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Yeah. Fabulous. Ok. So, um my name is Lia, I'll be talking to you about rheumatoid arthritis. Um It's a really broad subject. Uh So we'll try and head to the things that are most pertinent for the exam. So it's an autoimmune disease characterized by chronic inflammation of so your joints um in the hands, it presents as asymmetric polyarthropathy and it's got muscular fetal, sorry. Have you moved on to the next slide? I don't know if everyone else can see it, but it's still on the initial introductory slide on my screen. Uh The one that says rheumatoid arthritis. Yes. Yeah. Uh It's on the powerpoint display as opposed to the, you know, like the presentation mode. So I don't know whether that now it's moved on, it's moved on now. And if it does, it's funny how um it comes up, it comes up as having changed slides on my screen. So if you, if I move on to the next slide and you can't see it just, just interrupt me with this. Ok. So I'm not sure what's happening today. Um So it's an autoimmune disease characterized by chronic inflammation of synovial joints. Um And it's got uh musculoskeletal and systemic manifestations. So, um it's characterized by the formation of panus tissue which leads to joint destruction. Um and early in uh early diagnosis and the use of disease, modifying anti rheumatic drugs. So, dmards can significantly affect the disease course and progression. So I've just changed slides. I hope everyone can see this. Um So just talking about the epidemiology. So it affects 1% of the population. Sorry. Again, it's stuck on the Rh A slide. Yeah. All right. Now it's moved on. Perfect. We, we may have had, we may have to go, um, sort of like this. Uh It's not ideal. Um But uh I'll see, I'll see how we can move between the slide transitions and I'm not sure why this is happening. So, uh we'll, we'll, we'll give it a go. Um So in terms of epidemiology, the prevalence is 1% of the UK population. Um, it affects 1.5 men per 110,000 and about 3.6 women per 10,000. Um, and the peak age of incidents um is, uh in their, in their seventies for both men and women. Um, it's 2 to 4 times higher in women. And uh if you have a family history of rheumatoid arthritis, you have a 2 to 4 fold increase in the risk for first degree relatives. Um So the antibodies that are implicated are rheumatoid factor, which is I GM antibodies against the constant uh region of human I GG. So I GM is this big snowflake type uh antibody um and it's against the constant region of I GG antibodies and these are present in about 60 to 70% of patients. Uh The other antibodies are anticyclic, it related peptide autoantibodies and they have a sensitivity of about 6061 to 75% and verity of 94 to 99%. So, in terms of the pathophysiology, um it's a multifactorial disease. Uh there are some genetic risk factors. So, HLA Dl one and Dr four are the sub susceptibility genes that have been identified. Um It's worth just mentioning mentioning that these are mainly for sero positive arthritis, sero negative rheumatoid arthritis has a different set of genetic associations. Um And there are some gene environment interactions that affect the reactivity of these autoimmune uh antibodies. Um So they're autoantibodies against citrullinated antigens. Now, these anti CCP antibodies are uh can be detected a long time before the onset of joint symptoms. So, um and there there's a number of potential trigger sites. So, lungs, so for example, smoking or silica dust has been implicated uh periodontal disease in the gut microbiome as environmental triggers to um genetically susceptible patients. Um The immune system is no longer able to recognize its ari proteins as self proteins and there's a whole bunch of them. Uh Vimentin collagen, two histones. Uh I wouldn't expect anyone to be able to list these. But um I II think if you can remember just one or two examples that'll be good. Um And uh these antigens are taken up by antigen presenting cells such as dendritic cells and B cells. Um And these cells then migrate to lymph nodes to activate T helper cells. Um Now, th one cells um that induce interfering gamma and TNF alpha and interleukin one leading to joint destruction. Um were the ones that were mainly outlined. Um Th two cells secrete uh interleukin four and interleukin five as well as 13. And then, most recently, they've identified a new subset called uh T helper cells uh 17 which secrete uh interleukin 22. And these uh promote proliferation of the s overall fibroblast and through um induction of uh chemokine ligands. So that's quite a, a sort of extensive view of the pathophysiology. Um Essentially, there's uh the synovial joints are then infiltrated by leucocytes. And these release a whole set set of cytokines which uh produce an inflammatory cascade. Um And you can see here that there's a number of different cytokines that are implicated with all of these different cells. Um Essentially there, there is eventually the, the formation of panis um which is a special type of tissue. Um So uh panus forms, which is a type of distinctive tissue located at the interface of the synovium and the cartilage bone interface. So, panus is um Latin for cloth or covering um And then uh there's certain types of cells called fibroblasts, like synovial cells that predominate this tissue um activated neutrophils from the pace release lysinal enzymes and free radicals. Um And mediators include interleukin one TNF alpha, um matri meal proteinases and a whole load of other cytokines. Um And this leads to the destruction of articular cartilage and soft tissue. Um And you, you have these marginal erosions which is essentially bone invasion by the panus. Um in terms of diagnosis, uh this is very sort of medical student days. Um But I think if you can remember these, if anyone does ask, um in terms of uh diagnosis of rheumatoid arthritis, the American Rheumatism Association um have uh seven criteria um for the diagnosis of rheumatoid arthritis. Um The uh it sort of teaching is that you need four or more criteria to be present for six weeks. Um And the first four have to be present. Uh But if you have four or more for more than six weeks, it's likely that you, you will be diagnosed. Um So it's uh morning stiffness around joints for one hour. And so at least one hour before improvement, swelling in more than three joints or more, uh which is observed by a physician arthritis of the hand. So MCP joints and PPP joints and wrist, uh systemic arthritis. And then the other sort of less uh likely ones are rheumatoid nodules, uh being rheumatoid factor positive. Um and x-ray changes. So, erosions and, or periarticular osteopenia and hand wrist joints, um and decalcification. Um And this was based on the study of 262 subjects with rheumatoid arthritis um versus 262 control subjects with other rheumatic diseases. Um So, uh in terms of presentation, um uh there's a number of rheumatoid presentations which are quite classic for exams. Um but uh just thinking about joint pain, tendon rupture or subluxation, uh nerve compression um in an atlantoaxial subluxation. Um and then extra articular manifestations which are just useful to, to keep in mind. Um uh So, pericarditis, vasculitis, and then something called FTI syndrome, um which is rheumatoid arthritis, splenomegaly, and leukopenia. Um So, within the history, uh we want to particularly ask about hand dominance occupation, uh pain, weakness, loss of function, uh past medical history, um including medication and operations, uh social history and employment history. Um So, in terms of the examination, um we want to get them to lift their hands above their head, you just get a general impression of shoulder and elbow function. Um any rheumatoid nodules, um proximal to distal and then extensor to flexor. Um So, looking at the finger cascade posture, if there's any extensor lag or flexion lag, uh any deformity, um the presence of rheumatoid nodules, which may be in about 25% of patients. So, you have this collagen capsule uh with fibrous and central necrosis. If it's large um and functional tests. So, uh key uh coin pen grip and power grip um and then just looking um at the extensor side, there may be evidence of extensive tendon rupture. So Vaughan Jackson syndrome is uh quite a classical sequential um er extensor tendon, extensive tendon rupture and it's U usually ulnar to radial um er E PL rupture, uh MCP joint, subluxation and ulnar drift of the fingers, uh finger deformities such as male finger, bouton and swan neck, uh Z deformity of the thumb. Uh and Kett on a uh so kit is misspelled on that one. Uh So you may see a prominence of the ulnar head and that's due to var subluxation and supination of the carpus due to the laxity of the extrinsic vow ligaments which are usually quite strong um uh distal radioulnar joint disease and ulnar subluxation of the eu. In terms of other examination findings, um you may see volar ulnar subluxation of the metacarpal pharyngeal joints. So there is radial deviation of the metacarpals which alters the line of the pool of um ec and there's also capsular laxity. So, in this diagram, you can see that the metacarpals go radiately and then the ulnar there is ulnar deviation of the fingers. So that's kind of one of the classic deformities that you might be able to see on the flexor side. There may be a cleaner wasting. So, ca carpal tunnel syndrome, um there may be an f pl rupture. Uh This is called Manel Norman syndrome. Um and it's uh loss of thumb, inter joint flexion. So that's the sort of classic pos posture that you may see. Um uh and uh this is usually due to a nutritional rupture um from a scaphoid spur or a roar plate. Um There may be some trigger finger as well. Um So you want to just sequentially test um sorry for examination. So, uh in terms of uh palpation, uh ask if the, if there is any pain. Um And then you want to look at uh MCP, joint subluxation and stability, see if the uh deformity is correct or not. Um check the extensor tendons. So E pl uh you want to look at if they, if they can uh retropose the um uh thumb um and then test the flexor. So FDP, uh you want to test each one individually. Um So you uh ask them to do resisted D IP joint flexion um and then uh check the F DS. So this is a mass action muscle. Um And you want to stabilize the other digits and extension to inactivate FDP and then ask them to flex their and their finger. Um So there should be P IP joint flexion with the other digits immobilized in extension. Um Just a word of note for the little finger. Approximately 10% of people have no F DS to the little finger. Um And then other flexors that you may want to test uh F PL so resisted thumb, pharyngeal joint flexion and with the MCP joint held in extension. Um And of course, we want to check the nerves. So uh there may be compression um and especially look out for carpal tunnel syndrome. Um special tests which may be helpful. Um So you want to check for the uh tenodesis effect um to see if there's any uh intact extrinsic. So you want them to go from uh wrist flexion. So, passive wrist flexion which causes the MCP joints to extend to passive wrist extension, which causes uh the uh MCP joints to flex. Um And the other test that you may want to do um if you do see cap or um what may want to check for er Dr instability. So, um the piano key sign um and this evaluates the stability of the Dr and the T sec. Um So there if you depress the ulnar head palm award um and stabilize the pisi form, uh you may see the ulnar head coming up like a piano key. Um and that's a, a sign of dr and stability in terms of x-ray changes. Uh 30% of people will have x-ray changes at diagnosis and 70% will have um x-ray changes at 33 years. Um You may see marginal erosions. Um So uh the these are a relatively early findings. So you may see these bare areas. Um and this is particularly affects the radial side of the me carpal MCP joints, um soft tissue shadow, uh which may be swelling, joint, effusion, edema or sinusitis. This may be the only sign uh especially in early onset um uh osteoporosis. So you may see juxta articular uh osteoporosis and then a bit more generalized later on uh with disuse and steroids, joint space narrowing. So, symmetrical, concentric and uniform joint space narrowing, um and periarticular erosions And with, within the hands, you may see the small synovial joints that are classically involved are the MCP joints and the P IP joints of especially of the index and middle finger. Um the ULN diagno and the tricho um D IP joints in the hands are uh usually relatively spared and you may see some late changes. So, subluxation with um uh subluxation with uh radial uh deviation, I should say radial deviation, uh Pia swan neck, um hitchhiker thumb deformity and there may be some scapholunate dissociations um and ulnar translocation um in terms of the differential diagnosis. Um so uh osteoarthritis um especially uh lesions that involve the thumb and the D IP joints. Um You may just want to confirm what sort of prominences you're seeing. So, Heberden's nodes and D IP joints and Bouchard's nodes and the P IP. Um uh Lupus um may have joint subluxations and dislocations. Um but the joint space is normal and there won't, won't be any evidence of any erosions. So, in this radiograph, you can see uh subluxation and dislocation um of the MCP joints, but there's no erosions and the articular surface is well preserved. Um gout uh which is a form of um mono usually monosodium urate crystals, uh the position around joints. Um these are negatively birefringent on polarized light. Um And you can see these punched out erosions with sclerotic margins. Um They may have some overhanging sclerotic edges. So they, they sort of classically called uh rat bit erosions. And you can see in this picture here, um these overhanging sclerotic edges um and psoriatic arthritis. Um So you may find um a number of deformities there. Um So it's a symmetric polyarthritis. Um so it can mimic rheumatoid. Um You'll get erosive changes in bone proliferation. It's more common to be affecting uh distal than proximal joints. So, pharyngeal joints more so than metacarpophalangeal joints. Um Patients are usually that are HLA b 27 positive and 50% of the time. Um You may find these pencil and cup deformities um but they're not uh pathic for psoriasis, although they're more likely to be seen in psoriatic arthritis. Um You may find dactylitis, so swelling of the entire digits and, and this may be um seen as a soft tissue shadow. And if you do ultrasound on these digits, you may see sinusitis and tar cyano um acro osteitis which is resorption of the distal phalanx. Um Again, it's not necessarily pattern pneumonic for p ps psoriatic arthritis, but it's um more likely to be seen uh then um and something called arthritis mus, which is a rare form of destructive arthritis, particularly affecting the hands and feet. Um And you may find uh in the very, very late stages. So, II suspect this may be more uh for example, like a, a clinical photograph, a historic clinical photograph that's presented in an exam, um telescoping of the fingers and something called opera uh glass hand um which is where the soft tissue collects near the base of the digits because there's such a degree of erosion and it's uh named after the uh telescopic Opera glasses that people once had. Um It's a rather unkind name for that deformity. Um So the treatment of rheumatoid arthritis, um you want to, you want to um manage them according to an M BT approach. Um So nice guidelines have been updated in 2020. I have to say it's been a long time since I suspect any of us may have read about rheumatoid arthritis guidelines. So hopefully this will be just uh a good summary to just remind ourselves of what uh the updates are. Um They've introduced something called it a target, a treat to target strategy. So multiple dmards can be offered um one by one to achieve treatment targets. Um And the first line now is conventional uh dmards uh monotherapy. So, rather than com combining different dmards, um they're trying to introduce um just one, ideally within three months of the onset of persistent symptoms. Um and uh they may be bridged um with other treatments when they're starting a new, uh DMA. So, ideally monotherapy, but they may I introduce uh an, a second da if, if uh need to be. Um, and that bridging is usually with steroids. Um a step up strategy, a step up strategy is something that's been introduced as a term. So it's adding a another er conventional dmard when needed. Um So that's a favored over replacing um the these drugs with another type. So it's favored over sequential monotherapy. Um They believe the clinical out benefit is outweighed by a potential increase in a number of um side effects. Um And then there's also biological uh dos so, anti TNF drugs, um there's a whole host of them. Now, antiinterleukin one, which is Anakin one, which is a human recombinant interleukin one receptor antagonist. Um And then there's also some new drugs called uh antiinterleukin six monoclonal antibodies. Um And uh there's three of them at the moment. Um So just a word on Anakinra, it's a recombinant interleukin one receptor antagonist. Uh and it blocks the proinflammatory effects of interleukin one. It's a competitive inhibitor of interleukin one binding to the interleukin one receptor. Um But it's only recommended um for controlled long term clinical studies. So, uh they don't believe it should be a routine drug that's offered based on the cost analysis. Um and they wouldn't recommend combining it with anti TNF alpha. Um other medication that's used uh nonsteroidal antiinflammatories and selective cox two inhibitors. Um ideally at the lowest effective dose for the shortest possible time, use them with a uh protein P inhibitor. Um and they have potential gi liver and toxic effects. Um and just as an overlap for other areas where these may crop up. Um So, pharmacology, uh uh sort of pharmacological and uh so you may be asked to draw, for example, um exactly how er nsaids affect uh prostaglandins um and thromboxane synthesis. So, uh this is a pathway that's taken from Ramachandra. Um So, starting with phospholipids um which are then um converted into a aic acid uh and the peroxidases. And then you've got thromboxane, thromboxane prostaglandins and prostacyclin. Um uh corticosteroids affect and the lias and then you've got nsaids which uh may affect cox one and two or may affect cox two selectively. Um So I think just being comfortable with drawing, this may be quite helpful um as an add on to some questioning uh on rheumatoid arthritis treatment, um other, other avenues of rheumatoid arthritis treatment. Um Glu glu glucocorticoids. So, um short term treatment uh of rheumatoid flares. Um and er the current nice guidelines don't recommend them. Um long term only if uh all other treatment options have been offered. Um And there's a whole number of side effects for uh steroid treatment. So, um I think it's worth just being able to reel them off. Um, if asked. So, uh we're gonna just do some cases. Um If uh anyone would like to just tell me what they can see on this er clinical photograph, that would be great. Um I'm happy to take this mirror if no one else is thanks for. Um, so this is a clinical photograph of a 70 year old lady that seems to show an appearance of dropped fingers affecting the two digits. Um So that's what I can see in the photograph. I would obviously want to take a detailed history from the patient looking at their general um how long they've had this deformity for and how it affects them from a functional perspective. Um Looking at any systemic disorders or diseases that they may already have if they are known to be a rheumatoid patient already on medication. Um And also obviously their hand dominance and whether they um they're 70. So I'd expect them to be retired, but what their general hobbies were and their functionality at home in terms of activities of daily living. Um I then want to examine the patient. Um I'd want to look at whether the uh deformity was fixed or flexible. Um So passively, whether I was able to achieve full extension. Um I would want to see whether they had any active extension at all at the MCP joints and also look at the general movement affecting the P IP and D IP joints. Um I would want to look for any pain associated with it. Um as well as look for any features at the wrist, for example, a ulnar in this case, um or any other bony boss or prominence um that may have caused a nutritional rupture, for example. Um I'd want to have asked already sorry in the history about any trauma again, um to look for any sort of lacerations or indication of injury to the extensive tendons. Um and look for other sorts of differentials that may have caused dropped fingers. So again, examine the patient to check whether it could be a subluxation of the extensor tendons. So try and hold the fingers out into full extension and see if they were to drop back down suggesting a possible sagittal band rupture. Um So basically pinpoint what's going on. Uh But I think based on this, that this is possibly a Vaughan Jackson um case. So then I'd go down that kind of pathway. Yeah. And um what's your differential diagnosis? Um So apart from Vaughan Jackson, the differentials I'd have is traumatic extensor tendon injury, um arthritis, uh causing a fixed flexion deformity. I'd want to look also on the um palmar aspect for any signs of duress disease which could be causing an M CPJ contracture. Um and also neurologically as well, obviously do a neurological assessment to ensure that there was no neuro neurological compromise. Sorry, that was causing the drop in the fingers. Yeah, great. Thank you so much. Thanks for that. Um So um dropped fingers. So let me just move on to the next slide. Thank you very much for that Chrissy. So um dropped fingers, um your differential diagnosis, as you quite rightly said. Um So Vaughan Jackson syndrome, so ruptured um EDM um which is in the fifth extensor compartment or EDC in the fourth compartment. Um You may find it AAA really good sort of special test for that is the um tenodesis effect. Um So you'll find here that the tenodesis effect is disrupted. Um Another um sort of possibility is sagittal band rupture um uh caused by ulnar sublux extensor tendons. Uh So they'll be unable to actively extend their fingers, but they can maintain finger extension. Um If the MCP joint is passively extended, um because that uh relocates the extensor tendon um centrally. So they might not be able to uh a actively um extend their fingers. But if you put their um fingers in extension, you, so if, if um you relocate their extensor tendons, they'll be able to maintain them um pin palsy. Um So you'll find that the tenodesis effect is intact with that one. There may, there may be um radial deviation of the wrist um because uh a CRL would be intact. Um And that would cause um uh wrist, um extension and radial deviation. Um There may be some dislocation of the metacarpal fungal joint um which would need uh reduction in x-ray uh or it may just be a locked uh trigger finger. Um But as you quite rightly said, you want to do a full history examination. Um And then this is your sort of differential with some special tests to help you um just going back to potential drawings that you may be asked for. Um drawing the extensor compartments is a relatively simple thing. But I think in an exam setting, it's always worth having that at the top of your head. Um especially when you see this because uh it's easy to kind of um panic in, in that situation. So, um and and then classically which conditions may affect which compartment. So um just being able to uh just draw that would be quite helpful. Um And er as we saw um so it's er Vaughan Jackson is classically in the fifth compartment. Um And you may have this um honor to ra progression. So maybe in the history, they may say, oh, it was just um my er little finger that this happened to initially, but now I think my ring finger is gone. So um they may give that a history. So that will be another helpful thing to decide. OK, so we've just got a another case. Um Does anyone want to go for this one? I'm hoping everyone can still see, see this which should say case two. Obviously me, I wanna let someone else have a but if I was gonna ask, let me know and I can try and work. OK? Um It's like an A so going on then twice anyone there. OK. Well, pretty, I think you will have to do the honors again. So thanks for, thanks for, that's all right. Um So I can see a clinical photograph as well as a radiograph showing an ap and lateral projection of um a wrist as well as the proximal aspect of the carpus. Um On reviewing this, I can see that there's been a distal radius fixation. Um And as per soon's index, you can see that the plate looks fairly prominent. Um um not only above the watershed line but also kind of prominent on the volar aspect, which would make me concerned that there could be a potential for an FPL rupture. Um Looking back at the clinical photograph, this seems to be supported by the fact that I believe we're trying to get the patient to extend at the IP joint which they're able to do on the right hand. But on the left, they're maintaining a flex, a flex attitude at the IP joint of the thumb. Um So that would suggest sorry, we're trying to get them to flip and they were unable to do that on the er right side suggestive of af pl rupture um on the right um photograph. So I'd obviously want to take a history and examine this patient looking for any active movement, um as well as passively checking whether the joint was um mobile or fixed. Um as this would help with determining possible management options. Um And I'd want to see the chronicity um in terms of how long ago the fixation was and when they noticed um that they no longer were able to actively flex at the IP joint to once again help with management options. Um It would be important to determine from a history perspective, their functionality hand dominance uh because there is always an option to leave these and treat these non operatively if the patient found that it wasn't affecting them from a day to day, kind of uh activity of daily livings perspective or job perspective. Um But yeah, then it would have that discussion with the patient and if they wanted an operation, discuss with them, the potential uh tendon transfers that we could consider. Yeah. And just as a as a random guess how long after their fixation do you reckon they presented like this probably about kind of six weeks. So 4 to 6 weeks where they come back for their follow up. So 6 to 8 weeks classically, possibly because that's when we make follow up appointments for people, but well done. Yeah. So it's always tricky working out uh which side is normal, which side is abnormal with those um photographs because you don't exactly know what's being tested. So you have to work through and ask. But, um, as you quite rightly said, um, so we're suspecting an F pl rupture. Um And er uh this may be due to um, uh a, a scaphoid spur that has eroded through the volar wrist capsule, um or um a following volar plate fixation. Um, your differential would be um anterior intraosseous nerve palsy or it may be a trigger thumb, but that's quite unlikely. Um um And uh in terms of management options, um depending on the chronicity of the injury, um you may be able to um repair this primarily or, or a delayed um repair and that may be with an N 10 suture or an advancement. Um Looking for tendon grafts, palmaris Longus, it's a classic one, but not everyone has a um a Palmaris Longus. So, in this photograph, just here on onto this side, you can see that um just by asking the patient to put their little finger to their thumb, you can see whether they may have a um Palmaris Longus uh tendon present. Um other uh tendons are a um may be um useful in that case. Um And you may also consider doing tendon transfers um such as F DS of the fourth. Um and similar results have been achieved with grafts and transfers. Um So, uh case three, OK. Any anyone apart from pretty, I'm hoping you can see case three photograph there Yeah. Uh like I said, Mary, if you, I don't particularly, I just wanna give, if someone else wants to speak. I don't know if uh OK. II can't, can I see anyone else there? OK. You may have to take this, just go for it. Yeah, I can see a picture. Yeah. So um this is a clinical photograph of a 78 year old um patient who's right hand dominant. Um And we can see that we're attempting to perform a retropulsion um which they are unable to do with the right hand suggestive of a possible rupture. Um So I'd want to examine this patient, obviously take a thorough history, look for any indication of trauma that may have caused this such as a laceration. Also find out if they may have had, for example, a distal radius fracture that was managed non operatively as that can be one of the indications for any pale rupture or one of the causes, sorry for any pale rupture further down the line. Um And um after kind of taking this history from the patient, I would organize for any appropriate investigations. So, in this case, if I was suspecting that there was a pill rupture, I may get further imaging in the form of an ultrasound scan or even an MRI scan. Um And then once again, have a chat with the patient because they're 78 years old, discuss both non operative and operative management options. Um And if they decided that they did want operative intervention, um I would then discuss with them about possibly doing a ei to transfer. Um um But again, before determining that I would want to get a radiograph to make sure that there was no arthritis within the joint and the joint was supple on examination um to kind of obey our tendon transfer principles. Yeah, brilliant, excellent. Um So, uh so you, you, as you quite rightly said, uh rupture can be due to inflammation um and also just inflammation in rheumatoid arthritis. It may also be due to distal radius fractures, um and uh displaced fractures in particular. And again, we've got our um extensor compartment um drawings. Uh If we need to um show that um one of the classic parts of a vi may be then to uh sort of um outline which um incisions you would use for an E IP to E PL transfer. Um And how you would do that. Um So uh the three incisions that are described um um for example, in longitudinal um incision, um proximal to the extent of retinaculum, um and oblique um uh incision um over the thumb, metacarpal pharyngeal joint to identify the APL tendon distal to the rupture. Um and uh transverse incision over the index finger, metacarpal head. Um So you want to confirm APL is absent and explore around the list as tube cool. So that's you can do that through your first incision um identify that E PL stump at the thumb MCP joint um and uh identify uh E PL um which is usually sorry, that should say um uh E IP which is usually honored to the EDC. Um So here you can see E IP um is honored to the EDC. Um And uh you want to cut um EO P at the level of the index, anger metacarpal head and deliver it um at the extensor retinaculum level, um tunnel through the old line of E PL and deliver the E IP tendon through the incision at the metacarpal frontal joint. And then uh you can do a PVI taft weave um with a 40 PD suture. Um And I would say that there's a really useful video um by the writing group um which tells you about how to do this operation sequentially um which is quite useful. Um Also uh from the previous series uh last year. Um I think flexor, flexor and extensor tendon um injury, injuries were covered in the trauma term, which is also really helpful. So, um you can also go back and just have a, a look at that. Um Other things that we may find with the rheumatoid hand. So, um PIAs deformities. Um So P IP joint, flexion and P IP joint hyperextension, um it may be flexible or fixed. Um And the mechanism is that the head of the um proximal phalanx buttonholes through the extensor hood. Um usually due to essential slip rupture caused by sinusitis in this case. Um and there is vus subluxation of the lateral blood bands mirror. It's just stuck on the ei pe L transverse light. Yeah, that's it moved on. Sorry. Uh Thanks for reminding me. So, um just talking about the flexor and extensor tendon injuries from the last time. So it's useful to just go back and have a look at them um as a good reminder of how to manage them. Um And then we'll just go over the baton. So um other deformities that we may find in the rheumatoid hand um via is one of them. So, uh characterized by P IP joint, flexion and D IP joint hyperextension. Um It may be flexible or fixed and the head of the proximal phalanx button poles through the extensor hood um due to essential slip rupture caused by sinusitis. In this case, um There is var subluxation of the lateral bands um uh due to triangle ligament disruption. Um Elon's test is usually for acute central slip ruptures, but they may still ask you. Um So uh to describe how you would do the test. Um So uh you want to uh ask the patient to place the hand over a table. Um and then uh look at the D IP joint with resisted extension of the middle phalanx. So the uh D IP joint remains uh floppy, which is a negative test. Ie normal examination. Um and this indicates that the central slip is intact. Um And so they will try to extend the P IP joint and the lateral bands will remain slack. So the D IP joint will remain relaxed. Um If the D IP joint goes into rigid extension, this is a positive test which is an abnormal finding. Um and there is a ruptured central slip leading to a weak P IP joint and allowing tensioning of the lateral glands. Um This can be uh classified um uh according to the nail buffer me classification. Um it's a grade 123 classification which is mild, moderate and severe um for mild, uh there's a dynamic imbalance. So, uh the the deformity is passively correctable at both the P IP and D IP joint. Um and there is an extension lag of uh about 10 to 15 degrees. Um in moderate deformities, the contracture is not correctable. Um And you may see an extension lag of 30 to 40 degrees with severe um deformities. There is fixed selection of the P IP joint, um and contraction of the Bolar plate and the collaterals. Um the management um can be according to the um to the degree of the deformity. However, in rheumatoid, it's usually going to be a a chronic deformity. So, um cap splints may not be so um useful um but they may still ask you about that. Um Options for um rheumatoid patients. Um soft tissue reconstruction may not be very helpful um because there is there will be ongoing inflammation. Um so, lateral band relocation or terminal tendon releases may not, not be so helpful. Um And arthrodesis needs to be considered carefully for risk factors for non union. So, medication and um activity. Um Other deformities are swan neck again. Um uh So this is um characterized by uh P IP, joint, hyperextension and D IP, joint flexion. Um And there is an imbalance of forces um with the lax fo plate. Um The NB classification um describes this um as uh 1 to 4. So one is a flexible hyperextension of the P IP joint. Uh Two is intrinsic tightness is present. So the P IP joint flexion is limited when the MCP joint is held in extension. Uh Three, there is limited to P IP joint flexion in all metacarpal fungal joint positions, but the P IP joint surface is still preserved for there is stiffness of the P IP joint and with articular destruction. So, uh you want to manage these patients according to the grade, um you may, may send them um for a cast and splints. Um intra intrinsic releases, um volutin ades of the P IP joint, um or arthrodesis. Um Other manifestations of rheumatoid um pancarpal disease. So, there may be uh synovial proliferation and inflammation, um and ligamentous laxity and joint destruction and they, they may have end stage changes. So, autofusion um or you may see palmar dislocation um and ulnar translocation of the radiocarpal joint. Um and uh other conditions such as um dru instability um may be managed with um a number of procedures. So I know last week we talked about um uh so, so Kanji, um I think we'll talk more about those procedures in another session. Um So just to summarize in terms of uh treatment, um you want to approach this with an MDT approach, system history and examination, think about differentials at every stage. So um examination uh special investors, a special test to help you to reach that diagnosis um differentials uh during x-ray um and then uh management according to the patient factors and expectations. Um One thing to say just at the beginning um because I think we may have missed out this side um is um it affects 1% of the population. Um And um if you're diagnosed with rheumatoid, one third of people stop working within two years of disease onset. So I think that's really key to keep in mind that um especially if people of working age or um have to look after themselves. Um and they live on their own. This may, this can be a really debilitating condition. So it's really worth having those details when you, when you're thinking about management options. Um Thanks uh everyone, thanks Chris in particular. Um So I think we can go back to uh see if there's any questions and um happy to answer any questions or anything else that might have come.