Harold Schoenhaus, DPM will discuss how changes to the anatomy of the foot result in hallux valgus. Dr Schoenhaus will discuss proper surgical planning to achieve optimal correction as well as how the biomechanics of the foot must be addressed to prevent recurrence.
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Male Speaker: I’m going to talk a little bit about pathomechanics of hallux abducto valgus. I mean, you certainly heard some good talks by Dr. Kalish and other speakers talking about this deformity, how you go about dealing with this deformity. But one of the things I’ve done for the last 45 years is teach biomechanics at the Tampa University School of Podiatric Medicine. I like to consider myself a surgeon, but always utilizing the principles of biomechanics and pathomechanics in my approach to correcting deformity. When you think about it, what differentiates us from any other profession who is doing foot and ankle reconstructive surgery? We have a community of orthopedic surgeons who are fellowship trained for about a year in the foot and ankle. That’s our competitors in a sense. I have always looked upon that as, okay, they’re there. They have very little clue about biomechanics, don’t care about it. We want to surgerize, correct deformity and send the patient out and that’s the end of the game. That’s not what we’re all about and that is what separates us from any other profession. The moment we lose focus on the fact that pathomechanics and biomechanics is a driving force in what we do, we will fall into another category, which is similar to a foot and ankle orthopedic surgeon. When you think about the numbers, we outweigh that category of people by a ton. Let’s not lose focus. Alright, disclosure information, I don’t make any money. I don’t know, what I’m going to disclose anyway? Learning objectives. Assessment. We want to isolate and identify degree of deformity. Talk about hypermobility of the first ray, metatarsus primus adductus, elevatus, functional versus structural. There’s certainly PASA, DASA. We put all these crazy initials on everything to evaluate a deformity. But I’ve always looked upon hallux abducto valgus as a deformity that develops over time. Now certainly, you could say HAV in a rheumatoid arthritic is a different animal than the typical slow insidious development of hallux abducto valgus that we see as somebody matures. We heard on one of the presentations about a hereditary component or a genetic component that moms got the bunion, my grandmother had one, my aunt’s got one, they weren’t born with that darn bunion. You’re not born with that bunion. There’s got to be an etiologic component to the development of hallux abducto valgus. Let’s try to go through a little scenario of thought that leads to development of this deformity. The underlying component is not that they were born with a bunion, they’re born with a foot type that’s led to the development of the bunion. Shoes, when I first came out 45 years ago, hallux abducto valgus, those tight shoes the women wear cause bunion deformities and hallux valgus. Well, that made no sense to me. Maybe an aggravator, if you put your foot in a pointed shoe, there’s no place for toes to go than other than in that point. Okay, that’s a problem. We’re smart. See, men are smart. We don’t develop that many bunions because we wear sensible shoes, right? But let’s look at HAV. Transverse plane, hyperpronation, you hear a lot about that, alright? We recognize a subtalar joint and a midtarsal joint have different axes of motion. They’re both pronatory, supinatory. We’re going to look at the oblique axis as it opens up, which dominates in the transverse and sagittal plane and why we lead into forefoot subluxation, which ultimately is HAV around the great toe joint. We’re going to look at oblique midtarsal function. The pull of the adductor, we’re going to relate to that somewhat. Hallux sesamoid displacement, Dr. Trepal talked about the position of sesamoids, where they seemed to sit in the interspace and why they appear in the interspace. Subtalar pronation, hypermobility of the first ray. It amazes me how many articles are written, identifying there’s no such thing as hypermobility of the first ray.
Orthopedic literatures replete with that. That’s a nonsensical component, doesn’t exist. I don’t buy that for one bit. We see too many abnormalities around the great toe joint including HAV, sub met to keratomas in more advanced stages, and we look at x-rays, and we can evaluate changes in position of a first ray. We’ll talk a little bit about that. Functional versus structural elevatus. Over time, elevatus becomes a structural deformity, whether it’s at first met cuneiform articulation with adaptive changes. Or is it a functional elevatus which is something that is potentially reversible by good orthotic management and control or controlling hyperpronation, and also the element of hallux limitus that exists. Yes, you can look at genes and say, here’s a mother and son. The mother has got HAV deformity and the son is developing HAV deformity. But what do you see happening in the midfoot, rearfoot? Hyperpronation syndrome. When we take a look at the bottom of the foot in the anatomy, we recognize very nicely that the adductor has a transverse and oblique head, inserting into the sesamoid apparatus. Mike gave a good anatomy review of what’s going into that apparatus. Well, we recognize that as the foot goes in a lateral direction with transverse plane hyperpronation, the adductor is arising from the more lateral aspect of the foot. If I transpose my forefoot laterally, the adductor is going to be pulling on the sesamoid apparatus and ultimately, into its insertion on the fibula site into the base of the proximal phalanx. It is a pulling component. Once that starts to happen, we know that the first ray is losing some of its stability. You look at that one picture with the foot in a more rectus position, look at the peroneus longus. Tremendous effect, a large tendon inserting into the first met cuneiform articulation. It’s the stabilizer of the first ray as we go from contact phase, midstance, into propulsion. In order for it to be an effective stabilizer, the lateral aspect of the foot has to be stable. The cuboid under which the peroneus longus is traversing the foot from lateral to medial has to be stable. If everything starts to shift in a lateral direction and the arch starts to compress or drop down, peroneus longus cannot stabilize the first ray. Now we enter this element of motion occurring at a time when it shouldn’t. That’s the definition of hypermobility, by the way. Somebody who has ligamentous laxity has hypermobility. But in true definition, hypermobility of the first ray is motion occurring at a time when it shouldn’t and that’s in the propulsive phase where we see complete breakdown. When you watch somebody walk and do through gait analysis, you will see a forefoot going into an abducted position. You will see the hallux abducting and being limited in some of its dorsiflexion and that’s why it also is drifted and pulled laterally, far different than the hallux limitus. Now, when you look at the foot that’s pronated on the other side with the hallux abducto valgus deformity, look where the long flexor tendon is sitting. Suppose to sit in between the sesamoids, pretty much under the crista. As the hallux starts to drift laterally, we shift the location of the flexor hallucis longus tendon and we go into this bow stringing, so to speak. We all look at the top of the foot and say, “Ah, the extensor hallucis longus may be bow strung.” Years ago, it was not uncommon to lengthen the EHL. I rarely if ever lengthen the EHL. But on the bottom of the foot, we can’t see that long flexor tendon. Now you’re going, correct an IM angle, you correct an HAV. You straighten out the deformity and you actually increase the length tension ratio on a flexor hallucis longus. It had been bow strung in short.
What happens when you go into the propulsive phase after a corrected bunion with an IM angle that was reduced and a hallux which is now straight? You wonder why we don’t get the dorsiflexion we would like postoperatively. Now if you shorten the metatarsal enough, you will release the tension on the long flexor tendon. We’re looking at a transposition, if you will, of the hallux in the lateral direction with the abnormal biomechanics associated with it. We talk about success with HAV surgery. Every one of us here feels we are talented surgeons and correct deformity. Not even a question. That is what we are trained to do and will do. We have an arsenal of armamentarium available with every type of fixation device we can imagine so when that patient leaves the OR, we have a high five and say, “We did it.” Take a picture, because six months later, a year later, when the patient says, “My toe doesn’t look so good. It’s in a bad position.” You can now tell the patient, “Well, what did you to my surgery? Look how beautiful it was when you left the OR.” But the point of fact, it’s the biomechanics that we haven’t controlled postoperatively. We need to do that. Your preoperative assessment is going to enlighten you as to how much pronation is existing, what is the environment such as elevatus, increasing it to metatarsal angle, hallux abductus position, sesamoid position. Those are your parts of your assessment that you’re doing. Just as important, in my mind is, can I control that foot if it’s hyperpronating preop, can I control that postop? If I can’t, I can pretty much guarantee, unless I do a more advanced procedure like a Lapidus there's a high incidence of recurrence of deformity. It’s pretty much our fault. Now in a patient population, adults aren’t always going to wear inserts. A women who wants to wear a nice stylish high-heeled shoe, two to three-inch heel, maybe four, there’s not an orthotic I can make that’s going to protect that foot and stop the hyperpronation. Impossible. I do rely on clinical evaluation, biomechanical examination, and radiographic interpretation. You could get more sophisticated as Dr. Kalish showed with this 3D CAT scanner for $200,000. Wow, with our levels of reimbursement, you’ll get even before you retire. Proper patient selection, important. Is the patient prepared to undergo what really needs to be done? Are they going to be compliant? How old are they? How is their bone stock? And what’s the postoperative course that they are going to follow? My success, I would like to think is, one, performance of procedure. Appropriate criteria are used. Surgical technique is good. Sometimes my residents get in the way of that. Fixation methodology and the art of surgery. We are artists, we’re sculptorists. We’re working with human tissue. We’re altering position. We’re changing bone. Bone is a living tissue. It will undergo change. It will undergo remodeling. We need to recognize that. The postoperative management, we are too in a hurry to weightbear our surgeries postop. I hear it all the time. Oh, I get my bunions up in around within a couple of days, even my Lapidus procedures, that’s why I do them. I stabilize them. I put enough metal in it. Forget it, nothing is moving and they can walk on it. Well, surgery requires healing. Fixation is only being utilized to stabilize the position you achieved until the bone heals, until the fusion occurs at the met cuneiform articulation. I’m very leery of the emphasis we put on quick surgical. I’ll get you back to work in a couple of weeks. No, it’s going to take time to remodel, heal, and then you’ll be ready. You need to be the determinant of healing. The x-rays that are taken, the serial radiography to determine that the fusion site has taken, it’s healed, you’re ready to go on, or whatever procedure you’re doing. The osteotomy has healed.
Biomechanical control in foot gear. My partner this morning or this afternoon showed this. If mechanics cause the original problem preoperatively, it will continue to subsequent problems postoperatively. Yeah, the biomechanical exam, let’s just look at this x-ray a minute. LaPorta many years ago wrote an article about transverse plane hyperpronation looking at the calcaneocuboid joint. Instead of it being parallel along the lateral side, you see the cuboid apparently abducted. Look at the long axis of the cuboid, and now look at the long axis of the proximal phalanx of the hallux, they’re parallel, because the forefoot is transposing laterally. The ball and socket talonavicular joint allows motion, peritalar subluxation in the transverse plane and the sagittal plane. We see this deformity occurring in more advanced types of hyperpronation that compensated forefoot varus, the equinus patient, the patient who might have intoed who had compensatory hyperpronation syndrome, flexible forefoot valgus. We’re looking at advanced foot types with severe hyperpronation syndrome and the x-ray speak for themselves. The hypermobility of the first ray allows the first metatarsal to start to move in a medial direction. It’s mobile. It can. As the hallux continues to drift more laterally, you get a retrograde force back in the first metatarsal pushing it out more medially. The sesamoids follow the proximal phalanx. They are firmly attached to the base of the proximal phalanx through the mechanism of the ab and adductor hallucis along with the flexor hallucis brevis, which now proceed as a member and as expansion from the sesamoids to the base of the proximal phalanx and onto the shaft of it. Wherever it’s going, they’re going. The ligaments on the side will alter or change or be stretched or contract over time. Here’s a clinical picture. Look at the abduction of the foot, look at the hallux. I can’t identify why anybody would think that hyperpronation is not associated with development of HAV deformity. There’s the elevatus component and I need to know whether it’s structural or functional. Do I need to drop it down? You heard Kalish talk about doing an osteotomy that plantar flex if you have to along with transposing or rotating the metatarsal head. I will do stress hallux dorsiflexion views to see whether the first ray that is hypermobile can be pushed back down. Is it functional limitus or is it structural limitus? If the first ray remains elevated, I’ve got to deal with that as a deformity postop or I better identify it preoperatively and alter the selection of procedure, and you could see it beautifully here. The bunion itself, I wrote an article many years ago that was in Journal of Foot and Ankle Surgery talking about the bunion and what really causes that bunion and the proliferative disease on the medial side. You saw this picture before, too. It’s nice having a partner in my practice. He does a presentation, takes most of my stuff. But that’s part of partnership, I guess. Look at the proliferative disease on the medial side. It’s actually an enthesopathy. I’ve had bone evaluated by a pathologist and says, “That is enthesopathic type of bone because of the pull.” When you do a bunion procedure, the tenacious structures on the medial side, isn’t it? That’s part of the tibial sesamoidal ligament and collateral ligament that goes from the medial side of the head to the base of the proximal phalanx. The sesamoids moving laterally, the phalanx moving laterally pull on the soft tissue structure, bone reacts, just like a heel spur. This is an enthesopathy. Now Mike Trepal talked a little bit about the rotation that we actually see in the metatarsal. When it’s hypermobile, we talk about what direction is that ray going. Well look at the crista and look at the direction the metatarsal head is sitting. When you resect the bone, we need to remove enough bone to allow a shelf to exist plantarly for the sesamoids to be repositioned. But it’s almost like, look at the crista.
You want to take that head and rotate it so that the crista is back underneath where it’s supposed to be. Austin bunionectomy doesn’t allow you to do that. It’s almost like doing what was called the DRATO procedure, where rotated the head. The adjunctive procedures you’ve heard all about, there’s no question that’s important. I do use adductor transverse in foot types that I cannot control transverse plane hyperpronation influencing the first ray. If it’s hypermobile and that patient is not so encouraged to do something like a Lapidus that might keep him nonweightbearing for eight to 12 weeks, I can close that IM angle down and maybe transpose the adductor. If I can’t control the pronation, it’s okay because now the adductor will have its effect on the first ray and keep it more inline. I do, do enter the sesamoid release in the inner space careful to avoid the vessel that Mike talked about plantarly, and I’m not going to bore you with all of that because we’re running out of time. I see I’m over and I’ll get yelled at. There is just transposition. If you wish to restore position, you do it with osteotomies at whatever level you need to use. I like Lapidus. I will tell you this, if you cannot control the pronation postop, the Lapidus procedure is giving the more lasting result because it keeps the first ray straight and we’re not going to get into the type of fixation or what you have to do. Postoperatively must think in terms of hyperpronation. In the younger patient, juvenile hallux abducto valgus do not think you can correct that deformity and then it last without doing a tendo-Achilles lengthen or your gastroc if you need it or deal with the hypermobile flatfoot, whether it’s through arthroereisis or any of the other procedures that are necessary based upon degree of deformity. The surgery does not eliminate recurrence by itself. I’m not going to keep going because I’m over already. The importance, I cannot stress enough, is pathomechanics and biomechanics is just as important in preventing recurrence in hallux abducto valgus deformity. Realize the pronation is the deforming force. Identify it, neutralize it, and by all means, use a good orthotic which the majority of which are not effective is the way we use them. That’s a whole other talk. Thank you for your time.