you hyperpronate, the forefoot goes that way, these guys have great mechanical advantage and now shift the entire position. And the peroneus longus which comes right up along the lateral column and can only function from low to high if their stability here can no longer stabilize the first ray. And there were just about supinatus, and here is a good example of a youngster who I actually did an arthroereisis with an Achilles tendon lengthening and changed the entire posture of the foot just by repositioning the subtalar, which directly influences the midtarsal joint and now look at the superimposition of metatarsals before and after, how you can now see the differentiation of mets. So we know that triplane soft tissue deformity didnât need a Cotton osteotomy, it needed a repositioning of the rearfoot to allow the peroneus longus to reposition the forefoot. And if equinus is present, youâre going to do a TAL or a Gastroc.
From an orthotic standpoint, post-operatively, 95% of my patients go into orthotics. And once, letâs say, they donât want to wear orthotics or wonât, I may have to alter my surgical approach or explain the problem associated with not following through with functional control. And there are numerous laboratories that provide excellent orthotic management and control for you as long as you have a good understanding of what youâre trying to accomplish with an orthotic, good casting technique or use these 3D imaging whatever, itâs an integral part of your practice. Just donât stop in the treatment of deformity by doing this reconstructive surgery. And the younger the patient, the more critical it is, because not only do they have foot problems, these patients usually have pathology of the leg, shin splints, deep pain, chondromalacia of the patella, low back pain, genu valgum. And your orthotic, neutral position, good controlling orthotic now gives you the totality of good patient care, that allows for a first MPJ to be loose enough to dorsiflex and get 65 degrees when I go into the propulsive phase. So, I share these thoughts with you to open up your mind again, itâs there. Please take advantage of your knowledge of biomechanics in treatment of your patients. Thank you.
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