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Good afternoon. It's Lucy mailing. I'm the outgoing Adam Brooks take hand fellow wrist pain on the side of this pain is common. Why? Well, this intentionally busy diagram shows that there's a lot of stuff in this area. Why is it so painful though, often more so than raided complaints? And that's probably secondary to its richly innervated soft tissues. Well, why is it so richly innovated as well? See, it has because proprioception is essential in this real construct because there's lots of stuff that can go wrong over here, it can be a difficult diagnosis to make. And hopefully by the end of this talk, we'll demystify this list into something that looks more like this. The FRCS and real life practice is all about generating structure out of chaos. So we'll classify the differentials into intracapsular and extra capilla. So bones and joints and the things that we're used to and then some other squidgy bits, I should add that there are many, many ways to skin a cat. And although I hate that phrase, it's become a running joke that I must shoehorn it into every teaching experience. So there you go, Mr Johnston, it's there. Um So let's go. We're going to talk about intracapsular pathologies first. And let's start with the bony infections, oc carpal abutment. So the ulnar normally takes 20% of the load from the carpus. In essence, it is the fibular of the forearm, the radius and the ulnar should be within two millimeters of each other in order for this normal distribution of load to occur. If the ulnar happens to be too long, either primarily because that's just the way somebody was made or secondarily to an issue with the radius, then problems can occur. Secondary positive ulnar variance can be from a problem during growth such as mad lungs or much more commonly due to a distal radius fracture, malunion with shortening. Now to make an assessment of the relative length, it is crucial to get a true pa view and this slightly grainy image shows how that should be taken. So the hinge should happen at the shoulder to 90 degrees of abduction with the elbow and 90 degrees of flexion and absolutely no rotation happening at the forearm level. This would of course give a false assessment of this parameter. So how do we treat it well? As always with hands, we start with conservative measures and these are Sympton Reef. If we're going down the surgical route, once we've exhausted our conservative measures, the question is between shortening the relatively long ulnar or lengthening the relatively short radius. And when would you choose each. Well, with everything, there are pros and cons to each option. But I would recommend the default as an ulnar shortening osteotomy. It's a reliable operation. It's easy. The patient doesn't need immobilization, but there is a role for radial ostectomy as well, particularly if this radius malunion has led to a 3D problem that also needs correction. For example, rotation that has interfered with the distal radius ulnar joint. There are other procedures such as the Wafer procedure where a tiny amount of distal ulnar is excised. The procedure where the whole ulnar head is excised, the where the distal portion of the ulnar was excised and the D I UJ fused into one bone mass and an ulnar head replacement whereby one can choose the length of the neck and head. There are other infection syndromes that can occur between the, the styloid and the trr. Um I've learned that this is more common in tennis players, presumably it's their backhand move. So they have pain on extension, ulnar deviation and supination hamate tri hamate. So this is golfers and radial ulnar impaction, which can be an iatrogenic problem after one of those aforementioned DRE procedures. And we'll talk a bit more about the D and why we hate it later on. Now on to some other bony pathologies. K book who is Kimber, he's actually not this guy on the bottom left. He was a radiologist from OSA. You notice that on a series of radiographs there were some quirky looking lunates. What is K UPS? It's avascular necrosis of the bone. But what on earth is vascular necrosis is rare though not in an exam setting. And it's a heterogenous disease. And these two facts mean it is very difficult for us to fully understand its natural history. It's been classified by Liman and this is something that does come up quite frequently in the M CQ. So it's worth having a look at that patients with P typically present with central or ulnar side of wrist pain. And they may point to the dorsum of their wrist when trying to localize it. What is actually causing the pain? Is it ischemia to the bone or infarction within the bone? Is it increased pressure within the bone? Is it due to sub collapse? Are you fractured? Is it due to the resultant change in the biomechanics of the carpus? Or is it due to the subsequent arthritis that ensues it could be any number of the above? And really, we need to try and drill down into what is causing the pain before we can treat the cause. There are infinity treatments proposed for the treatment of this condition which means none of them works very well. We start with simple things like rest and immobilization. You can decompress the urinate. Now, we're not sure whether this reduces back pressure and stimulates um revascularization or whether it's just the injury causes a human response. One can try to directly revascularize the unit by way of the 12 intracompartmental supraretinacular artery uh front. But if sed's dead, he's not coming back, one can unload the lunate. Now, these patients, unlike our abutment folk, they tend to be negative. So the luna is carrying too much load. So there are procedures to bypass urinate either by S TT or even by capitate fusion. You can just de innovate the area and hope for the best. And to be honest, this has the best evidence base. And beyond that, we're looking at salvage procedures. So the fact that there are multiple options tells us that none of them is ideal. So who is this person on the bottom left? It's Voltaire who wisely proclaimed that the art of medicine consists of amusing the patient while nature cures the disease. And I think he's probably spot on for this condition. Kook tends to have a symptom duration of an average of seven years though it can be highly variable. But essentially, if you can amuse and entertain your patient for that long, you might not need to do anything much more. What else can go wrong with the bones in this area? Fractures? So how many hip fractures um this is seen in people who um have a full on an out stretched hand more on the ulnar side or anyone who tries to use the heel of their hand as a hammer or orthopedic surgeons in other words. So you can palpate your ate about two centimeters northwest or northeast of your p depending on which hand you've chosen. And it should feel slightly unpleasant but not agonizing. Now, if there's a fracture there, the patient will be off the chair. Um, you can then ask for a car tunnel for radiograph, which looks like this middle picture and that's with the wrist hyperextended, looking through that carpal tunnel. Once you've diagnosed it, what are you gonna do? Just because you can fix it, does that mean you should, it's actually less painful with a faster return to activities including sport by excising it. Now, of course, we should try conservative measures first, but they are a bit notorious for no union. And I think that's because the ligament protection is constantly trying to, to go away. Poor fractures, not common can be treated with immobilization or excision as above and tr fractures over this side as well. These are typically a ligamentous ul and you get that Dawson flake that you can see on the lateral view. And that's because the extrinsic ligaments converge here. So, although the fracture itself isn't significant, it may represent a more interesting soft tissue wrist injury. And if in doubt, get an MRI moving on from bones, now they're remaining intra, we'll talk about your joints, the distal radar on the joint. I feel sorry to be on that. I think it gets a bad press. It gets blamed for carpal. So it's more, it's more likely to be the radius as well and it gets blamed for problems of instability. But the ulnar isn't unstable. It's a stable bone. It is securely attached at the elbow and it cannot rotate, it stays still once the radius rotates around it. So let's think about through instability, instability equals laxity plus pain. It is possible to be lax without having pain and that's not a problem. Some patients have pain and no laxity, they're not unstable. So what does keep the Jewish in place? Again, we're classified into primary and secondary stabilizers. Primary, we've got the TFC or triangular fibrocartilage complex, secondary stabilizers can be separated once again into static and dynamic ones. The static ones are the things that don't move. So the shape of the bones, the ec U subsheath more on him later and the interosseous membrane. So a more global forearm disruption such as a essex lepre um injury affects the druze as well as the pe dynamic stabilizers are the muscles immediately either side of that area. So the ec U in supination and pronatal quadratus in prom. And here we were thinking it had no purpose other than to get in the way of our radial plate. So you can see from this list that instability can result from an intracapsular or an extracapsular problem or a combination of both. Once we're here, let's take a deep dive into the TFC. It sounds complicated as it's comprised of this six item list and that's an exam favorite as well in the MC QS. But really, if you think of it as a hood over the ulnar head, then you won't go wrong when the ulnar wears his hood up, he keeps his head down. Oh, of course, the meniscal homolog second on this list down is just like the meniscus in a knee. It is a vascular central and that has an impact for its uh recovery potential. So this TFC ZH keeps the radius and the ulnar approximated, it protects the ulnar head from impaction by the carpus, but it facilitates rotation through an almost 100 and 80 degree arc. If there is injury or laxity of the TFC patients may have a piano key signed. So this is where the ulnar head looks prominent dose. And when you rest their forearm down on a desk, you can push the ulnar head down and it will ping straight back up again. It's important to test the stability of the distal radio ulnar joint in three positions. So you can a lot from dorsal to P in a neutral position. But it's also important to do this in super and pro nation. And you must compare it with the other side because there is huge variation. The dorsal stabilizers of the TFC should be taught in pronation and the palmar stabilizers should be taught in super. Hence, when you have a dorsal ulnar dislocation it's stable when you immobilize it in supination. And of course, we shouldn't think of it as a dorsal ulnar dislocation. It should be a palmar radiocarpal subluxation. How else do we test the TFC? Well, patients will have focal tenderness at the fovea. So if you just work your way along your own ulnar on the subcutaneous border, just as you get to the end, there's that little soft spot and it can be uncomfortable to press but it shouldn't be extremely painful. Uh You can do a TSC grind test which I don't advocate during in the exam, which is very uncomfortable and you can ask the patient whether they have pain or rising from a check. TFC injury is classified into type one, which is traumatic and type two, which is degenerative beware that up to half of over fifties have a degenerative TFC on MRI. It is a highly innovative piece of kit and this is why it's not injured more because it's actually quite small and flimsy, but it's extremely proprioceptive. Aside from MRI, one can use arthroscopy as a diagnostic tool and this involves the trampoline test and the hook test. There are all manner of treatments possible for TSC pathology. As always, we'll start with conservative measures and therapists quite often will supply a wrist widget or K tape or a monster splint which helps to limit some of the pro supination in the surgical realm. We've discussed arthroscopy which can be diagnostic and therapeutic certainty of tears are amenable to repair and just like in the knee, if they're in the red, red zone or more peripheral zone, they have a much greater recovery potential. A TFC injury may be part of a fracture. Um And in that setting, when they choose to fix an ulnar styloid fracture, you can reconstruct the DDI UJ stabilizers by way of the Adams procedure, which is where you take Palmaris, our favorite spare tendon graft in the world and you wrap it around in sort of figure of eight to reconstruct the dorsal and palm radio on the ligaments. You can perform an ulnar shortening procedure so that abutment is less of a problem and therefore pain reduces. And as before you can do arthroplasty. So we've digressed a little bit from joint to ligament, but it's difficult with the D IU to separate the two. So let's just get back to our joint issues. Sinusitis. It's common especially in rheumatoids and often responsive to steroids, arthritis. Now, this can be both rheumatoid and in the D UJ rheumatoid remember is a disease of Synovium. So it can destroy all the stabilizers that we just discussed and it can lead to instability with the classic prominent ulnar known as this as a folk might recognize the rings on the hand of this right hand image because this is in fact, my wrist, which sports one of the finest that I've seen. I'm sure you'll agree and it's good to understand your patients by having a selection of your own minor ailments that are seen in your practice. Um So do U arthritis also on examination patients will have pain on the radio, on the compression and especially if you compress the two together and ask them to pros, they really won't like that fawn Jackson syndrome. This is a subsection of bru arthritis which involves the overly of tissues, the extensor tendons glide right over the D IU. So anything that changes the changes the shape of the bones makes and craggy is likely to affect those tendons too. Historically, it was described as a consequence of rheumatoid arthritis, but it is actually more commonly seen in osteo now. And that's just because of the rheumatoid drugs um that have kept the physical destruction at bay for many. So extensor tendons rupture by a process of attrition at the site of the D I UJ and the most susceptible are the ulnar, most tendons. So that's EDM and number five followed by DC four and so on. So here's a question, why not EC in compartment number six, this diagram shows how the tendons in compartments, 1 to 5 are tethered by way of the extensor retinaculum to the radius. But the EC U here number six has its own sheath. It's tethered here. In other words, it dances with the ulnar. So when the radius is rotating all around the place, the EC U stays still and this is what protects it from Vaughan Jackson syndrome. Um, patients with Jackson syndrome used to complain that they couldn't drink tea with the queen but more accurately. Now it's the king and as a slight, as side. But whilst we're in this territory, I think it's important to cover this favorite exam question. What is differential diagnosis for a dropped little finger? We've spoken about Bourne Jackson syndrome or an extensor tendon rupture, sagittal band rupture can lead to a subluxation of the extensor tendon usually off the ulnar side. Now, in this setting, when you lift the patient's finger, they will be able to then actively hold it up. MCP dislocation can lead to a dropped finger and this is a classic rheumatoid presentation, pin palsy at the elbow. This is likely to affect more than just one finger, but you'll know that the Tenodesis effect is intact. So the tendons are all present and in the correct location and then don't forget pathology on the other side, masquerading as a dropped finger. So anything that causes a flexion contracture such as um is is on your differential list and don't forget, trigger fingers as well. Treatment of through pathology as always pro the underlying cause. Acute instability often follows a distal radius injury and restoration of the bony anatomy will suffice in re stabilizing that joint if not consider the primary and secondary stabilizers. And which of these were meant to be repaired if they are irreparable or the injury is chronic or the patient has poor collagen, consider reconstruction with the Adams procedure. This is where we fashion a figure of eight using long synovitis. We mentioned took a steroid injection and then arthritis. These implants here are two options for joint replacement in this area. On the left, we have the the head of prosthesis, affectionately known as the Herbert and on the right, we have the uh total DJ replacement, um known as the ACTIS or the sheer. After the surgeon who designed it, the form is easy, it's reliable and it has good survivorship. The arthroplasty on the right arguably has a super learning curve and because it's more complicated, more could potentially go wrong. And I'd advise you to use this with caution because the surgeon who designed it claims that he's never had any complications with it at all. Not alarm bells to me in the middle, we've got the medieval Dre procedure which might feel like you're treating the problem. But remember that the ulnar is a stable post. So if you take that out, you can end up with all sorts of instability and that is painful. Um Finally, there's a Swapan option, which is a distal radioulnar joint fusion with an ulnar neck resection. So it's the same problem as the DRE before, but it's more complicated. So, really don't do this for Vaughan Jackson syndrome. We need to treat the underlying cause as well. As consider the soft tissue reconstruction of these tendons and often just buddy them to the next door neighbor will suffice on to some other joint pathology. Carpal instability. I won't go into great detail here because it's a whole lecture on its own couple in stability can be classified as non dissociative and dissociative. The former includes the midcarpal instability. So this is essentially a kinematic dysfunction on on the deviation. And it's one of those party tricks that certain spending people can do a dissociative instability is where neighbors dissociate. So it's bones within the same group. So you may be familiar with the scun association, but that tends to be more uh central wrist pain. So for this talk, we're looking at the lunar dissociation to test this, you can blo the lunate against the triquetral and this will feel wobblier than the contractual side and will generate pain. If this is injured on x-ray, the patient may have a Visy deformity. Remember the scaphoid is Arnold Schwarzenegger, it always wants to flex. So that must mean the triquetra is the opposite. It always wants to extend, both want to take the lunate with them and usually neither will win. And that's why the lunate sits in a neutral position. But if the lumen ligament is lost, the scaphoid wins and the lumen flexes with it busy is actually reasonably well tolerated because patients are still able to extend their wrist and extension of the wrist is its functional position. Uh an exam M CQ that often comes up is asking which portion of each ligament is the strongest. So ate is strong dorsally, meaning the L must be the opposite. It strong on the palmar side. What else can go wrong with joints around here, we can get arthritis at the pisotriquetral articulation. And this a bit like with thumb base oa is common in older females with a lifetime of laxity. I'm not sure what the official test is called, but I call it the wiggle test where you essentially let the patient's uh wrist flex um to detention the FC and then you just grind that Pisa form up against the bone from side to side. And if it's particularly symptomatic and steroid injections aren't doing the trick, you can excise it. The pisiform is a border of ions canal. So we must be aware the arm clockwork if we're going into it, poor translates as P shaped bone. But in this condition, it actually becomes more of a bowler hat as the articulating surface grows a rim of osteophytes. And that explains the difficulty in cutting out, cutting it out and the relative ease of neurovascular injury. Um when it looks like it should be so straightforward to shell out. Finally, chondrocalcinosis. So, calcium pyrophosphate dihydrate deposition, it commonly affects the T FCC and not infrequently, the Jewish as well. If you ever see isolated S TT arthritis, that's really quite specific for CPPD. By the way, there is no cure for this condition that crystals don't dissolve and treatment is symptomatic or salvage for the ensuing arthritis that some will develop. Ok. We got in there. Let move on to extra capsular issues. It's OK. We're getting there. We've covered intracancellous pathology. So let's move outside the joint and look at some extra capsular issues, tendinopathy. The ec U can present with tenosynovitis, instability and much less of rupture. We've seen earlier that the EC U dances with the ulnar whilst the other tendons move around with the radius. And this is why it's safe in Jackson. But to test an unhappy ec that may have, you can do the synergy test. So ask the patient to contract their APL against resistance and they will inadvertently have isometric ec contraction and this causes pain for instability of this area. It's the ec subluxation test. This is another common party trick. Essentially, it's the ice cream scoop test and people will know if they can do it and they'll say, oh, I've got something that pops in and out over the ulnar head. It's usually not a major issue. Um So it can be managed conservatively, you can leave it completely alone or you can try out a period of immobilization and therapy. Um It can be repaired the EC U subs sheet and failing that it can be reconstructed using a sling made from the next or um extensor retinaculum, the ec subsheath, by the way, just refers to it being sub or beneath the main extensor retinaculum. So it's still over the top of ec and this confused me for ages. So hopefully, it's provided some clarification and finally rupture, I've never seen it. Um But if it happens, we've got our friend Palmaris Longus who is always willing to provide a reconstructive graft. The ulnar nerve can be a source of risk. It has two popular sites of compression. Those being the cubital tunnel at the elbow and GS canal down at the wrist. How might one differentiate the two sites of compression from a sensory perspective? The dorsal sensory ulnar nerve will be spared in Guillain canal but affected in cubital tunnel. It comes off at the distal quarter of the ulnar and it tends to cross over just around the ulnar styloid level. From a motor perspective, we have to check when the FDP to bring in little. And the FC have been denoted and as a cubital tunnel sur fiber, I can tell you that I knew exactly where my nerve was compressed and patients will often feel uh that and describe it. I'm sure some of you can relate 6% of orthopods have this, which is twice the general population. I'm not sure whether it's all that time spent holding retractors with flexed elbows. But if in doubt, neurophysiology will help locate the site and it's useful for prognosticating too. So let's talk about a favorite exam topic. And that is the paradox. It seems to tie people in knots and it's not rocket science to understand, but it is surprisingly difficult to articulate. I think. So, feel free to or this um or not, you may have a more concise um description that you can reel off yourself. But this is 11 explanation. So the ulnar paradox describes a more clawed attitude of the hand with low lesions due to the preserved, unopposed action of FDP for the ring and little fingers, not the term attitude or posture, not deformity. Hand surgeons prefer the form high lesions, take out the intrinsics and the extrinsic. So that means the lumbrical which do finger extension and MCP flexion as well as the FDP. So, although more muscles are taken out with a high lesion at the elbow, the overall appearance is less noticeable because there is a balanced loss intrinsics plus extrinsic. So the paradox describes a more clawed attitude of the hand with low lesions due to the preserved, unopposed action of FDP to the ring and little the end claw attitude. By the way, describes finger flexion as well as MCP hyperextension. The lumbar claws are MCP flexors and finger extensors. So if you take them out, the opposite will ensue without the MCP extension. It isn't through ching. It's just a fraction deformity or attitude I should say. Um and going back to the perfectly correct terms, I'm sure the word claw is due a rebound any day now. But I digress the treatment of nerve compression is to decompress that nerve. Usually these are the possible signs of compression at the elbow. Historically, a giant incision would be made and all of these factors addressed. But there is a school of thought that simply doing Osborne's ligament, the the most common site of compression is sufficient in the vast majority. The more you unzip, the more you risk devascularized the nerve, which could actually exacerbate the problem. The next question should you transpose? So that's from brain, the nerve from behind to the front. And if so, should that be under the skin under the fascia or under the muscle? I would advocate only doing this for proven nerve irritability or instability. So you tested on the table by flexing flexing and extending the elbow and seeing whether the ulnar nerve pins around over the medial upper condyle. I also suggest only ever doing a subcutaneous transposition because fascia and muscle to me are new sites of compression. Surely an alternative to that is by shaving off the medial epicondyle. And proponents of this procedure will say that it creates a more gentle path with less risk of tethering. But of course, it causes some burning bleeding and this might irritate the nerve lead to scarring. The jury is out over which is better. But the latest literature recommends a simple decompression as first line for cubital tunnel, it can be done widew under local anesthetic without a to but a prerequisite is that the patient must have mobile shoulders and be able to externally rotate. Um One alternative to this is to have the patient supine with the elbow across the body. Um And I know elbow surgeons prefer this because the scar ends up a little bit posterior, which is less in the way when you're leaning. But the downside is that as a surgeon, you'll have to stand up, which is uh not our style as having surgeons. It's important to counsel patients that the outcomes for cubital tunnel release are less good than for carpal. There may be a greater physiological component to pure mechanical compression and the compression site is much further than the nerve's final destination. An alternative, more exotic site of compression is Eon's canal. Consider a space occupying lesion if you have compression here because when you go in and find that palmar carpal ligament, which is the roof, you will be so disappointed by how flimsy it is. It's so underwhelming. You can't comprehend how that could possibly cause compression. You incise this and you will see two branches of nerve sitting atop the transverse carpal ligament, which is the floor of canal. And you might assume that one is motor and one is sensory but no both are sensory. The motor branch comes off on the under surface and you will not see it unless you go looking for it. And this is actually often squashed within the fascia of the hypothenar eminence. So you really must go deep to find it and free it and that releases much more. Whilst we're here. Why is the magnitude of double crush? Now, double entrapment syndrome greater than the sum of its part. It's due to the interruption of axonal transport, not just at a single site of compression, but in the entire length between those two sites. So that entire section of nerve from elbow to wrist becomes pathological. It can't import nutrients and it can't export metabolites and for vascular, not very common but may in exam, hypothenar hammer syndrome, rare in the general population, but perhaps overrepresented by orthopedic surgeons who prefer to use their hand as a tool. And it is defined as a posttraumatic thrombosis in the ulnar artery um in the hypothenar area. But some will use it to describe an aneurysm in this area as well. And of course, it may be a false aneurysm as a result of that trauma. The ulnar artery is the main contributor to the superficial palmar arch and this supplies the digits. So patients may present with ischemic sounding pain, um affecting the digits and that's not always very nice. So just keep it in mind. So we've done a deep dive into the various anatomical causes of side of wrist pain. And we've classified them as interim and extra capsular on any list of differentials include infection and tumors I haven't gone into these specifically here, but of course they can happen, aim to find the pain generator and then focus on treating that as with all things, hand start conservative and work up towards more jazzy options. I hope very much that this has been useful and I'll have to answer any questions. Thank you.