Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

There was swelling in the same region and a loss of range of movement. There is often reduced wrist strength. However, it is not uncommon for late presentations. And you will find those groups of people. Personally, I found usually manual working men who tend to present later than other groups of people. Once you've seen the patient in clinic, you perform a clinical examination, you will find usually a reduced range of movement as previously discussed. And you will also, once you've seen the patient in clinic, you perform a clinical examination, you will find usually a reduced range of movement as previously discussed. And you will also be able to identify where the the area of the pain is in clinic. You will start off with an X ray, but it's quite common whether or not you find something on the x-ray to move on to cross sectional imaging, especially if you are suspecting Kembo disease. This could be in the form of MRI scan or CT scan. Often we will use both of them. The exact etiology of KV disease is not always clear and may be multifactorial. There are several theories of things that may contribute towards K box disease. These may be negative on the variants, decreased radial inflammation, lunate morphology, lunate arterial supply, lunate, venous drainage and systemic causes such as SL E Raynaud's disease and scleroderma. However, these are rare and often in the literature. You will find that patients do not have systemic causes associated with their key box. The first factor we look at is the variants, as you can see from the picture of the right. This shows that you can have negative, neutral and positive ulnar variants. The radiograph that you take should be apa view taken with elbow flexion and shoulder abduction at 90 degrees with neutral forearm rotation. We are looking for a variation of greater than 2.5 millimeters from neutral to say that it is either negative or positive, negative on the variance is associated with King box disease. Whereas positive on the variance is associated with on the lunate impaction syndrome or on the lunate abutment lunate morphology is also an important factor to look at. There is the Tuia Zico classification which is a type one, type two or type three lunate also described as trapezoidal rectangular and pentagonal lunates. The type one lunate is associated with negative ulna variant and an increased incidence of king box disease, vascular supply of the lunate is also something that has been talked about many times over the years. Gelman described the patterns of the vascularity in the lunate to be of a yx or I pattern. The most common of these would be the Y pattern followed by the I and then the X within these patterns. There is a dorsal and volar supply. In 92% of lunates and a single vus supply. In 8% of lunates. Unsurprisingly, the single vascular supply is thought to be a contributing risk factor. However, it is worth noting that following a perilunate fracture dislocation where you would expect compromise of the vascular supply of the lunate post injury. Kee Box disease is rarely if ever seen. Perhaps the theory that has gained most traction in recent years is concerned with the venous drainage of the lunate. The disruption in the venous drainage supports the theory of an interosseous compartment syndrome within the lunate caused by venous hypertension. There are two potential methods for this to happen. And the firstly is an obstruction of extra osseous venous drainage, especially where there is only a single point of drainage. The arterial supply will have an adjacent venous drainage point. And so the lunate with the single volar arterial supply would be at risk. However, this is now felt to be more likely due to a disruption of the subchondral venous plexus in the proximal lunate secondary to micro fractures caused by the risk factors that we have previously talked about. And I'll discuss this in a little bit later, repetitive injury to the proximal aspect of the lunate as it engages the distal radius leads to a stress fracture of the thin subchondral bone. And you can see this on the diagrams to the right hand side where you have ac is the articular cartilage. And you can see the venous plexus demonstrated just above it. Disruption of this subarticular plexus then occurs which then leads to interosseous hypertension within the lunate itself. Further propagation of the micro fractures will lead to a lunate collapse. But there is potential for fracture healing as there is in all other bones and potential for that process to stop. This is especially in younger patients. And later on, we will mention that it is therefore important when you have your very young patients, especially those under 15 years old or you hold off operative treatment for as long as possible as it is likely that these patients will go off for spontaneous healing. When we mention the lunate and the factors that are affecting Ken Box disease. If you see diagram a on the left, this is a type one lunate and you can see the negative on the variants. This is an uncovered or at risk illuminate. And you can see how the lunate itself is hanging over the edge of the distal radius compared to B which is a covered lunate. This is a type two lunate with normal like normal variant and the lunate itself is not over the edge of the distal radius. This is important as when the wrist is used with the deviation whilst in a power grip, it produces a nut cracker effect from the capitate, pushing down on to the lunate, then onto the edge of the distal radius. Looking at this diagram, you can see why the uncovered lunate would therefore be at risk of having this nutcracker effect, which is then gonna cause the micro fractures at the approximal edge of the lunate leading to disruption of the venous plexus. And therefore, leading to the venous hypertension within the lunate itself. Once this process starts lunate collapse, then causes proximal migration of the capitate. This in turn leads to degeneration of the central column of the carpus. And proximal row instability will develop and this is comparable to a chronic scapholunate rupture where the capitate again will try to migrate approximately the scaphoid is then forced into flexion. And if you look on the X rays, if you see scaphoid flexion on plain radiographs, this can be an indicator of disease progression within K box disease. Following this, the radial column degeneration will then occur. There have been a number of classification systems throughout the years. I'm going to discuss the most common ones and the common classification systems have all been brought together for one algorithm which has been described by Bain and Liman and I will show you this in a few slides of time. The most common classification is the Lichtman Radiographic classification. This is what they describe as an osseous based grading and this would obviously, firstly happen in the form of an x-ray while you're in clinic. But to identify changes such as the three C changes, you would need a CT scan. So stage one is a normal radiograph. Stage two is increased density without lunate collapse. And you'll see sclerosis on the radiograph. A three A is lunate collapsed with the radiocaps angle less than 60 degrees. So the scaphoid has not yet yet gone into that Flexion three B is lunar collapse with scaphoid palmar flexion radios scaphoid angle of greater than 60 degrees. And this is the thing you can look out for when you're playing films. Three C will only really be identified on CT and that's lunate collapse with a coronal lunate fracture. And that shows it's chronic. And at this point traditionally is when we think about salvage procedures, and then we have stage four, which is lunate collapse with radiocarpal or midcarpal degenerative arthritis. The next classification system is the Schmid MRI grading system and it's a grading system based on vascularity. So as you can see from the images here, the one on the left side is for T two weighted fat side images, then we have T one weighted images and then T one weighted, which are gadolinium enhanced and they show a normal ischemic, partially necrotic and completely necrotic innate. And the changes that they show. The next classification system is the bain and be arthroscopic classification system. It is a cartilage based grading system. And it is looking at four articular surfaces. In particular, the proximal capitate, the distal and proximal lunate and the lunate facet of the radius. In grade naught all surfaces are normal. In grade one, there is what they call a nonfunctional surface. So degradation to the proximal lunate in grade two A, the proximal lunate and lunate facet of the radius surfaces are affected in grade two B, the proximal and distal lunate articular surfaces are affected. In grade three, all surfaces, apart from the capitate are usually affected. And in grade four, all four articular surfaces are affected and said to be nonfunctional bay. And lignin have devised an algorithm which can be used, which includes the osseous vascular and cartilage assessments of the lunate to classify the lunate and to devise some treatment principles. I won't concentrate too much on the treatment principles at the moment using this algorithm. But it certainly is there in the published literature and something you can can mention in the examination. What I'm going to do is now go through the individual treatment principles and say when we may or may not use treatments for king box disease should really be classified into non operative decompressive treatments, revascularisation, operations, unloading procedures, and then finally salvage procedures, non operative. Unsurprisingly, we'll start off with analgesia and splints. As for most things we do in hand and wrist surgery, we'll also offer steroid injections and then we'll move up to wrist denervation. Although I do realize this is actually an operation, but it doesn't quite fit into the other groups. The common standard operation in terms of a risk denervation is now the partial risk denervation. This is a denervation of the branches of the A in and Pin Hilton's law would suggest that you need to deal with all other nerves that are crossing the joints. And indeed, when wrist denervations were first devised, all branches were considered as part of the denervation. However, the a in pin denervation has been popularized in recent years and the results are equivocal to a full risk denervation. Before you attempt to denervation, you can assess the potential effects of the operation by trying a preoperative guided injection into the A in and pin at the operative site. If you then proceed to the denervation, it is a dorsal incision which is longitudinal at the level of this transverse line that you can see in the image which is about four centimeters proximal to the Droge and then you excise of one centimeter of the pin as you go down, go through the intraosseous membrane and then excise one centimeter of the A in the next type of therapy sometimes used in Kee Box disease is a decompressive procedure. The theory is to decompress the lunate with a compromised venous return to reduce the intraosseous hypertension. The common procedure is a core decompression of the lunate known as forage. This can be performed arthroscopically plus minus bone grafting and plus minus cy ectomy. This can of course be performed without an arthroscope. In which case, it is usually a fluoroscopically guided technique with a guidewire placed into the lunate and a cannulated d then used to perform a core decompression. You may also read about the forage procedure to the distal radius or the kappa tape. And even though these are not the bones which are affected by the intraserous hypertension. These are actually thought to be an indirect revascularization operation as they will lead to an increase in local vascularity and will therefore help with vascularization of the lunate. The next operations that can be performed for king box disease are revascularization procedures. They are direct vascularization of the lunate and involve a bone graft on a pedicle. There are a variety of choices that you may see in the literature, but the common ones are to use a four plus five extensive compartment artery graft or 1/4 extensive compartment artery graft. The graft will be taken from the area into which these arteries perforate and they will be rotated along with the artery back in towards the lunate. Other types of grafts include distant grafts. And one example is the middle femoral trochlear graft which can be taken as a free graft and placed into the lunate as an osteochondral graft. Unloading procedures are another type of operation that is undertaken in Kee V disease. Common ones are the radial shortening osteotomy, the capitate shortening osteotomy and the saper capitate fusion. The radial shortening osteotomy is used in patients with negative ul the variants, it will correct the negative ulna variant, it will reduce the radial inclination and is commonly fixed with a plate. Although you will see some descriptions of people forming this operation and fixing these with compression screws through the radial styloid. A less common operation is the capitate shortening osteotomy. And this would usually be used in patients with positive or neutral on the variants bay. Here has described the technique to perform this with a single sore blade. So he pre drills the capitate. This will be via a dorsal approach. He will debride the dorsal aspect of the third metacarpal. Once he's pre drilled this, he will then use an oscillating saw and often you will not be trying to remove more than the saw blades, width of bone. Once this has been removed, the guideway can be replaced in your to your pre drilled hole and a headless compression screw can be used to compress the osteotomy site. Another unloading procedure is the scaper capitate fusion. This allows stabilization of the radial column. And as you can see from this X ray image here, this will also stop proximal migration of the capitate. This helps to unload the lunates. This will increase load through the radiocaps articulation. And as with all partial carpal fusions may require further surgery in the future. Another treatment option, which is sometimes seen is the lunate replacement off the shelf replacements used to be available in the UK. And the example of this is in the picture on the slide. However, these are no longer available due to the recent EU MDR regulations which has led to a number of these small volume implants being removed from the market. You will see this with some of the pyrocarbon implants around the hand and the wrist as well. They certainly have been around. And nowadays, if you want to have one of these, you will usually have to get a 3d printed lunate. However, you need to consider which shape to pick your 3d printing will usually be based on your contralateral lunate, but this will of course be a normal size and may not fit into the gap where your degenerate lunate has come out of. So you may need to consider that the size of your 3d printed lunate is closer to the generic lunate. In the examples that I have seen in practice, the surgeon has printed both sizes and implanted the best fit salvage procedures. Generally, once you see that coronal split usually on your CT or MRI, this is when you'll have to resort to a salvage procedure, unloading procedures, revascularizations and decompressions will not work at this point. But do remember that the lunate is now compromised and cannot be used as part of the salvage procedure. So don't say four corner fusion in the exam cos the lunate is one of the four corners. The salvage will of course depend on the pattern of degenerative change as well as patient factors and what they decide to go for a proximal row. Carpectomy is an excision of the proximal carpal growth. It relies on a healthy lunate fossa of the distal radius and it relies on the proximal capitate articulation being in a good condition as this will now help to form the main articulation of the wrist. This should allow a greater degree of range of movement compared to a partial carpal fusion, but the grip strength will be reduced and this is due to a reduction in the car or height. This has been shown in multiple studies and usually forms the basis of an MC. We have already mentioned scale for capitate fusions, which may also be used as a salvage procedure as the condition of the lunate will reduce the number of partial carpal fusions available as previously discussed. Perhaps one of the final options available for salvage procedures is the total risk fusion and this is a reliable management option for end stage risk degeneration from any of the common causes including king box, slack or snack wrists. The dorsal plate is commonly used. There may be may be some variations on this including short bend plates to accommodate for APR C. These are also good for neuromuscular patients and plates that do not cross the third CMC. J. However, intramedullary vices are now becoming more popular and you will see these advertised that they have a stem going into the distal radius into medullary. And another one going usually through the capitate into the third metacarpal, they don't have various connection devices in the middle which do allow greater adjustability and a lower profile. However, the obvious disadvantage is if you have to remove the metalwork, this is going to be much more difficult, especially if the patient has gone onto fusion. Another potential option is a total wrist arthroplasty. These will be discussed in more detail. Next week, these would require a referral to specialist centers as overall, these are low volume implants compared to total hip and total knee replacements. However, these are rarely used and are unlikely to be suitable for the classic Ken box group, which is your 30 to 50 year old male patient. You may also hear of the concept of team box, which is key box in the younger patient for this group. We advocate a more conservative management and really try to avoid operating on those less than 15 years of age. You can cast these patients for 6 to 12 weeks. And another technique is to cast and temporarily pin the S TT with K Ys in order to perform an offloading procedure on these patients. In summary, the treatment of king Go disease remains controversial. Authors such as Bain Liman have produced a treatment algorithm in recent years, which I've shown you on these slides. But the treatments offered will vary depending on local skills and experience. Once degenerative changes have set in the salvage options are less controversial. However, it's important to remember how to identify when we have got to the salvage stage. And remember that Coronal split in the three C classification. It is known that in several cases, the disease will not fully progress. So observation is appropriate in the early stages. These are the references used in the production of this talk. I would really like to highlight the Lichtman and Bain papers. Those three that I've got there. If you really want to learn about Ken Box disease, pretty much everything you're gonna need to know, especially for the exam is gonna be within those three papers. They have the etiology and the pathogenesis of Kee Box disease. The assessment of classification and treatment and an algorithm for treatment which has been designed in 2017 by Li Ba.