Section: CME Category: Surgery

First Metatarsophalangeal Joint Arthrodesis

Michael Troiano, DPM

Michael Troiano, DPM discusses the etiologies that can lead to hallux limitus and hallux rigidus, reviews surgical techniques and pearls as well as possible complications involved with performing a first metatarsophalangeal joint arthrodesis

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Goals and Objectives
  1. Review the etiologies that lead to hallux limitus and hallux rigidus
  2. Review surgical techniques and pearls for performing a first metatarsophalangeal joint arthrodesis
  3. Review complications associated with performing a first metatarsophalangeal joint arthrodesis
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  • CPME (Credits: 0.5)

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    Release Date: 03/16/2018 Expiration Date: 12/31/2020

  • Author
  • Michael Troiano, DPM

    Center for Foot and Ankle Disorders
    University of Pennsylvania - Penn Wound Care
    Adjunct Clinical Professor, TUSPM
    Philadelphia, PA

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    Michael Troiano has disclosed that he is a consultant for Stryker and Smith and Nephew.

  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Troiano: Welcome to the end. It’s over. This is a painful lecture, because it's really, really long. And there's a lot of words, and the reason being is the first MPJ is a very, very difficult joint to understand. There's a lot going on biomechanically and pathomechanically [Indecipherable] [0:00:22] this fusion. So those of us that are residents in the room, take this and review it before you take your Boards or what have you, because there's a lot of principles that are important. Like the difference between hallux limitus and hallux rigidus.

    Obviously, hallux limitus rigidus is an interchangeable term, in that limitus turns into rigidus as time goes on. Most importantly, characterized by inadequate sagittal motion, hallux limitus is the precursor to hallux rigidus. The primary factor that differentiates the two is actually the sesamoids. So sesamoids and hallux rigidus actually hypertrophies and ankylose [phonetic] [0:01:06] themselves to the plantar surface of the first metatarsal. That's the primary difference, and when you look at an x-ray, you can actually identify the difference between limitus and rigidus based on hypertrophy or size of the sesamoids. And if you have access to a C-Arm in your office or even preoperatively, you'll see the sesamoids easily move in hallux limitus and not so much in the rigidus.

    Lapidus described a paralytic deformity or congenital clubfoot to help that type of deformity. As to why hallux limitus and rigidus develops, we're going to get into some of that route. Identify the long first metatarsal hypermobility, met primus elevatus, DJD, trauma. And of course, osteochondritis dissecans or early arthritic process, from dropping a can of soup or what have you, on the toe obviously will lead to hallux limitus rigidus.


    We’re always taught in school that 65 degrees of first MPJ motion is necessary for normal gait; however, Hetherington did a study identifying that even in a normal joint, most of us in everyday walking only use about 31 degrees when we weight-bear. And therefore, some of this may be kind of a learned pathology, such that, if we're not concentrating heel-to-toe walking, which our patients obviously are not, right from not using the joint properly or to the maximum 65 degrees, the train kind of goes down the track, such that the joint models itself to not articulate dorsally.

    Clinical examination of hallux limitus rigidus; you want to do a weightbearing stance and actual gait. Assess the first MPJ independent of the IPJ. So when you grab the toe at this point here and start to dorsiflex, it really makes it look like you have a lot more dorsiflexion than you do, because of the IPJ. So instead, the toe should be grabbed closer to the first MPJ when you're assessing. And stance of the hallux, may be plantarflex relative to the first metatarsal and what that does, it pushes the first metatarsal dorsally accentuating the dorsal bunion. In gait, the point of ground contact maybe the IPJ which hyperextends to accommodate propulsion.

    So here comes the pathomechanics, what causes the hallux limitus and rigidus. Hypermobility of the first ray, repetitive trauma of the FHB, to stabilize the medial column, adaptive changes occur within the joint, and arthrosis result from the repetitive impingement. First ray length abnormalities; you can get hallux limitus rigidus from a long first metatarsal leading to excessive loading of the joint and eventual adaptive or degenerative changes. Short first metatarsal, obviously, you may experience lesser metatarsalgia gripping the ground with a hallux in attempt to reduce the symptoms in lateral forefoot. So basically, the first ray, when short, grabs the ground and creates the joint anomaly. This can lead to a hyperactive FHB and, of course, adaptive contracture then begins.


    Uncompensated varus deformities; especially in the rear foot, first metatarsal is going to grab the ground and force it downward. Varus deformities can occur at any level. Sagittal plane elevation prevents the middle column from bearing full weight, and compensation occurs within the first MPJ through plantar flexion of the proximal phalanx and the first metatarsal. Over time, the first metatarsophalangeal joint becomes fixed in equinus and that fixed equinus leads to ongoing accommodation of the joint. So realistically the suspects which will cause hallux limitus rigidus are forefoot varus or rear foot varus, residual clubfoot to form a metatarsal coalition, and a malposition fusion.

    We can cause this with inappropriate or unsuccessful bunion surgery, malunion, leading to met primus elevatus, first metatarsal elevation, infection, AVN, connective tissue disorders; all can lead to hallux limitus rigidus. Arthrosis and trauma. Gout obviously, psoriatic arthritis, rheumatoid arthritis. Very hard to fuse the first MPJ with psoriatic or rheumatoid arthritis, without taking these patients off of their salt preps or they’re sterilely prepped first which they oftentimes will not do.

    Osteochondritis dissecans obviously is the process whereby injury has been present and occur sometimes years before, so it’s very difficult to discern or delineate what trauma leads to the first MPJ arthritis.


    Traumatic defects in the articular cartilage of the first metatarsal again can be as far back as kicking the soccer ball as a little boy which can lead to the osteochondritis dissecans, oftentimes not seen on an MRI. So, you know, you’ll order the MRI looking for an osteochondral defect and not see it. And obviously MRIs are taken in five-millimeter cuts. So, it's very possible that joints just skipped over in toto.

    Lapidus, again, described weakness of the peroneals with a strong TA and FHL causing the varus position of the foot as it pertains to the ground, inability of the medial column to contact the ground. Weak dorsiflexors of the foot with strong plantar flexors and, of course, calcaneus deformities with active plantar flexion on the hallux will lead to what Lapidus described. Hence the reason to do a metatarsocuneiform joint fusion with plantar flexion with that first metatarsocuneiform joint fusion, making the peroneus longus again competent.

    Flexor hallucis longus recruitment in weightbearing propulsion locks the IPJ against the ground. The problem here is the IPJ, once locked against the ground, cause retrograde elevation of force to the first metatarsophalangeal joint which can cause a large portion of degeneration.

    The plantar structures can lead to arthrosis. Plantar fascia via the windlass mechanism; dorsiflexion of digits creates tension on the plantar fascia, aids in resupination of the rear foot during propulsion and loading of the MPJ’s secondary contraction of the plantar fascia occurs in hallux limitus and rigidus. The FHB obviously inserts into the sesamoid apparatus and is an important stabilizer of the first MPJ and then contracture compounds the degenerative process with first MPJ by not allowing the joint to dorsiflex.


    Sesamoid degeneration immobility occurs primarily through the FHB which prevents gliding in the metatarsal head and then the normal gliding mechanism of the plantar structures actually becomes more of a hinge-type phenomenon. When the hinge-type phenomenon begins, the sesamoids actually will jar that joint plantar flexed position and will contribute to ongoing hallux limitus rigidus.

    Etiology; cyclical events proposed by Watson-Jones, and then verified by Jack; spasm of the short flexors lead to a secondary contracture of the plantar structures which leads to subsequent osteoarthritis. All of these are articles that hopefully you’ll put into your [Indecipherable] [0:08:49] as you go through your residency and finish your Boards.

    Micro versus macro trauma. Obviously macro trauma, stubbing injuries speak for themselves. But micro trauma, repetitive dorsal impingement eroding the articular surface. So this is the female wearing high heels. This is the dancer. This is the toe walker. This is the soccer player. So repetitive micro trauma can certainly lead as well. That’s how all of us feel.

    Radiologic examination, joint space narrowing, osteophytic lipping, subchondral bone cystic changes with sclerosis. Obviously, this is grade II/III hallux limitus, which we're going to get into grading in a second but you'll start to see the lipping develop and major hypertrophy in the sesamoids here.

    The best hallux rigidus classification system is the general osteoarthritis classification system. So small osteophytes in grade I; grade II, definite osteophytes; and then grade III, extensive loss of joint space with sclerosis and subchondral bone.


    There are two classification systems that you should know for your Boards, the Regnauld and the Hanft [phonetic]. Regnauld is by far the most common. We're not going to get into each except for grade I is more of a simple hallux limitus whereas grade III is more of a hallux rigidus.

    Measuring the met primus elevatus on radiographs; you have to measure the angular divergence of the dorsal cortical surfaces of the first and second metatarsus. Sieberg and Jack [phonetic] [0:10:34] 1994 showed the exact measurement. It's a landmark article that we should all read. If the distal number is greater than the proximal one, then a true elevation is present. So we can actually measure radiographically and see how much plantar flexion needs to be performed by Lapidus procedure, or plantarflexory osteotomy. Hopefully avoiding fusion down the line. [OFF MIC]

    Fusion position should be 25 to 30 degrees dorsiflexed on the first metatarsal, not at the MPJ, but the first metatarsal. So that translates to about 10 to 15 degrees dorsiflexed to the ground. So we want to find a functional position which is 10 to 15 degrees dorsiflexed to the ground. Most plates that we use now have this dorsiflexion built into them. Screws or K wires can be a little tricky. What you don't want to do with the fusion is fuse it perfectly parallel to the weightbearing surface, because a person will inevitably begin to toe-off through the IPJ and create the same problem at the IPJ which can actually be even more painful than hallux limitus rigidus to begin with. You want to fuse into 10 to 15 degrees of a valgus position, reason being is obviously we're going to twist off when we walk into a valgus position.


    Flat foot will need less of valgus position because they're valgus to begin with, and the cavus foot will actually need more reduction of the IM angle, what will occur proportional to preoperative findings. So we can actually correct a bunion with the first MPJ fusion as well, just by positioning the joint where we want it. The bunion would reduce over time as the soft tissues begin to stabilize at the metatarsocuneiform joint.

    Any way you wish to prepare the joint, it’s up to you. Whatever you're more comfortable with, you can cut it and you can curate it. And Cup & Cone reamers obviously are pretty fantastic as well. So long as you understand that the position that you ream the joint in, is ultimately the position that you have to fix it. So in other words, if you ream this whole joint, and then put the proximal phalanx onto the joint, and you've pushed a little bit more dorsal, that toe is going to take a more dorsal position. So the reaming should be actually head-on axial to each one, then you have a nice ball and cup to put the joint exactly where you want and fuse it into position.

    This is Wright Medicals plate. It has a slide here, compression slot for a trick screw which we're going to get into. One of the ones that I favor to use for fusion. Someone obviously with a congenital hallux varus, this person had, I believe polio and obviously very painful. Can't wear any shoe here whatsoever. So first thing we're going to do is our capsular tendon balancing by lengthening the EHL. If you don't lengthen the EHL in this case, it's going to be impossible to tell what position of fusion you should be in. So in other words, if we look back here, how much of this is actual soft tissue and how much of this is actual joint accommodating, the only way you know is if you release the soft tissue. So the first thing we're going to do is in a roundabout way, release all the medial structures, and then assess the joint at that point.


    So once we've released the soft tissue structures, we see where the hallux actually wants to articulate on the first MPJ. And obviously, it's not as bad dislocated as it was; therefore, our soft tissues were contributing a fair amount to that varus component. In this case, I use the saw just to kind of ream the joint across. So in other words, I feathered the cartilage off of the joint, and put the joint end-to-end at this point. So now we're going to provisionally fixate with a K-wire from both sides and verify our position. This is actually the K-wire cover to dorsiflex the toe a little bit to the ground, again at about a 15-degree level. Our end product, with a K-wire; one of the K-wires I threw a screw across in that plate into position. And you can see your pre- and post-op results. So preop here, postop with the x-rays.

    And again, a nice end-to-end covering with that trick screw that we saw. The idea being that we locked the proximal phalanx screws, we offset this screw, and as this screw bites, it will actually pull the whole construct towards us locking the position into place and then one screw just through the joint for some insurance.

    This is a cross plate. This is actually by Stryker. It's a lag plate very similar to the one that I showed for the Lapidus procedure, but basically going from stable to unstable pulling the proximal phalanx north into the first metatarsal. Again, we're going to ream a hole here, across the joint. And then our trick screw was put in via this little mechanism as targeting guide. So you can see it's a nice stable construct where you grab the proximal phalanx. Cross plate is the way to do this, grabbing again and pulling the proximal phalanx into position.


    This is failed implant. You know, I will tell you that the vast majority of hallux limitus surgery and hallux rigidus surgery I do, is not fusion. Most of them are LPT joint replacements from Wright Medical to replace the proximal phalanx. I don't do a ton of these first MPJ replacements. Reason being is the snowplow down or recess down the metatarsal, and you're left with the same problem you had except for now there's a metal piece in there with a ton of loosening. So I don't like the metatarsal replacement heads, as I don't think the success rate is great. I'd much rather replace the base of the proximal phalanx before fusion. So in a case like this, the implant has to come out. And we have to go past the recessed bone caused by the ortho-biologic failure of the implant. So we're going from the farthest points possible to make this as stable as possible.

    Again, in some cases, when the joint is accommodated, if we replace this joint, realistically, it's still going to function bullying the second toe out of position. So fusion in an in situ position, it’s probably the best, just to get rid of pain whatsoever.

    Complications; nonunion, malunion, elevation, infection, hardware failure, positional error, nail bed irritation and trauma. If you spend a second here, this is important. If you dorsiflex the toe too much, when this person walks, they're not going to be able to wear any shoes, because the toe is constantly banging at the nail level against the underside of the shoe. It can be very, very painful and unsuccessful outcome. So you look at it yourself on the table and everything looks fantastic, but this person can't walk or wear shoes.


    So this is something that if they start to get nail bed trauma, and you try to have them cut their toenail a little shorter, or wear looser shoes, nice shoes or what have you, this is actually a reason to redo the fusion right from the beginning, and relatively successfully. You can go right to the core and just take a plantar-based wedge to get the toe down a little bit. Limited IPJ motion, recognize that you're going to cause arthritis 10 out of 10 cases to that IPJ. So if the person does not have limited IPJ motion to begin with, it's going to get even worse once that becomes their new functional MPJ. So it can be very, very painful. This is the case where you want to use those carbon inserts that we were showing earlier today to stop this person from having to toe-off and said the rigidity of the carbon insert will take position.

    [OFF MIC]

    Thank you very much. We're done.


    TAPE ENDS [0:19:07]