Harold Schoenhaus, DPM discusses the anatomy of the first ray and how its abnormal function during gait leads to the development of either hallux limitus or hallux abductovalgus. Dr Schoenhaus also discusses procedures that may be employed to correct those pathologies.
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Harold Schoenhaus has nothing to disclose.
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Male Speaker: Dr. Harold Schoenhaus is the chairman of the Superbones Conferences, he’s a co-chair of several of our other conference with us. Harold has become a good fried over the years.
He has a wealth of surgical knowledge. I remember listening to him many, many years ago and always being impressed with his knowledge about surgery and very importantly, surgical biomechanics which is something that we cannot forget.
So I always liked to listen to his experience and his message in regarding his approach to surgical problems, so we’ve asked him to come and speak on Reconstructive Surgery of the first ray.
Let’s welcome our conference chair Dr. Harold Schoenhaus.
Harold Schoenhaus: All right. I’m going to share with you some things that I’ve gleaned over 47 years of trying to understand the first ray and the implications associated with it, and certainly the pathology that we see.
So we won’t bore you with those kind of things. Learning objectives, we want to understand the anatomy of the first ray, developments of conditions such as hallux limitus, hallus abucto valgus, function of the first ray during gate and considerations for reconstruction.
I have nothing to disclose other than my wife spends all my money. What we’re trying to accomplish is isolate and identify degrees of deformity, understand hypermobility of the first ray, metatarsus primus adductus, metatarsus primus elevatus, functional versus structural elavatus, [Posa, Dosa] [0:02:00] HAV angle, evaluate pronation.
All critically important components associated with the deformity, most of which, in my mind, are associated with faulty biomechanics or the pathomechanics of what happens to this foot, from point of heel strike to toe off.
And it’s interesting to me, through the years how most of the seminars I go to and attend, speakers relate primarily to surgical intervention. Rarely do I see an association and understanding of the mechanics, or at least a thought process of how the mechanics might be influencing the deformity, and most importantly what happens after you surgically intervened.
We’re all great artists, if you will, in an operating theater, and give ourselves high fives after we accomplish a beautiful correction, and then something happens over a period of time that we watch deformity recur, and wonder why.
So when we look at motion, for example, of the great toe joint, we find that we have a significant amount of dorsiflexion available, but primarily it happens in the final stage of gate when the heel comes off the ground, and we also know we get a retrograde force from the intrinsics going to the hallux against the first metatarsal head, pushing it more proximal so that we can get the additional dorsiflexion we need.
The joint itself, the first metatarsal phalangeal joint is well encased and surrounded with a nice capsule. Tendons, dorsally and planarly, tendons somewhat medial planar and lateral planar, so we have adductor, abductor, we have sesamoid apparatus, we have ligaments on the side from the sesamoid to the side of the metatarsal head, deep trans versus ligament.
We recognize the size of the hallux and the amount of intrinsic power going to the sesamoid apparatus and then hallux, to enable us to have a propulsive phase of gait, which is extremely active. The sesamoid apparatus, keenly important in my mind in the great toe joint function. And I will talk a little bit more about the intrinsics as we go.
So these two little guys called sesamoid, separated by the [indecipherable] [0:04:50] inferior aspect to the head, have certain influences placed on them by the intrinsic musculature that’s actually inserting into them on the lateral side by the conjoined head of the adductor hallucis, along with the flexor hallucis brevis, fibula side.
And it’s interesting that as pronation occurs in the transverse plane, the hallux and the sesamoid apparatus are pulled in a lateral direction. And then there’s this motion of the first ray that we talk about called hypermobility, which allows for a change of the first ray going in the medial direction. And as time goes on, the influence of the abnormal mechanics becomes that much greater.
When we think about first ray function, during the contact phase of gait, the foot has to pronate, that’s a normal finding. When that happens, the first ray actually moves up somewhat, it’s dorsiflexing and inverting as we talk about the first ray.
But that’s not hypermobility, that’s normal function. And then as we pass into midstance and then the propulsive phase, we get a reversal of that. So the first ray is actually going to be pulled down or stabilized against the supporting surface by the peroneus longus, which is coming around the calcaneocuboid area to reversing the arch coming from low to high, pulling down the first ray, stabilizing it against the supporting surface.
When anything interferes with the normal transition of contact phase pronation and it extends into midstance and propulsive phase pronation, that’s where we lose stability of the first ray. And all hell breaks loose.
So what is the first ray by the way? It’s obviously the first metatarsal and the medial cuneiform, the hallux is not part of the first ray. When we talk about elevatus, you take a lateral X-ray, weak bearing, you look at the long axis of the cortex of the first metatarsal as you go from proximal to distal and there’s the second metatarsal going from proximal to distal. And when you see the first metatarsal or first ray seemingly elevated and not parallel, there’s a potential of what we refer to as elevatus.
Now, this could simply be an X-ray finding and have nothing to do what happens in the propulsive phase of gait. So when I see the potential of elevatus, I like to take what I refer to as a stress lateral hallux dorsiflexion view. And then look at the position of the first ray. Is the first ray able to be brought back to the position that it is parallel to the second and actually a little posterior to allow for dorsiflexion of the hallux?
Or does it stay elevated and when it does it has to jam the great toe joint?
So if I’m going to surgically intervene to correct for hallux limitus rigidus, I have to take into account structural elevatus, not functional. Functional is related to the hypermobility component. If I can control a hyperpronation into the propulsive phase, I should be able to reduce that elevated position of the first ray.
Obviously, as time goes on, we developed changes in the great toe joint. Now other than trauma to the great toe joint, elevation of the first ray, associated with hyperpronation syndrome leaves the jamming of the great toe joint. And when you lose the ability of curvilinear motion, we’re going to get a compressive force at the joint level, leading to narrowing and thinning of the cartilage, squaring at a metatarsal head, and now we’ve got the adaptive changes that we see happening, leading to hallux limitus first, and then a form of hallux rigidus.
Now, when we’re looking at goals of surgery, because surgery is what I love to do, because I don’t think orthotics are going to make a big difference, or steroid injections or anti-inflammatories, when we move toward what I refer to as more end stage arthritic change, surgical intervention is going to be a consideration.
So what are my goals? One alleviate pain, two, improve the range of motion, three, improve quality in motion, and four, reduce to deformity.
I have been a proponent of great toe joint implantation for my whole career. I always believe that motion is life. If I can avoid fusion, I want to do it. Now, in the process of thinking about doing implantation of the great toe joint, materials become important, and your surgical approach is more important than a material selection.
Now on occasion, if I have used a material like, silicon and put that in the bone, it creates disastrous effect. The bone does not like silicon, so you use the fuse grommets to try to avoid irritation and granuloma does change within the synovial limited joint, the inflammatory process. I have really moved away from silicon for many, many years but I do like hemi-implantation.
In hallux limitus rigidus, one, we need to decompress the joint, deflector mechanism, those tendons I talked about early on, have not move, have not dorsiflex, have not extended for a number of years. So, the muscle belly has contracted, the length is no longer there. I need to decompress the joint. I never like decompressing on the head side because you affect the sesamoid apparatus, and the weight bearing capability, going to the second and third metatarsal heads, where you’ll develop a lesser metatarsalgia. So the best place in my hands, in my mind, to decompress the joint is at the base of proximal phalanx.
That being said, one has to be extremely careful of the resection of the amount of bone, because I don’t want to violate the plantar intrinsics. I’m resecting enough bone, and I only cut through the dorsal surface of the bone, down to the plantar cortex, and then take an ostial tone and break it.
Do not remove the intrinsics from the base. If you remove the intrinsics from the base, you will end up with apropos of hallux, or cock-up hallux, and trying to sew the intrinsics back to the base, in my mind, is not very effective. So here’s the amount that I usually resect. The disease, as people will tell you, is often on the head primarily.
The other element in hallux limitus rigidus is the sesamoid apparatus. These guys have not moved with hallux limitus rigidus for years. You have a sesamoid disease that has occurred. If you think you’re going to get dorsiflexion of the toe when the sesamoids are still attached to the head inferiorly, you’re going to be misled. So I do separate those if they are involved, and I do a radical resection on the head, which I actually, I’m going to resurface the head, where significant disease is present.
So, when I’m done resecting, I remove the portion of bone from the base of the proximal phalanx and prepare for an implant. I remove the sesamoid, sesamoid disease if you will with the McGlamry elevators, break them up, free them up, I have no removed the cartilage and subchondural plate from the metatarsal.
So you’re looking at spongy bone. Why? Because through that, you have mesenchymal stem cells that you can put to work. So now with that being left, what I have done is actually resurfaced the metatarsal head by using acelluar dermis, and that membrane not only goes over the head, but underneath the sesamoid apparatus.
So between the sesamoid and the metatarsal head, I now have a sheet of acellular dermis, and it’s just the technique that I use, I won’t bore you on how to do that, here it is elevated, we wrap around the head. I tie it rather tight and secure, cut off excess, here’s my hemi implant in place, I have removed enough diseased bone and cartilage, but not so much to create a significant problem of weight bearing transfer. With the sesamoids now protected plantarly, the head glides beautifully along with the base of the proximal phalanx.
This is the most shocking thing that I have seen, probably in my career, other than some of the train wrecks I have created with patients. But here’s one of my early cases. This is about seven years ago. I did the entire resurfacing, remodeling. She called me up and said, “I have a bump on the top of my foot, I want you to take it off. It’s by the big probably the big toe joint.” I said, “Okay, I will do that, but I want to go into the joint and see what we find,” because it’s been a number of years since I did the resurfacing, and that’s what we found.
So I opened the joint and take a look with what you have, cartilage on the head. If you come back here, you’ll still see suture from where I used the acelluar dermis that wrapped around the entire head. You got a differentiation right into the acelluar dermis from the mesenchymal stem cells, and then we have a joint that has cartilage, which has a nice surface to it, a nice spherical shape, and there’s the hemi implant in place.
So that is the approach that I use for resurfacing of the head along with base procedure.
Now let’s go to a little bit more of a difficult case, which is hallux abducto valgus, far more involved. Transverse plane hyperpronation, oblique midtarsal function, the adductor pull, hallux sesamoid displacement, subtalar pronation, hypermobility elevatus, and limitation emotion in the propulsive phase.
Interestingly, you don’t get as much degenerative disease of the sesamoid apparatus relative to the head. You may get some deformation and change in shape, but you don’t fuse, like you see, in end stage hallux rigidus.
Now hereditary change or effect is definitely a factor in HAV deformity, you’re not born with a bunion, but a mother who has a bunion and a son or a daughter has a bunion, or develops one over time, one has to think there’s got to be an association, and what is consistent, is the presence of hyperpronation.
And when you look at a skeleton or anatomy specimen showing you the patient with HAV versus a rectus foot, you see how the anatomy has changed dramatically. Look where the flexor tendon is, it goes with the sesamoid apparatus, it sits right between the two sesamoids, it now has a bowstringing effect holding the hallux lateral and encouraging deformity, as opposed to a straight position. Here’s the peroneus longus coming down to the first ray, and look where the flexor should be, directly straight.
So if you do HAV correction and straighten out this toe, what’s going to happen to the bowstring, you’ll get a flexor hallucis longus. You’re increasing the tension on it, unless you did something concomitantly to decompress the joint, or osteotomy of the metatarsal might be helpful, such as an Austin or a closing base wedge or a lapidus. But we never see the inferior part.
The only thing we do inferiorly is actually come into the interspace and do a dissection to release the transverse and the oblique head of the adductor pulling on the sesamoid along with the lateral head of the flexor hallucis brevis. This is not simple surgery. And yet it’s one of the most common procedures we all do on a regular basis.
So when I look at successive HAV, it’s A, the performance of this procedure. So obviously, you’ve been trained technically to do it well. Appropriate criteria, surgical technique, fixation methodology, and what I call the art of surgery. We are artists.
Post-operative management, you can fight this from today until tomorrow, weight bearing, non-weight-bearing. How fast should you weight bear something?
If you’re breaking bone, bone needs to heal. Give it the appropriate time. I’ve never been an advocate of doing a lapidus and putting six screws and three plates and whatever else so that patient can walk on it. No, if you need that kind of surgical approach and procedure, give me the time so that it ultimately will heal the way I need it to heal. And then your hardware is doing nothing anyway at that point.
Biomechanical control, I think that’s important. It was the cause, in my mind, to begin with. If it’s the cause to begin with, what are you doing about it post-operatively?
And selection of footgear. This is a phrase I coined a while ago, stating if mechanics cause the original problem pre-operatively, it will continue to cause subsequent problems post-operatively. All you’re doing is repairing deformity and realigning things. Like the air in your tire, you fill it up, everything is good. When the air goes down, the tire is uneven. Same thing is happening here, the ideology, the leak in the tire, the hyperpronation. So biomechanical exams are important.
Look at the transverse plane effect. Here’s a youngster which is hyperpronating significantly. The transverse plane, the TN joint is showing that. Here’s the cuboid because the forefoot goes in a lateral direction. It pulls the hallux and the sesamoid apparatus. And the hypermobility, the first ray over time, is going to enable it to move over.
The transverse plane, dominant motion coming out of the midtarsal joint, which is a difficult joint to control with standard types of orthotics, by the way. And we could just look at the parallelism of a hallux and the lateral aspect of the foot to easily identify the transverse dominant effect on the great toe. And of course, the elevatus component, as I stated before.
So the bunion itself, by the way, associated with the hyperpronation, sesamoid displacement, bone production, increased IM angle, and hypermobility to the ray. So if I look at the head of the metatarsal straight on, here’s my nice sesamoid grooves on the inferior aspect to the head, here’s the bunion. Never cut straight down into here because you’ll be right in the groove.
So I always make an angular cut.
And then the other thing I want you to see is some of this rotational component, which I think, Dr. Richie, I’m going to leave to discuss some of that for you in the next talk.
Adjunctive procedures. I can do any osteotomy and break bones and use all these fancy plates and screws, but you’re going to make a determination of whether you’re going to take out a fibular sesamoid, which I will tell you, I rarely if ever do.
Extensor brevis tenotomy, I don’t do that very often. Extensor hallucis longus lengthening, rarely, if ever do that. Capsulorrhaphies, yes. Adductor transfers, yes.
Adductor transfer could be a powerful procedure. If the forefoot’s moving laterally, and I can’t control the hyperpronation, take the adductor, which is arising from the lateral part of the foot, and reinsert it into the first metatarsal head. Now it pulls the first metatarsal and keeps it in a straight aligned position.
So soft tissue releases, all these stuff. There’s controversy as to whether you should do these in the interspace, I do it. I release that fibular sesamoid, I do a fibular capsulotomy. I want that joint to be loose as a goose as long as there’s no degenerative of changes.
And here we are just transposing the adductor. I do like Austin bunionectomy, so I think it’s the best place of the bone to heal. I don’t care what your fixation is, it’s going to heal beautifully. I usually like to use two screws. Realign the metatarsal relative to the sesamoid, close down your angle.
I don’t do a lot of capsular correction, of resection, Washington Monument, YUL. I don’t know about doing that crap.
I do what I call a tension capsulorrhaphy. I pull the capsule immediately when the toe is over in correct alignment, and then I sew it.
So my goals of bunion surgery are relocate the first metatarsal, establish link ratios, weight-bearing status is important, soft tissue imbalance.
Lapidus has become very important today. I don't know why everybody loves lapidus, why we’re going to stop the hyperpronation of the first ray. We’re going to control it, so that we get a significant reduction in the potential of deformity, that it can recur. And of course, there’s a million different plates and screws now, and other procedures like lapiplasty and beaming of the first ray so that we get adequate correction.
It’s a simple enough procedure to do as long as you understand the mechanics of that joint complex. I’m not going to spend a lot of time on that. The purpose of the lapidus is to lock the first metatarsal to the medial cuneiform. Is that enough?
Other things that I consider, arthrodesis, Evans, Koutsogiannis, Cotton, TAL, gastrocs. I’m always thinking in terms of the mechanics of the foot concomitant to what I’m doing surgically.
And here we have a lapidus procedure with a sinus tarsi plug. You have to stop the hyperpronation. Also, recognized you can have hypermobility of the first ray between metatarsals 1 and 2, and metatarsal 1 with the cuneiform. Just locking first met to first cuneiform does not guarantee a straight correction for years to come.
If hypermobility of that ray exists between 1 and 2, you better put a transfer screw across there and lock that joint as well.
So I’m very aggressive. Here’s a transfer screw, I don’t care what other fixation you’re using. We like to consider that we’re doing triplanar control, which Doug Richie is going to talk about. It’s trans-positional, rotational planar flexary.
Unfortunately, complications can arise. I rarely have any. I always blame it on the patient or my resident. But to conclude, understanding the anatomy of the first ray and its impact on function will allow the surgeon to properly assess the patient preoperatively and determine the appropriate procedures for restoration of long-term function.
We are the best in what we do. And what separates us from any other profession doing foot and ankle surgery is the knowledge of biomechanics, gait, and how that foot’s going to function post-operatively.
I thank you for your time.
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