Most of the surgical corrections discussed today require subtle deformities without arthrosis. Chronic mallet deformity involves DIP flexion due to an injury to the terminal extensor tendon. Non-operative treatment includes DIP extension splinting. There are a variety of operative treatments that we will go through. Of note, central slip tenotomy and spiral oblique retinacular ligament reconstruction will be discussed in the swan neck section. Patel et al showed in their study that even chronic mallets can be treated with extension splinting. In their study, mallet fingers that presented four to 18 weeks after injury had a successful outcome with DIP extension splinting. Their protocol was 10 weeks of continuous splinting followed by two weeks of night splinting. Their end extensor lag was five degrees and they had no loss of flexion of the DIP joint. Garbaman et al found a similar result with their protocol including seven weeks of splinting and their end extensor lag was 10 degrees. Lind et al advocated for their abbreviato procedure. Their series included 40 patients with nearly 50 months of follow-up. The chronicity of the injury ranged from five to 75 weeks. The average preoperative extensor lag was 38.2 degrees. The surgical procedure included DIP joint pinning and slight hyperextension for six weeks. An S-shaped incision was placed over the DIP joint and the extensor tendon was transected and then sutured with 4-0 silk. Despite the word abbreviato meaning to shorten, they did not tighten, overlap, or shorten the extensor tendon. They felt that natural scar formation would tighten the tendon. 60% of patients ended with an extensor lag of less than 20 degrees and loss of flexion of less than 30 degrees. The remaining 40% of patients though had a suboptimal outcome either due to an extensor lag or lack of flexion. Aislinn et al recommended tenodermadesis. They indicated this for deformities that were at least 12 weeks old and had passive extension on exam. The technique involved a transverse elliptical excision of skin and tendon and then suturing the skin, tendon, and dorsal capsule as one unit. The original article did not include joint pinning but others have advocated for protection with a transarticular pin. Instead, Aislinn et al splinted an extension for 35 days followed by 15 days of night splinting. Out of their series of 26 patients, 22 had satisfactory results with an average range of motion of 10 to 60 degrees. There are varying techniques for reconstruction of chronic mallet fingers. Gu et al described mallet reconstruction with palmaris longus graft. It was anchored into the distal phalanx at the terminal tendon insertion through a 1.5 millimeter drill hole and it was tied on the palmar aspect. The graft itself is sutured to the extensor tendon with PDS sutures. The joint was splinted in extension for four weeks and with the average followup of 12 months, 66 patients had less than 10 degrees of a residual extensor lag. Suzuki et al described an alternative technique with palmaris longus graft and their technique, palmaris graft was folded into a V and anchored at the terminal tendon. Then it was reinforced with sutures in a suture anchor. The radial and ulnar limbs of the graft were routed under the transverse retinacular ligament and sutured to the lateral bands. The DIP joint was pinned in extension for four weeks and then subsequently intermittently splitted for another 12 to 16 weeks. This in theory provides a more anatomic reconstruction. However, the reported result is a singular case and does not include a series of cases. Wang et al described using ECRB tendon bone graft for reconstruction. Through a dorsal incision over the DIP joint, a bone trough was made at the terminal tendon insertion. ECRB was harvested at the base of the third metacarpal. The DIP joint was then pinned in hyperextension and the graft was secured with suture. The tendinous portion of the graft was overlapped by the residual terminal tendon by one to one and a half centimeters. Postoperatively, the finger was splinted in extension, I'm sorry, in intrinsic plus for four weeks, at which time the K wire was then removed. Motion was held until x-rays showed bony healing. In their series of 28 patients, 24 had an end extensor lag of 10 degrees and four had a 20, I'm sorry, 10 to 25 degree lag. As a criticism though of this series, the time from injury to surgery was short at only 74 days and patients may have actually responded to non-operative treatment with extension splinting. Treatment of chronic mallet fingers that is not passively correctable or with degenerative changes or in patients who would exchange lack of motion for correction of the deformity is with arthrodesis. High union rates are reported with a variety of techniques including K wires, intraosseous widers, headed and headless compression screws. My preference is for a small caliber headless compression screw that can fit in even very narrow distal phalangeal canals. Swan neck deformity involves DIP flexion and PIP hyperextension. There are a variety of ideologies including extrinsic, intrinsic, and articular. But the commonality to the pathoanatomy is tendon imbalance with the extension force being larger than the flexion force at the PIP joint. The lateral band sublux dorsally to act as an extension force at the PIP joint. There is also contributory volar plate laxity. Swan neck deformity is often seen in the setting of chronic mallet deformity. Figure of eight splints can be used in supple swan neck deformities. However, there is limited data in using them in the non-rheumatoid patient. In the rheumatoid setting, it has been shown to improve dexterity. However, there is not improvement in strength or in pain. There are a variety of options including metal ring splints, prefabricated splints, and custom thermoplastic splints. Battler central slip stenotomy is one surgical option for the treatment of not only swan neck, but also mallet fingers. The idea behind this is that by dividing the central slip, the extensor mechanism migrates proximally, decreasing the extension force on the PIP joint and increasing the extension force on the DIP joint. The original description of the technique involves a mid-lateral incision, division of the transverse retinacular ligament, elevation of the extensor mechanism to allow for stenotomy of only the central slip. Post-operative regimens vary. However, the early description by Bauer included splinting the PIP inflection and the DIP in neutral for two weeks at which time active motion was begun. Bauer et al. reported an improvement in average extensor lag of the DIP joint from 57 to two degrees in five patients. They did note a 10 to 15 degree extensor lag post-operatively in the PIP joint. Rumberg et al. did their stenotomy from a dorsal approach and their post-operative regimen was to allow for immediate active motion. They had less improvement in the extensor lag of the DIP joint from only 37 to nine degrees. The PIP joint had correction of 10 degrees of hyperextension to two degrees of an extensor lag. Chao et al. showed in an anatomic study of 15 fingers that this procedure typically yields an average correction of 36 degrees of DIP extensor lag. Swan neck deformity due to injury causing PIP laxity may be improved with FDS tenodesis. Prior to proceeding with this, it is important to assess DIP extension lag with a distal bouvier type maneuver. If by blocking PIP hyperextension, the DIP extensor lag corrects, then this may be the appropriate procedure. If it does not, then another option should be considered as this procedure will not correct a DIP extensor lag. The technique involves a slip of FDS to secure the PIP joint in about 20 to 30 degrees of flexion. This can be achieved with the FDS slip anchored to bone at the proximal phalanx or metacarpal neck or with a slip looped around the A1 or the A2 pulley. The joint is splinted in slight flexion for six weeks with motion within the confines of the splint beginning around two weeks. Catalano et al. published a series of 12 patients but only three in their series actually had a swan neck deformity. The average PIP hyperextension of 31 degrees corrected to 12 degrees of a flexion contracture. Tonkin et al. described lateral band translocation for swan neck deformity. The technique involves a mid-axial radial incision. The radial lateral band is isolated from the central extensor mechanism dorsally and the transverse retinocular ligament volarly. The accessory collateral ligament is divided from the palmar plate. The A3 pulley is divided to expose the radial slip of FDS. The radial lateral band is mobilized volarly and then held in place by a sling created by suturing that radial slip of FDS and the palmar plate. If DIP extension lag remains, then the DIP joint is either pinned in extension for four weeks or it's fused. In their series of 30 fingers with 42-week follow-up, PIP hyperextension of 16 degrees was corrected to a flexion contracture of 11 degrees. Thompson et al. described reconstruction of the oblique retinocular ligament with a spiraled-free tendon graft as their solution to correct mallet and swan neck deformity. Their technique involved harvest of either palmaris longus or plantaris. This was then anchored just distal to the terminal extensor tendon through a bone tunnel with either a button or metal clips over the finger pad to secure this. The tendon graft was then passed subcutaneously over the middle phalanx toward the radial aspect of the PIP joint. Then it's passed volar to the PIP joint, specifically superficial to the flexor tendon and deep to the neurovascular bundles. It was then passed ulnar to radial through a transverse bone tunnel in the proximal phalanx. The graft is anchored on the outside of the radial skin over a button or with metal clips. The DIP joint is pinned transarticulately, but that's only if it's a very long-standing deformity. Postoperatively, an intrinsic plus splint was placed and active motion was begun at three weeks. In their series of 10 patients, for the cases with hyperextension at the PIP joint, hyperextension was improved from 20 to 40 degrees to zero to 15 degrees. And the DIP flexion deformity was improved from 20 to 90 degrees to zero to 15 degrees. Kanaya et al. had a similar technique and they had similar results with their seven patients. Kleinman et al. modified this technique. The course of the palmaris graft around the finger was the same. Differences, though, included a more extensile incision along the entire course of the graft. They also routinely pinned the DIP joint in neutral and the PIP joint in 10 to 15 degrees of flexion. They did not use any bone tunnels, but instead used pull-out sutures or pull-out wires for distal fixation. And then proximately, they sutured the graft at the fibro-osseous rim. K-wires were sequentially removed. In their series of 12 patients, compared to Thompson's approach, they had more flexion contractures of the PIP joint and hyperextension deformities at the DIP joint. Durand et al. recently published on a new technique for spiral oblique retinacular ligament reconstruction using only half of FDP. Proximal to the A1 pulley, half of FDP is harvested. This is brought out of the sheath distally. It is then routed dorsally through an oblique bone tunnel that is distal to the FDP insertion and at the terminal tendon insertion. Then it is routed dorsal to volar, deep to the neurovascular bundle. It is then inserted back into the flexure sheath between the A4 and the A3 pulley. It is then retrieved through a window in the mid-substance of the A2 pulley. Then it is sewn to itself in the adjacent fibro-osseous rim with tension set with the DIP joint in neutral and the PIP joint in 20 to 40 degrees of flexion. A dorsal splint is placed with the finger in this position for four weeks. While their series only included three patients, they had complete correction of DIP joint flexion and PIP joint hyperextension deformity. There was also no loss in DIP flexion. Boudinier deformity involves DIP hyperextension and PIP flexion. The pathoanatomy includes an injury to the central slip and triangular ligament, allowing volar subluxation of the lateral bands. Non-operative treatment of Boudinier deformity involves splinting the PIP joint in extension. If seen acutely, this typically involves six weeks of static full-time splinting followed by a course of night splinting. If seen on a more chronic basis without initial full passive PIP joint motion, that initial treatment involves serial casting or dynamic splinting to achieve full passive PIP joint extension. Then the PIP joint is statically splinted for another six to 12 weeks in extension. Literature search does not provide robust outcome data on the success of non-operative treatment in the chronic post-traumatic setting. One surgical treatment for Boudinier deformity involves terminal extensor tenotomy. This involves a dorsal incision over the middle phalanx with oblique division of the extensor mechanism distally to the triangular ligament. On one of the earlier series by Stern et al, it showed that while DIP hyperextension and flexion is improved in the vast majority of cases, this does not improve the flexion deformity at the PIP joint. Thus, patients should be counseled on the expectation for DIP joint but not PIP joint improvement. Littler described rebalancing the lateral bands by dividing the lateral bands and suturing them to each other and to the central slip. The PIP joint was pinned in extension for two weeks. While good results were reported in the article, it was not descriptively quantified, and so I can't recommend this necessarily. The MTEV procedure differentially divides the radial and lateral bands over the middle phalanx. The band divided proximally is sutured to the central slip. The band that is divided distally is sutured to the other band's distal remnant. The PIP joint is pinned in extension for six weeks. In delving into their series of 20 patients, the majority of patients had correction of PIP joint flexion deformity and DIP hyperextension. In being critical, though, of their results, about half of their patients developed an extensor leg at the DIP joint, ranging from five to 30 degrees. Curtis et al described a staged approach to boutonniere deformity. A prerequisite for the surgery was passive mobility of the PIP joint, either by splinting or release of the palmar capsule. Stage one involved tenolysis of the extensor tendon and transverse retinacular ligament. Stage two included division of the transverse retinacular ligament. Stage three involved lengthening of the lateral bands of the middle phalanx or performing a phalartonotomy. Stage four included excision of central slip scar and then advancement of the central tendon to the central slip insertion. After each stage, active finger motion needs to be checked. If after stage two, an extensor leg of 20 degrees was seen at the PIP joint, then stage three was skipped and stage four was performed. The flexion deformity at the PIP joint was not completely corrected in their series, but led to an average improvement of 31 to 38 degrees. Urbaniak et al also described central slip reconstruction, but they used the dorsal capsule. The procedure involves division of the transverse retinacular ligament and then creation of a larger proximally-based flap between the lateral bands and then a distally-based capsular flap. The lateral bands are slightly centralized with suture. Then the distal-based capsular flap is weaved through the proximally-based created flap. The PIP joint is again pinned in extension for four weeks and then splinted for another four weeks. Flexion deformity at the PIP joint improved on average from 56 degrees pre-op to 12 degrees post-op. Hyperextension deformity at the DIP joint improved on average from 15 degrees to one degree. There are also central slip reconstructions with tendon graft. Lou et al described this first technique. In their technique, they released the transverse retinacular ligament to allow the lateral bands to be centralized dorsally. Then the scarred tendon slip is excised. A palmaris longus graft is used at one end of the split. At one end of the middle phalanx, a Y-shaped bone tunnel is created. This allows for central docking of the graft with the split limbs passed radially and annually through the bone tunnel. Before looping the graft on itself, the graft is passed around the lateral bands to ensure that they stay centralized. Then the graft is sewn into the proximal extensor mechanism. The PIP joint is pinned in extension for four weeks. In their series of 18 patients, flexion deformity of the PIP joint was improved on average from 48 degrees to 11 degrees, and active flexion in both the PIP and DIP joints were improved significantly. Ahmad et al described central slip reconstruction by tunneling a slip of FDS from palmar to dorsal through a three millimeter bone tunnel at the base of the middle phalanx, and then weaving the slip into the extensor over the proximal phalanx. Ahmad described this in a singular case for a rheumatoid patient. At 12 weeks, the patient was reported to have a PIP joint arc of motion of 30 to 85 degrees. A robust case series is not available in the literature, but a recent biomechanical study by Maslow et al showed that FDS central slip reconstruction has higher load to failure compared to the MTEV procedure and also primary repair. In summary, there are a lot of options. And overall, a close look at the literature shows that there is imperfect correction with most of the options. It is my bias to avoid an excessive amount of non-absorbable suture dorsally as I've had wound complications from this. For supple mallet, I would offer a tenodermadesis, Fowler central slip tenotomy, or sorrel. If the deformity is rigid or has degenerative changes, then I would perform an arthrodesis. For supple swan neck deformity, only due to PIP joint laxity, I would offer FDS tenodesis. Otherwise, for supple swan neck, I would offer the sorrel procedure. And for supple boutonniere deformity, I would do the Curtis staged approach as it incorporates many of the available options. However, with more data and in the setting of loss of dorsal extensor substance, using FDS for reconstruction may be promising. Here are my references. Thank you for your attention. Dr. Goitz will now take over. Actually, Dr. John Fowler will now discuss the deformities due to inflammatory synovitis and arthropathy. Thank you. And then the polling should now be open, and so if you want to submit your questions through the app, I'll be monitoring those questions. Thanks. Those are my conflicts. So I know Jennifer probably just talked about a little bit of this, but I think it was interesting doing my research for this talk that when you have rheumatoid arthritis, that's really we talk about inflammatory issues, like really RA or some version of that's going to be the main issue. A third of all RA patients get a boutonniere, which I thought was kind of shocking. And then 14% of them get a swan neck. And when they first get diagnosed, that's often maybe one of the first things that we'll see. So in the first two years after diagnosis, 18, 8 to 16% of people present with one of these two things to a hand surgeon, which I thought was kind of crazy. I know Jennifer just talked about boutonniere deformities, and it's a little bit different in the non-traumatic setting. So in the traumatic setting, it's going to be central slip rupture, and that still kind of occurs, but for a different reason. So you're going to get synovitis of the PIP joint. That's going to loosen the dorsal capsule. That's going to make the central slip attenuate, and then you're going to get the flexion at the PIP joint. Because of that, the lateral bands are then going to displace palmar to the axis of rotation. They become fixed and then hyperextend the DIP joint. So we love grading things in orthopedics, especially hand surgery. So if you get a stage one boutonniere, which we would define as a passively correctable PIP joint with an accessory lag of only about 10 to 15 degrees, you usually can treat that with a nighttime extension splint, and a lot of times that rebalances and you're done. You can try injections to control the synovitis, and if that doesn't work, then you're talking about going in and potentially doing a PIP joint synovectomy, and then doing a terminal tendon tonotomy, which is called the Fowler tonotomy, but I had nothing to do with it. It was well before me. I think one of the important points is you want to get relatively proximal, which might sound weird, but you don't want to get too close to the DIP joint because there's some capsular attachments, which can cause more DIP flexion than you want in the long run. If you get a stage two boutonniere deformity, this is where the flexion deformity is worse. Remember, stage one was 15 to 20 degrees. Stage two is 30 to 40 degrees, and the important point is there's still a normal articular surface. You'll see in stage three, once you get arthritis or at least cartilage loss, all bets are off and you're going to bail to some type of salvage procedure, either arthroplasty or arthrodesis. And then, of course, we have to subdivide things as we always do, and so you've got early and late. If you have a fixed deformity, that's where you have to do a two-step process. Step one would be to correct that fixed deformity, so you're doing some type of vulvar plate release. Maybe you're going to do it in one stage or two. Sometimes you talk about pinning it in extension and then coming back later. Step two is reconstructing the central slip. So we know that it gets stretched out because it's the synovitis, and so kind of in general, people recommend actually excising part of it, or there's some other things I'll show you on the next slide, and then you still go in and do that terminal tendon tenotomy. These are pictures on the right of finding that central slip and then just basically trying to tighten it up so that your finger doesn't go back into flexion. As I mentioned just, you know, 30 seconds ago, if you have a fixed PFE contracture and joint-based destruction, I think arthroplasty is a little bit tricky in those, so I usually do an arthrodesis in that situation. I pulled this from one of Jim Tang's articles with Paige Fox. So you're going to go in between the lateral bands and the central slip. That's going to give you access to the joint to do your synovectomy. And then I thought this was kind of interesting. They tightened up the central slip and then they pull the lateral bands dorsally to block the flexion. It's kind of a pants-over-vest type treatment. I've never personally done that, but I thought that was pretty interesting. One of the important things, as we'll talk about MCP joint stuff later, because that's part of RA as well, is that you'd like to try to correct the boutonniere before you address the MCP joint. Because a flexed PIP joint, as you can see in the picture on the right over here, is going to lead to decreased MCP motion. And volar subluxation of the proximal phalanx can then contribute to your PIP hyperextension. All right, so that's boutonnieres of the fingers. Let's move on to swan necks of the fingers. There is a classification system. I didn't find it super useful, so I'll kind of skip through that. Just like with the nighttime extension splinting for boutonniere, you can do a flexion splinting for swan necks. So remember, swan necks are going to be hyperextension of the PIP with flexion of the DIP. So same thing in milder cases. You can do this, and sometimes it rebalances things, and people are happy enough. When that doesn't work, we start talking about operative treatment. So remember, in this scenario with hyperextension of the PIP joint, your lateral bands are going to sublux dorsally. And so all of what we're doing initially is trying to release those, get them to go back volarly below the axis so the finger will actually flex again, resect the dorsal PIP capsule. Sometimes you have to release some of the collateral ligaments to get that flexion back, and then sometimes you have to Z-lengthen the central slip. Other options can include, maybe in addition to some of those releases, the Zancoli or FDS tenodesis. Zancoli is always confusing because there's multiple Zancolis, and they'll describe like five different procedures. So maybe FDS tenodesis is the right answer here. In this procedure, you would excise or cut the ulnar FDS slip, fold it back on itself, and sew it to the A2 pulley. And that's basically just going to cause a tenodesis effect so that your PIP joint doesn't extend, which helps fix the swan neck. I was trying to find some outcome results. Believe it or not, there's not a lot of outcome data on almost any of these procedures, but I found this one out of France. They did 23 of these ulnar slip FDS tenodesis. They splinted in 20 degrees of flexion for four weeks, and then got reasonable motion afterwards. I'll show another slide next that has a little bit more flexion. I think probably what happens when you take the FDS and sew it to the pulley, it's just not going to be able to pull through as much, so you lose a little bit of motion. But they didn't get any hyperextension, and the DIP flexion corrected in most of these. This is the procedure that I've kind of gone to, and I really like. This is another Zancoli procedure, which again is super confusing. So in this one, you make mid-axial incisions on either side of the PIP joint. You release the lateral bands, and you basically bring them down and sew them either to the FDS insertion and or to the vulnar plate. So you're forcing those down as much as you can. And I like it because it's a little less exposure, like the mid-axial approach is nice, and I've done this in probably four or five patients, and they all have been very happy with it. Kind of one of the more, I think, extreme things to do, and I wouldn't recommend it, I'm curious if anybody in the audience has done this type of procedure, but the Thompson-Littler approach. So I have the top picture up here kind of looking at the classic Thompson-Littler. So you're gonna take the ulnar lateral band at the level of proximal phalanx and transect it, and you kind of pass it around over to the radial side and sew it either to the radial lateral band or sew it to the extension mechanism on that side. They've done this modified one here, but I think it's a lot of exposure. You can see those other two procedures we talked about, either going dorsally and releasing the transverse retinacular ligament, or doing that Zankole, or even the FDSTM thesis, just to me seems a lot less invasive, and you may need to do other things long-term, so I kind of like doing something a little bit less. I mostly put this in here kind of for historical value. So that is finger boutonniere. There's also thumb boutonniere, which I've only seen a very few of kind of in my career. This is actually one of my patients that I put on the right over here, came in with a thumb looking like that, and to me that was actually nice because it made the decision easy. You weren't gonna be able to salvage that IP joint, so that was an easy fusion for me. But you can see it's the same thing. It's the proliferative synovitis causes all these problems. Causes soft tissue laxity, the collateral ligaments start to go bad, and then all the tendons start going in the wrong direction. Again, classifications, type 1 boutonniere is just synovitis of the MP joint, and these are usually passively correctable when you can treat them in a splint. Once you get to type 2 boutonniere, now the CMC joint's involved, and your MCP joint is fixed. And then in those cases, talking about MCP arthroplasty or fusion, I tend to favor fusions for these, and an IP fusion as well. Once you move into type 3 thumb issues, now it turns over to the swan neck. So the swan neck starts at the CMC joint. You kind of get that Z pattern. Again, synovitis is the problem. And then once you get to type 4, you also add ulnar collateral ligament sufficiency. When you get to type 5, now the MCP joint is starting to really hyperextend, but it spares the CMC joint. And then when you finally get to type 6, that's the worst of the bunch. It's just completely mutilated, and fusions are your only options. So treatment in general for these type 3 to 5, CMC arthroplasty, kind of pick your poison there. It probably doesn't matter what kinds you do, although they tend to not favor some of the ligament procedures, because those are often bad in the synovitis-type things. And then you can either do MCP arthroplasty or fusion, and then do an IP fusion as well. Again, just kind of looking up, like how do these people do long-term? This study, Tom Kefauver and Jim Strickland from the Indiana Hand Center looked at this back in the early 90s. 92 fingers with swan neck deformities. They did that dorsal capsulectomy and lateral band mobilization. It increased their range of motion by 55 degrees, which is great, but they lost 17 degrees that over three months. And the reason I kind of put the study in here is that the results were unpredictable. And I think that really sums up a lot of treatment for inflammatory arthritis. I don't know if anybody looked at the handout, but one of the other things I kind of put in there was about sagittal band insufficiency. And it's kind of a chicken or the egg sometimes. Does the sagittal band rupture lead to ulnar drift, or does ulnar drift in rheumatoid arthritis lead to sagittal band ruptures? I put down two techniques here. This is kind of the classic Elson technique, where you take half or a third of the EDC tendon, you wrap it under the deep transverse intermediate carpal ligament, and then sew it back to itself. And that kind of acts to pull the tendon back over more centrally. You can also do this modification of the Elson technique. And they're talking about the index finger here, obviously, because we have an EIP. And they're kind of going underneath the interosseous tendon and kind of looping things around. I favor the Elson techniques. I think it's very reproducible. But if it's in the index finger, I think you can try this other technique as well. I found this really great article, Greg Bain, just really beautiful pictures here. But you can see, here's your central tendon. You can see the sagittal bands on either side. If you have an acute tear, which we're not really talking about here for rheumatoid arthritis, you can just sew it back together and it does pretty well. However, if you have kind of a chronic stretched out tear, you're gonna do a version of that Elson. And this is kind of what they showed there. You're passing it underneath the intermediate carpal ligament, and then bringing it back through and then suturing it to itself. And you can see in the picture how that centralizes the extensor tendon. We're gonna finish up talking about the MCP joint. Basically, you're gonna do an MCP arthroplasty. I think we probably all know that. You can do an MCP fusion in rare cases, but when you do the MCP arthroplasty, you really wanna try to correct the ulnar drift. And I kind of put this slide in here because I thought the results were kind of humbling in many ways. You can see that the ulnar drift started off anywhere from 26 to 48 degrees. And they did correct it, but you can see it never ends up being normal. And so much of what we do is kind of telling patients about expectations and what they're gonna get out of a procedure. Make sure people understand that even though they will improve by anywhere from 12 to 30 degrees, their finger still is gonna be ulnarly angulated. If you look at extension lag, same kind of thing. I mean, you look at this, the index finger still had a 32 degree extensor lag at one year after the surgery. And then the arc of motion too. One of my kind of lines to patients about silicone arthroplasty is it improves pain, but it doesn't improve motion. And it may even make it worse in some scenarios. So you can see at one year after an MCP arthroplasty, patients are basically gaining about 10 degrees arc of motion. But if their fingers are straighter and they don't have pain, most of them are very happy. Sometimes we talk about MCP arthroplasty, we worry, so you've got the boutonniere deformity, you've got the swan neck deformity, like is that gonna mess up my MCP arthroplasty? You can see in this study, they only had 19 boutonnieres, so that was a little bit of a complicating factor. But they had 178 with no deformity, and you can see that their arc of motion at two years was only 25 to 35 degrees, but it didn't seem like the boutonniere or the swan neck affected long-term outcomes. So at least we can hang our hats on that. What about that ulnar drift when we do the MCP arthroplasty? I think we all kind of struggle with that. I think the classic answer is probably one of these crossed intrinsic transfers. And you can look here, 73 hands, they did 28 crossed intrinsic transfers, and 45, they had no transfers. They had mean follow-up of 50 months, and you can see there was less ulnar drift in the transfer group. They showed that other study that showed 12 to 15 degrees of ulnar drift. You can see in this group, if you do the crossed intrinsic transfer, you get a little bit less. Basically, you're gonna cut that ulnar intrinsic at the P1 level, and then transfer it to the adjacent radial collateral ligament. If you read the initial descriptions, they transfer it to the extensor hood, but this group out of Britain seemed to think it was better to transfer it right to the collateral ligament. And then here's just another extensor centralization, those patients, and you can see they really decreased the post-op ulnar drift. Thanks. Thank you. So I'm going to introduce Dr. Bob Goitz, he's going to talk about malunion joint contracture and intrinsic extrinsic tightness. Oh, you want to do questions? There's one question for you. The question is, with the ELSIN, can you talk about tensioning the EDC slip, can you over tighten and decrease MCP motion? So yes, but I think that we already kind of showed that after those type of procedures, people don't get great MCP flexion anyway. And so I would probably favor more over tension. I think people end up being less happy with the ulnar drift, and they kind of don't, not that they don't mind as much, but they've had poor MCP motion for a very long time. And so I think they don't notice it. So I would pull it tight. Thank you. Thanks, John. All right, we're going to switch things up a little bit. You saw a lot of studies, a lot of procedures, and this is more of a practical guide to the stiff hand. And I would say, you know, lots of times on the two talks you just heard, the diagnosis is not too tough, but picking a procedure can be tough. And I find you need to have like a toolbox of options, and you try to pick what the best one is for that patient. Whereas in this situation, I find a lot of people will, you know, have questions about how to, what's going on here? You know, that's the hand, that patient that comes in with the stiff hand, and you're trying to make a, you know, reasonably quick diagnosis, and then come up with a reasonable plan with that patient can be a diagnostic dilemma. So this is going to be just a very practical guide of how I look at the stiff finger and the stiff hand. So we'll look at joint contracture, intrinsic and extrinsic tightness, and how bony anatomy can affect the stiff hand. So you know, and a lot of this is going to be directed to the PIP joint. You know, a lot of our arc of motion is at the PIP joint, so a lot of patients' complaints are related to the PIP. So contributions, obviously, would be, you know, joint congruity, the collateral ligaments, the volar plate, the tendons that move it, and then the soft tissues, right? So there's really three key features, I think, to when a patient comes in and you're trying to assess their problem, and it would be, I usually check their active motion, what's their passive motion, and I'll just write it down, and usually the answer will come out just by writing these things down, and what the effect of MP motion is on the PIP joint, for instance. And so we'll just go through this. So if, you know, this is the very simplest one, right? If a patient comes in, they have a stiff PIP joint, and their active motion equals passive motion, despite the position of the MP joint, then you know that's a joint contracture. Pretty straightforward, right? That's pretty, that's not the most common thing that will come in, because you'll have features of different things that can contribute, but when you see this, at least the diagnosis is fairly straightforward. You know there's a joint contraction when active and passive motion are equal. How about if passive motion is greater than active motion? Then it's not a joint contracture, right? And then it's either going to be something to do with the tendon adhesions or intrinsic or extrinsic tightness. So just to kind of review the anatomy, you saw really the finger anatomy related to the extensor mechanisms and everything. We're going to go through more of the, you know, the contributions of the different intrinsics and extrinsics, and how they contribute to stiffness. So just as a reminder, you know, the extrinsic, like the EDC is best represented for extrinsic extensors are dorsal to all three joints, right? The extrinsic flexors are volar to each of the three joints, and then you've got the intrinsics with your interossei and lumbar goals, and that's where it becomes a little bit more confusing. And they're volar to the MP joint, and then they become dorsal to the PIP and DIP joints. So how each of these contribute to stiffness will be based on, then, your position of one joint relative to another. So I think this anatomy slide is most important when you're thinking about stiffness. What may be contributing to the stiffness of that finger is based on what tendons may be involved, if we're talking about extrinsic causes of tightness. And so, you know, just as a model to look at this, you know, the intrinsic muscles that pull volar to the MP joint will flex the MP joint and then extend the PIP and DIP joint. So if there's decreased flexion with the MP joints in flexion, you know, if both joints are flexed and you have less flexion, then that's extrinsic extensor tightness, right? Because they're all dorsal to both joints, and so if both are, you're trying to flex and you're tight, then that's an extrinsic tightness. And I'll use this kind as an example. This patient had a grinder injury to the dorsal and the hand. We did a, basically, you could see the cross-sectional anatomy of her wrist and carpus and hand, and all the tendons were taken out and everything, and so we did a free latissimus flap to cover it and did some tendon transfers at the same time. And ultimately, this was, I can't remember how many months this is out, and you can see we asked her to make a fist, and she can't flex her PIP joints when she flexes her MP joints. And so that's extrinsic tightness, right? And I think that makes sense because, you know, we're talking about the tendons that were going across the multiple joints on the dorsum of the hand, which was all the injury. So this one's an easy, you know, way to, easy diagnosis. Flexor extrinsic tightness is also, can be pretty straightforward. This is a young woman who had, you know, a forearm injury, and we asked her to, with her, you know, make a fist, or extend her fingers, actually, with the wrist or MP joints and extension. She can't make a fist, whereas when she flexes her wrist, her fingers can extend. And so, and you can see here on the volar side, when you try to straighten the fingers, you'll see, you know, the dimpling of the skin, pulling with the tendons that are adhered to the skin, causing the reins of a horse pulling, keeping the fingers from fully straightening. So that's extrinsic flexor tightness. So if you have decreased PIP flexion with the MPs and extension, right, so this is the opposite of what we just saw. Like, you know, if you're trying to move both joints in the same direction, whether it be into extension or into flexion, that would be extrinsic tightness. Here you have the opposite. You have, with the MPs and extension, you're trying to flex the PIPs, then this would be intrinsic tightness. And so then you know it's the intrinsics that are causing this tightness. And so this would be the typical test here, where you hold the MP joints and extension and flex the PIP joints, and this would be the intrinsic tightness test, whereas with MPs flex, they can make a full fist. And so we'll come back to each of these now and treatment of each of them, right? So you've made the diagnosis now of a joint contracture, and then so what are the contributions to a PIP flexion contracture, right? So it's typically would be edema, scar about the joint, or a boulder plate immobility, which is the most common. So non-operative treatment obviously would be prolonged stretch, edema control, static nighttime extension splinting, and then we often use a dynamic daytime splint. Usually they can only tolerate about 30 minutes, so I typically will order for twice a day. And then if they fail that, the order of treatment for a flexion contracture release would be, you know, boulder plate would be the most common contract, structure that's contracted. Release that first, then the accessory collateral ligament component, the flexor sheath you may need to resect, and then lastly some of the proper collateral ligaments on the volar side. Lots of times just manipulating the finger after doing the top three, you'll get the last bit of those proper collateral ligament that may be contributing to the flexion contracture of the PIP joint. And then it comes down to exposure. You know, I think that's often a question, what's the best way to do this, and I actually think there's a lot of different ways, and I bet you if we poll the audience, there'll be a variability of how the people do it. And I've kind of used over my 25 years of practice done all of these, and I have somewhat of an algorithm for the different ways, but we'll go through it here, and the pros and cons of each of them. So for a PIP flexion contracture, you know, a lot of people would do a volar approach, that's where the money is. You're looking to get the volar plate, the flexor sheath, the accessory collateral ligament, so a Brunner approach would be probably the most common, but then you're extending the finger and then your wound may break down and have troubles. So I personally don't love Brunner incisions for especially severe flexion contractures. You certainly can do a Z-plasty, and that's a preferred approach, especially if the skin is involved and you have like a linear scar from a burn or something like that, then you might want to do a Z-plasty, and then you can, you know, mobilize the skin from lateral to give you more length of that incision, and that can be a very effective treatment. I'll do that a good amount when you think the skin is involved and you have to do something to affect the skin. There's also a number of different ways you can improve the amount of flexibility of the volar skin. You could do approximately base rectangular slide, basically, and then you'll have a defect distally, and that's that middle slide there, and, you know, as you extend the finger and you slide this approximately, there'll be a defect here that you skin graft, or you can take a lateral, approximately base lateral flap, transpose it, and then skin graft behind that. So these would be the most typical ways that we would address especially volar skin problems that are affecting PIP flexion contractures. Obviously the pro is that this is a direct exposure. The con is that you may have wound problems because you're going to then keep the finger in extension as much as possible and may even pin the finger in extension for a short period. So for a long time in my practice, I did lateral exposures just to minimize the wound issues approximately, or volarly, especially if there weren't any skin issues that I had to deal with, but, you know, so the benefit, obviously, is the wound healing issues, but obviously the problem is the indirect exposure. You're going from one lateral side across to the other side. Sometimes it would take a second lateral incision on the other side, so that's not ideal. But this is a very acceptable way to do it, especially if you want to minimize your wounds volarly. You can easily, you know, you can get to, you know, on the side you're making the incision, you take down the volar plate, the accessory collateral ligament component, go across, get your other accessory collateral ligament, take out part of the flexor sheath, and then manipulate, but sometimes if it's a real bad contracture, it's hard to get it all from one side. So I have done dorsal exposures for this, and it's not very well described. The one, the only real, I found a personal communication from Buck Gramco, and he had done this in his practice, and this was a patient who I found it was a necessity to do. It was a very severe, it was a 10-year-old with these chronic PIP contractures from a brain tumor or something like that, and I thought it would be hard to do a volar approach for all these. It was a pretty significant contracture of 90 degrees in all of them. Lateral would be tough because you got the fingers in the way, one finger's in the way of the next to do a lateral approach, and then so I did do a dorsal approach on this, and then since then I've done about 20 of these, and I find the dorsal approach to be quite nice. The finger's very accepting of dorsal flaps. You keep the neurovascular bundle within the flaps, and it allows you to get to both sides of the joint, take down the volar plate, the accessory collateral ligament, the flexor sheath, and you never have troubles with the volar skin. Sometimes the manipulation, like in someone with a 90-degree contracture, you'll get a little skin rip volarly, but that's usually not an issue at all. Just like when you manipulate for xyoflex or something, the skin wound usually heals pretty readily. So, transitioning from PIP flexion contracture to extension contracture, I'll take an extension contracture any day over a flexion contracture. Much easier. You know, you could fairly small dorsal approach, just got to take down the transverse retinacular ligament, elevate the lateral bands, get to the joint, take down the dorsal capsule, and then maybe some portion of the dorsal proper collateral ligaments, and then do an extensor tenolysis, and usually it's a 15-minute procedure, and they really don't have as much trouble as rehabbing it, and I find much less recurrence rates compared to flexion contracture. So, I'll take an extension contracture. It's pretty easy to deal with the neurovascular bundles, but this is basically, the majority usually is the dorsal capsule and maybe the tenolysis of the extensor mechanism. So this is just to kind of highlight, this shows you the exposure, elevating the lateral bands, you get to the joint, leave the central slip attachment, take down the dorsal capsule, just dorsal to the collateral ligaments, pretty easy to get across and take off the dorsal capsule, and pretty quickly get a nice flexion. So moving towards intrinsic tightness, as a reminder, the intrinsics, interosseion lumbricals are volute to the MP and dorsal to the PIP and DIP, and so I think it's important to identify a lot of these intrinsic tightness patients. In fact, Dr. Fowler didn't harp too much on this, but a lot of the rheumatoids, for instance, a lot of the boutonniere deformities are due to intrinsic tightness, so any rheumatoid patient that come in, I always check them for intrinsic tightness and will institute, like this splint for instance, when they have very mild intrinsic tightness, you may hurt off the boutonniere deformity early if you can work on the intrinsic tightness. So this would be a typical splint, I would provide a hand-based MP extension splint that allows the PIPs to flex, so all night when patients are sleeping, their extrinsic flexors want to flex, and so they're doing therapy all night, stretching their intrinsic tendons. So this is a very common splint that I order on most of my rheumatoid patients that come in for other problems, I'll always check them for intrinsic tightness, because it's really a precursor to a lot of finger deformities that were talked about earlier, and this just shows why this would be a stretch, because it wants to flex the MP joint, extend the two joints here, you extend the MP joint, allow the flex, the PIP and DIP joint. So there's three different intrinsic release procedures, and these are, I use in increasing severity, so the distal intrinsic release is the most common, and it's used for the more mild amount of intrinsic tightness. Intrinsic muscle slide, I use mostly for spasticity, CP, functioning but fairly significant amount of intrinsic tightness, but still functional, and then the distal, or the intrinsic tenotomy would be the most severe, maybe non-functional intrinsics, like after a Volkman's contracture or whatever. This is just from one of our articles that we looked at how much, you know, it's often, how much do you got to take of the, when you do a distal intrinsic release of the extensor mechanism, we kind of looked at this in the lab just to see, because it's very variable, you know, some people will just cut the triangular part of the extensor mechanism, either side of the extensor, the central tendon, whereas some will cut out a certain amount, and it really was never defined, so we looked at, you know, how much does it take to immediately get loosening of the intrinsics, and we found it was about 60% of the extensor mechanism distal to the transverse fibers of the extensor hood. So this is just an illustration of the muscle slide that I would do for more spasticity or, you know, functioning but significant intrinsic tightness, and then certainly the intrinsic tenotomy, which I typically will do on rheumatoids, I'm doing MP arthroplasties, I would just do a tenotomy. I don't typically do the transverse, although it looks like there's some data to indicate that it may be indicated. And then this would be the one that Wolfman's contracture, you know, that's one you're just going to do a tenotomy. You got dysfunctional intrinsic muscles, you're just going to do a tenotomy if you need to of the intrinsics. And then extrinsic tightness, you know, it's pretty straightforward, you know, you do a tenolysis and or muscle slide, for instance, on the flexors, you know, if it's pretty significant extrinsic flexor tightness, you might need to do a muscle slide, and again, there's that same woman, you know, with the grinder injury. We basically came back, did a, elevated the flap, did a tenolysis of the transfer, and then you could see she could flex her PIPs much better. She couldn't flex the ring finger, we had to fuse the ring finger MP joint just because there was no joint left, but you could see that she could quickly flex the PIP joints pretty well. So the last topic I'm going to cover would be bony contributions to finger stiffness, and so you could certainly have joint impingement from malunions of fractures, and you could see here, this would be an easy one to see why they would lose flexion. You can get certainly rotational malalignment, something that we deal with every day, right, with fractures of the fingers, checking for that. You can get extensor mechanism imbalance from, you know, different ways that the bones will heal and certainly get a combination of all those. So we all, all of us are checking for this every day in our office as an indication for surgical treatment, malrotation, you know, it's not uncommon, you'll get a patient come like this, they're a year out from their injury, look at the x-ray and you really don't, it doesn't look that bad, but they're pretty unhappy with their rotational malalignment, and the question is what to do. And so this one, for instance, if it's just a rotational malalignment, I'll typically do an osteotomy at the metacarpal level, even though this is a proximal phalanx level, especially if I just need to get some rotational alignment, and whereas, you know, you may find that a mild amount of shortening of P2, for instance, will end up with this, this mallet deformity of the fingers. And so I think the extensor mechanism is not very tolerant, especially with a slight amount of shortening at the P2 level, and you'll see this not infrequently, and this is my partner, Dr. Kaufman, had done this procedure, which was a pretty nice illustration of, you know, he did an osteotomy, lengthened it out, and the patient got back their full extension of the DIP joint. So how do I choose which site to do the osteotomy for a malunion? I'll do it at the site of the deformity to restore anatomy, and if, especially if there's a tendon dysfunction like that one at the P2 level, and I'll, whenever possible, I'll do the metacarpal base because it's more tolerant of plating and less tendon adhesion problems. So in conclusion, knowledge of anatomy is paramount, systematic physical exam is going to help you make your diagnosis, and then, you know, essentially, once you know the etiology, treating the cause. Thank you.

finger and hand stiffness

diagnosis

treatment options

joint contractures

collateral ligaments

volar plate

non-operative treatment

surgical options

anatomy of the hand