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Done a great job of organizing a very comprehensive program to talk about three conditions, ankylosing spondylitis dish and kyphosis. So they, they're all quite broad things. And um I don't want to sort of dwell too heavily on any of them. I just want to give you the basics for day to day orthopedics and mainly the FCS or um I think I'm in my penultimate year as an examiner. So a lot of this stuff might be more than you need. Um But hopefully it'll be more than enough. Um So the first thing I wanted to talk about was um ankylosing spondylitis, an axial spondyloarthropathy or spondylarthritis. This was a review article that might be, you know, if you had to read one thing, this was in the New England Journal of Medicine, um not too long ago and it's to do with Ank spon, ankylosing spondyloarthritis. And um uh one of the things that will be evident is that if you look at the characteristics of inflammatory back pain, it's in young people, it's been going on for more than three months. So it's more than a muscular strain. It's frequently associated with early morning stiffness and it tends to get better with activity, uh, and doesn't get better with the rest. So this is quite an important thing to when you get, uh, uh, when you, if you get a back pain in your, or you see a patient in clinic, what you want to do is ask them about early morning stiffness and, and whether or not paradoxically the pain gets better with exercise, you'd appreciate that mechanical pain will get worse with activity, um or with exercise, inflammatory back pain improves with exercise. Now, if you think about it, an orthopedic surgeon is unlikely to see somebody um with acute um inflammatory spondylarthritis, a young person in your clinic with back pain that's not getting better. They've got early morning stiffness and their pain gets better with activity. Think about an inflammatory spondylar arthropathy. I've tried to sort of take some bits off of this paper that I think are really helpful and um I've taken them out word for word because I think in your mind you have to have a simple concept of inflammatory disease of the spine in both rheumatoid arthritis and ankylosing spondylitis, bone is a target of inflammation. That's a really fundamental concept, isn't it? Both rheumatoid arthritis and ANK spon is associated with bony inflammation. And that second paragraph's important uh activated immune cells at the sites of the inflammation in the bone produce a wide range of cytokines which lead to bone resorption in ankylosing spondylitis and rheumatoid arthritis leading to bony erosions, osteitis and peri inflammatory and systemic bone loss. So, that's a really fundamental concept. Both R A and A S is associated with bone inflammation and localized bony erosion and osteitis. So, here's some examples from that paper from the New England Journal. I think that's a foot maybe with some er, inflammatory er changes. These must be fat, saturated. T two images mustn't they? Here's the, er, sacra ala and here's the er end the, the front of the inter disc. So, osteitis is the common endpoint of both rheumatoid arthritis and ankylosing spondylitis. But here is the fundamental difference. Peri inflammatory new bone formation is impaired in rheumatoid arthritis and that causes non-healing erosions and that leads to a vicious cycle of bone loss and osteitis. So, in other words, in rheumatoid arthritis, the inflammation is associated with impaired new, impaired new bone formation. By contrast, peri inflammatory bone formation is increased in ax bod and we don't know why and that leads to healing of the erosions ossification of the enteritis and potentially ankylosis. So, the underlying fundamental pathology is inflammation, but the reaction of the body to that inflammatory response differs in rheumatoid arthritis and ankylosing spondylitis. That's all I know about this. This is all I needed. Uh in terms of my understanding, I, I don't think we need to know very much more. I think we do need to know about this concept of the rank L the receptor activator of the nuclear factor. Kappa B ligand. No, nobody can remember all that. But if you're in the exam, somebody presses you and you're doing well. You, you've done, you've got a six and you're heading for a seven, they might say what, what, um you know, what sort of um molecular level um concepts are you aware of? And the rank L ligand I is believed to be er crucial in coupling osteoblastic and osteoclastic activity. I think that's all you need to know. Rank L stimulates the differentiation and activation of osteoclasts. And in all these pathological processes, there's an imbalance between new bone formation and bone resorption. Um This paper from arthritis research and therapy is a nice little summary. You can see that uh you have uh osteitis uh both in rheumatoid arthritis and ankylosing spondylitis. And um on the left side of the diagram, you can see that in rheumatoid arthritis, you get synovitis and cartilage degradation. And on the right side of the diagram, you can get periostitis, enthesitis, syndesmotic formation and bony sclerosis. So, on that side of the diagram, you're talking about the effects of ankylosing spondylitis. Um I'll just pause there for a second. II, I don't have any detailed molecular knowledge of these conditions. But does anybody have any questions or comments about what they understand the difference between R A and A S to be any, any useful input or do you think that's a, a fairly reasonable summary. Seb I'll pick on you. Um So, I mean, from what I, what I've seen is that R A is primarily focused around the, um the main limb joints as well. While a spontan focused around the um sacra IACC and um lumbar spine region. Yeah, the axial skeleton. Yeah, that's a good point. That's a good point. Um All right. But in terms of the pathophysiology, I mean, I think it's probably safe to say osteitis, bony inflammation, enthesitis is a common feature of both diseases, but it's the body's re re re uh it's the body's response to that that differs in Aon and rheumatoid arthritis. And I think that's the only point I was trying to make. Ok, let's move on. Uh So having given that as a little bit of a background, um this is, you need to have a vague idea of the classification of spondyloarthropathy. Um and the broad classifications are uh with radiographic sacroiliitis, you have um axial spondylarthritis and then you have the other conditions like psoriasis, reactive arthritis and inflammatory bowel disease. You, you just have to have that as a differential. So, I if you get asked by the examiner, here's a young person with back pain. You think it's of an inflammatory origin? What are the things you're thinking about? Have they got psoriasis? Have they got inflammatory bowel disease? Have they had a recent infection? Um or er other features typical for sacroiliitis and ankylosing spondylitis. Um This comes up again and again and um overly so I think this concept of osteophytes, which are these horizontal marginal outgrowth of bone shown on the right and Syndey which are vertical, er, flowing er overgrowths of bone, er, which are present in ankle closing, spondylitis, um of necessity. Um The talk is short but um we can talk about uh this uh when you guys come to our clinics, but what I wanted to say is more often than not, it's not the young person with back pain that presents to the spinal surgeon. It's the ankylosing spondylitis patient with a broken spine or the deformed spine. So, here's an example, there's C 234567, there's a fracture through the super end plate and through the middle column of C seven, exiting through the poster elements. And you can see on the plain radiograph that the fracture is not evident. Um There is an adage that we say to you guys all the time. If you have a patient with a bod with any magnitude of trauma with new onset spinal pain, beat in the neck, thoracic or lumbar spine, they have got a fracture until proven. Otherwise, er you plain x-rays are largely useless. So we use CT and if necessary MRI. So this CT scan shows a three column fracture involving the C seven vertebra. These are very common following low energy trauma in people with the A with an ankylo spine. This is treated typically by long segment, posterior stabilization. Although sometimes we use an anterior approach. Here's another example of an anterior column fracture in a patient who fell, had walked around with pain in his thoracic spine for many months before he came to A&E and on the x-ray on the left, you can see the the void, the sort of gap in the Antero longitudinal ligament ossification and it's even more evident on the CT scan. So the moral of the story is the spine is fractured until proven. Otherwise, it always is. Here's another patient with an ankylosing spondylitis picture who had a fall presented with what er very low energy trauma. Again, the plain radiograph looks completely blameless and you can see on the CT scan, this is a highly unstable three column fracture which required a poster stabilization over a long segment. Uh And the last point I wanted to make about fractures is that although patients um may present acutely, quite often, they present late. Um This man presented with uh you can see that he's got ankylosing spondylitis, he's got a fracture uh involving the uh lower cervical spine and most unwisely, um I decided to try and treat this non operatively with a halo. Um uh I think he was resist resistant to surgery and he wasn't particularly fit and watch what happens to this fracture at presentation at follow up in the halo and at further follow up in the halo. So he's gone from having a spine that's at about a 30 degree angle to the horizontal. I know it's parallel to the floor. So he's lost all his forward gaze uh like any other uh orthopedic problem. Uh We treat uh how would you go about addressing this or what you do is you put the patient on traction and you gently realign the head over the course of a week. You take the patient to theater positioning, patients with ankylo spondylitis is extremely difficult. You can see Bob Crawford on our retired colleague in the picture, er he was a master at setting up these operations and here we've um partially realigned the spine. You can see he still has quite a lot of um protraction of his head, but we've realigned the spine. So at least he's looking forward and this is him er in recovery. So the principles are um if the pain, if the spine, if the patient has pain in the spine, in the context of an ankle or the spine is fractured and it us and it almost invariably, not always but almost invariably requires surgical stabilization with long fixation and failure to do so can lead to a progressive deformity. Any questions on trauma in ankylosing spondylosis before we move on anybody at all? Um Mr Lutchman, do you always, so do you image just the um area that's affected or you go whole spine every time for these types of patients. That's a really good question. So I, I think what we tend to do is we um we try to image the whole spine. I've only shown representative pictures. Um But what we try to do is we'll get a CT scan of the affected segment. And when we get the MRI scan, we'll ask them to sculpt the whole spine because sometimes you're quite right, you can miss fractures at other levels. but that's an excellent question. So yes, always think about the whole spine when people you can, you can you effectively end up with a segmental fracture, don't you? You can have a fracture of the cervical spine, mid thoracic spine. And therefore you have like a femoral fracture. That's segmental, you have a spinal fracture, that's segmental, that's a very good point. Well made any other questions or comments with this case that you've presented in mind? Um Do you now treat like 99% of his operative then? Yeah, they, they have to be perfectly aligned. Um If there's any deformity, the reason this failed Mike is because if you look at where this guy's head is starting relative to the axis of weight bearing. When I put him on a halo, the halo is not acting through the weight bearing axis of the spine, it's acting anterior to the spinal column. So it therefore you're never going to achieve a realignment of the spine. So unless the patient has normal sagittal alignment, which is very unusual in ankylosing spondylitis or if they have a, um, an undisplaced fracture, I think that thoracic fracture that I showed, I think we treated that non operatively because he presented sort of months down the track and eventually it did heal. But in answer to the question in the exam, er, say there is an extremely low threshold for surgical treatment and in fact, surgical treatment is the preferred option unless there's an absolute contraindication to not doing so quick question. Um 3 60 versus posterior only. Yeah, that's a good question. So in, in all the cases that I've treated and, and I've treated dozens over the years, I've treated patients with posterior long instrumentation. I follow up with CT scan and I've not had any fail from a, from a lack of anterior support. The bone does fill in the healing potential is, is not any less than the a one patient people have a saying, don't they, they make bone for a living and, and I have not had a requirement to go anteriorly, but that's a good point. You need to follow these patients up and if there's evidence of a mechanical failure of your instrumentation, you need to do an anterior supplementation. The difficulty is anteria is often difficult, isn't it? Hasan because they're quite kyphotic. So getting anti access can be difficult. But again, that's a very good question. OK. The, the other reason a, a patient might present to a spine surgeon who has ankylosing spondylitis. Um again, we don't tend to see them acutely, but you can, you tend to see them at fractures and you tend to see them at deformity. So this is a patient who has a thoracic deformity. You can see he has a loss of his forward gaze. He went, underwent a posterior closing wedge osteotomy, a thing called a pedicle subtraction, osteotomy of C seven. And we realign the spine as you can appreciate, this is quite sort of high risk surgery. Um The colostomy III I hasten to add what preexisting and um um but what you the principle is is like you would treat a femur or tibia, you create an osteotomy and you realign the bone. Uh In this case, it just happens to be intertwined with the spinal cord. So you need to do it carefully under monitoring. So, deformity and fracture, that's before and after that leads me on to dish. Um This is a paper probably worth reading. Um It's a narrative review of conditions that mimic ankylosing spondylitis. Um You can see think about inflammatory bowel disease. There's an interesting fact that I didn't know that about 20% of patients with inflammatory bowel disease present with inflammatory spondyloarthropathy as the presenting symptom and they don't develop their bowel disorder. Uh until some months later. So 20% of people might have an initial presentation with spinal pain, uh and subsequently develop uh bowel symptoms, uh psoriatic arthritis, the prevalence is on the uh reactive arthritis and uh certain metabolic disorders can lead to inflammatory spondyloarthropathy. Um I won't dwell on this side, but again, it's, it's a paper possibly worth having a look at. It. Talks about the different clinical manifestations. The, the one we're most interested in is the one in the second column, ankylosing spondylitis, enthesitis is common, peripheral arthritis, including the hips and knees is common. It's associated with HLA B 27 but that's not universally positive uveitis is common, but nail and finger changes are uncommon. There's uh an increased risk of psoriasis and inflammatory bowel disease in patients with a bond and you can have decreased chest expansion and cardiovascular complications. That's the one that you need to know most about. Um there's a paper by this guy, um which I found useful and, and basically for the exam, you need to have some definitions. What's dish dish is a bone forming disease characterized by new bone formation in the axial and peripheral skele skeleton. But in the absence o of inflammation, uh this is believed to be a noninflammatory condition. It can be asymptomatic or it can present in a couple of ways which I will talk about in a second. But like I said, it's considered to be a non inflammatory condition that's debatable. Um But I think if you had to have a definition that separated from a bond, that's a useful way to look at it and this is from that same people and it's quite an interesting um series of pictures. These, they talk about the radiographic criteria set by somebody called Reni um and going from left to right, let's talk about these, these ct scans, the extreme left picture shows these very coarse overgrowths of bone and they're largely horizontal and there's a cleft between the vertebral bodies and this so called osteophyte or excessive bone. And that's typical of dish diffuse idiopathic skeletal hyperostosis. The middle picture is ankylosing spondylitis where there are these smooth vertical flowing um overgrowths of bone and there's obliteration of the disc space that's typical of ankylosing spondylitis. And the picture on the extreme right is what advanced spondylosis looks like. There's narrowing of the disc spaces but they're not fused and they are a horizontal overgrowth of bone um osteophytes er rather than sn desma phys. So left to right. You're looking at dish ankylosing spondylitis and spondylosis. I think AAA lot of people get really hung up on that. I think it's good to have a basic idea. Um But actually the principles of management for Di and Axon are very similar because bear in mind they're coming to you with deformity and with fractures. So, um Tom Barker and MS cartoon and Mr Gill wrote up a case of ours where we had this patient with what looked like dish, these massive Antero osteophytes and dysphagia is a recognized complication where the, you have these anterior overgrowth of bone. And that picture on the top right shows the osteophyte as access to an anterior approach. And on the left is the preoperative x-ray. On the right, the postoperative x-ray. So what we did was er barium swallow confirmed that this was the level of the um dysphagia and resected the osteophyte and he had a good result. So when you look at the papers, one of the ways this presents is with dysphagia. Another way it presents is with pathological fracture, just like ankle losing spondylitis. The spine is brittle and prone to three column failure. Uh And this is one of my patients. Um you can see on the top left hand picture, uh I'm not sure if this is dish or there's an element of a bond or whether or not there's an element of just age-related, degenerative change. And you can see that it's quite difficult sometimes to characterize accurately. But the principle is this is an ankylo spine with a three column fracture and it requires long stabilization typically posteriorly, sometimes anteriorly. Uh that's all I want to say about dish. Really a anybody have any questions or comments about dish, er their experiences and things they might have come across anyone at all. OK. So we'll move on now to degenerative kyphosis, which is the last topic that Mr Steele wanted me to cover and humans have evolved, evolved to be er bipedal mammals. Um But what happens as we get older is there's a failure of the spinal column and a tendency to become quadrupeds effectively. What you do when you walk with a walking frame, if you walk on four limbs and degenerative kyphosis is exactly that. If you look at the normal well balanced spine, you have a lumbar lordosis, a thoracic kyphosis and a cervical lordosis. And the spine is balanced by which, I mean, the head is above the pelvis. As we, if you look at the normal parameters of the spine, the one I want you to remember most is the one on the extreme left, which is called the sagittal vertical axis. If you drop a line, a plum line from C seven down, it should fall into the sacrum. And what happens as we get older and become kyphotic is the sagittal vertical axis becomes increased. And you can see that typically it's less than five centimeters. But I'll show you some cases where we see degenerative kyphosis leading to an increase in sagittal vertical axis. So here is the balance spine. And you can see from that picture on the right, what it means to have a balanced spine. It means that the uh line of force of the trunk goes through the middle of the pelvis. And that's er biomechanically the most efficient system as the spine becomes kyphotic. And you can see here, this person has a lumbar lordosis of 46 degrees and the sagittal vertical axis is 33.5 centimeters. Although they have a scoliosis, this person was relatively asymptomatic. We find that the main determinant of symptoms is the sagittal alignment, not the coronal alignment. So the scoliosis isn't the main consideration. The main consideration is the lateral picture is your head over your pelvis in the sagittal plane. So what happens as we get older, your head and is tipping forward your thoracic spine is becoming more kyphotic. Your sagittal vertical axis is increasing and you're becoming more decompensated. And here's an extreme example where the patient's lumbar lordosis is four degrees. Typically, it should be 50 to 70 degrees and the sagittal vertical axis is 24 centimeters. So this person's head is way way in front of their pelvis. And what that means is the energy expenditure for ambulation is considerably increased and the patient fatigues and experiences pain. So, here's an elderly person, their sagittal vertical axis is 10 centimeters and the head and weight bearing axis is anterior to the spinal column and increases the moment arm acting on the spine considerably. So why do we get kyphotic as we get older? We lose lumbar lordosis because our disc heights diminish, we get vial insufficiency fractures and our extensor muscles become weaker. We develop spinal stenosis and we have a tendency to stoop forward. We get lumbar facet arthrosis which causes us to lean forward to relieve the pain and that leads to a vicious circle leading to progressive uh lumbar kyphotic deformity. So this is, this diagram is a nice one that shows what happens when we age. You can see on the extreme left that's normal healthy balance. In the middle picture, there's loss of the low doses, but we compensate for that by retroverted the pelvis. And if we get lot further loss of lordosis, you then have to um retroverted your pelvis and flex your knees. And you can see you get hip flexion uh and that can lead to a contracture. So when you're asked to assess a patient with a spinal deformity, never, don't forget to assess the hips because the hips is part of the overall balance of the patient's posture. So here's some examples, some surgical examples. This is a patient with lower lumbar lordosis. It's now 10 degrees. They've got a pelvic tilt. We'll talk about these things when you come to clinic. But the sagittal vertical axis, which is the one I keep asking telling you about is 18 centimeters. It should be less than five. So this person underwent a poster lumbar antibody fusion and a pedicle subtraction osteotomy. Again, it's a closing wedge osteotomy. And what we've tried to do is to realign the spine. This demonstrates a really common complication of this type of surgery, which is this person developed a proximal junctional kyphosis. The upper part of the spine has become very kyphotic because it's trying to get back to where it started. But this patient had a good clinical outcome and their uh standing alignment was much improved. This is how we do it. This is the patient on the table. The picture on the right shows the spine exposed proximally and distally. And you can just see in the middle an osteotomy segment where the quina and thecal sac are exposed. And then we do a closing wedge of osteotomy. Again, you can imagine that's quite harrowing and carries a risk of neurological injury. Here's another example, using a different tactic. This person has a lumbar lordosis of minus 11 degrees. So they've got an 11 degree kyphosis, they're not lordotic at all. And Mr Khalil helped me do this operation. We did anterior lumbar antibody fusions. You can see some screws in the front of the spine at um L2, 334145. And by releasing the anterior longum ligament and doing an opening wedge osteotomy, we were able to realign the spine. Um And again, he had an excellent clinical outcome. His sagittal vertical ais went from 25 centimeters to four. The complication rate for this operation is 40% 40. This is the patient preoperatively and post-operatively. And you can see a lot of these patients are overweight and you can imagine that mechanically. Yeah, sometimes you're fighting a losing battle. Uh Finally, I would draw your attention to this er bit of this chapter in this journal that Mr Steele and I contributed to he and I wrote about inflammatory conditions of the spine. It's an orthopedics and trauma and we've done a section that covers most of this material. You need to come to clinics, you need to see these patients and we need to talk about them. But I hope I've given you an overview of how we approach these people. And I'm happy to take any questions is the sagittal vertical axis, something that you can only measure measure radiographically or is it like limb length discrepancy where you can get like a ballpark measure in clinic or do you need xrays and do it properly? Yeah. So, so you, you get a really good impression clinically, Mike when you see the, when you, when you drive to the, when you drive down the road, you see these people walking to the shops, don't you? They're walking on the walking frame, they're leaning forward and you get a really good appreciation that what you're dealing with there is somebody with a sagittal imbalance and, and that can be multifactorial. They might be bending forward because they're stenotic. So, you know, when you have stenosis in your lumbar spine, you bend forward, they might have facet arthritis. So instead of standing up, right, they lean forward, uh and they might have extensor muscle weakness. So those things will be passively correctable, won't they? Then you'll have the structural aspects of it, the disc height loss, the, the fractures and the ankylosis of the spine. You know, sometimes you get auto fusion with the spine, the lumbar spine in kyphosis. So there'll be passively correctable postural elements and there'll be structural elements, but you get a really good impression in clinic. Um And um you get a, you have to do radiographic. The reason I do radiographic parameters we all do is if you're going to do an operation, if you're going to do a hip replacement, you take an x-ray to make sure you've got the stem down the fairway. It's not in Varus, you've got the hip center in the right place. So really, you have to have a surgical target, don't you? So we, we measure all these parameters, the sale vertical axis, the pelvic incidence of pelvic tilt and the sacral slope. And those are the things that you're aiming to improve in, in very advanced units where they, they have a lot of money to throw at it. What they do is they prefabricate a rod with an idealized correction. And what you do is you break the spine and realign it to the idealized rod. What we do is it's sort of, you know, typical sort of British orthopedics, you kind of fly by the seat of your pants. But the, the, the, the, the tendency now is you have preplan software, you work out what your osteotomies are going to achieve in terms of an angular correction and an S va correction and you, you send off the the details to a, a manufacturing facility with pre-op cts and x-rays and they manufacture a prefabricated rod for an idealized correction. Um Navigation kind of comes into that as well because with modern navigation systems, you can pre you use preplan software to help you execute the operation. Um So I think that's, that, that's, that's the direction of travel. Answer to your question, you get a really good impression. So when you're in the exam and you see this woman or man bending forward, you say this man or woman has a sagittal malalignment, they've got an increased um sagittal vertical axis because their head is several centimeters in front of their pelvis. I'm gonna lie them down to see if it's passively correctable. Is it extensor myopathy? Is it facet arthropathy? Is it stenosis or is it structural? And you really have to come to our adult deformity clinics? They, we do one every sort of two or three months at Norwich where all the consultants are there and we have all the adult deformity patients because we have a joint MDT where we decide what to do with them. And it's an excellent clinic. So if you're coming up to the exam, contact our secretaries and come to that clinic, we also do a pediatric clinic every Friday morning when we're not doing complex spine and you can see the Children coming up to the exam. But I, I really would recommend come to at least two or three of our clinics before you do the exam. It's very simple. It's just like limb surgery except you have to see it in the spine. It's just like having a tibia vera. How do you correct? A tibia vera? Well, you do an opening wedge osteotomy and you realign the tibia so that the mechanical access of the limb is reconstructed and that's exactly what we're doing here any more questions? Excellent. I look forward. I want to see all of you in my clinic. Ok. All of you. Good. Can I go, sir? Thank you. Sorry, I just been still trying to sort out Mr Steele this connection. Sorry. Um Yeah, I'll call you back. Sorry, Mr Lutchman. Um Cool. So uh we're still trying to sort Mr Steele out. He's unable to get into the event now. Um But we will work on that. Uh Is that um is that the end of your talk, Mr Luman? It is any any questions? So, so, so really, I, I like.