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Common Orthopaedic Conditions, Dr Rick Gardner, International Healthcare Executive and Chief Medical Officer (CMO) of CURE International

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Summary

This on-demand teaching session will provide medical professionals with an introduction to common orthopedic conditions, such as bone infections, congenital conditions, metabolic issues, tumors, neuromuscular issues, hip dysplasia, and brachial plexus palsy. It will review radiological changes of acute and chronic osteomyelitis, how to diagnose and manage these conditions, and different ways the body can form invulcera. Join Dr. Rick Garner, a children's orthopedic surgeon trained in the UK and Canada, to learn more about common orthopedic conditions in this informative and enlightening lecture.
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Learning objectives

Learning Objectives: 1. Define the terms ‘acute osteomyelitis’, ‘chronic osteomyelitis’, ‘sequestrum’, and ‘involucrum’. 2. Explain how infection can cross the physis and cause osteomyelitis in infancy but is not possible in older Children. 3. Analyze the difference between acute and chronic osteomyelitis and describe how the two conditions can differ in treatment. 4. Recognize the radiological signs for acute versus chronic osteomyelitis. 5. Describe how the body produces new bone (involucrum) in cases of chronic osteomyelitis.
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Mhm. My name is uh is Doctor Rick Garner. I'm a children's orthopedic surgeon. Um I'm based in, in Zimbabwe. Uh I've done uh my training in the UK um and then fellowship training in Canada. Um and I've been living in Africa these past 10 years or seven years in Ethiopia. Um and the past three years in Zimbabwe uh with Cure International, uh where we focus on children's uh disability surgical care. So, really, um it's a great um honor to be with you today for me. Um and my, my rema today um is um common orthopedic conditions. Um and um I'm just going to turn off my video for now just whilst I'm giving the, the talk. Um but I'll put it back on at the end. Maybe there'll be some questions. Um And so yeah, so my room is common orthopedic conditions and um the breadth of this is obviously very, very wide. Um and um I hope that you'll see this um really just as a, as a summary to walk through some conditions that many of you will see. Um, you've probably seen many times already and things that you'll see throughout your career. Um And um I really would just, I was trying to work through what might be most helpful. And so I've taken a fairly broad spread. Um So the conditions we'll talk through for the next hour will be infection, acute and chronic osteomyelitis, a congenital um condition. One of the most common that you will see which is club foot metabolic condition is rickets. Um Of course, there are wide breads of all of the different conditions you can see in each one of these subgroups. But these I think are probably some of the most common. We will be touching on tumors. Looking at benign and malignant tumors using exostosis and osteosarcoma by way of example, and looking at neuromuscular cases, trying to understand what is the difference between cerebral palsy and spina bifida. And to have some idea about how we diagnose and manage these conditions uh with hip dealing with hip dysplasia, Children who are born or in their early infancy, develop a dislocated hip and then sometimes um that can go on to osteoarthritis of the hip as well as other conditions that can also cause that and then also just one upper limb condition where we'll look at brachial plexus palsy. So um please see this as being an overview of these common conditions and really an introduction to orthopedics. Um I hope that in time that each of these conditions and others will merit in their own sessions. Um And, and we'll see how the curriculum pans out. But that's my, that's my hope for this as well. Um So we'll start off. So um talking about infection, a lot of the issues that infants and babies have with infection is partly due to the difference in blood supply for them and when they um and the difference for them in their infancy and in their later childhood. So, um in newborn infants, the metastases of the arterioles from the nutrient artery. So you see this vessel coming in here being the nutrient artery can actually penetrate across the physis. So, the py is another word for the growth plate. So they can penetrate across the growth plates and then come into the epiphysis of the bone. So we've got the end of the bone known as the epiphysis. You've got the uh growth plate here, which is the physis and the area here, the metastasis and of course, the diaphysis. But in infancy, blood vessels can penetrate across the physis. So if you develop osteomyelitis or a bone infection in the most common area of high blood flow in the meta region of the bone that can penetrate across the growth plate, coming into the epiphysis of the bone. Sometimes it can discharge and cause infection of the joint as septic arthritis. Now, in older Children, the feces act as a barrier and it's not possible for the bacteria to cross the growth plate. Um And so a meta sele this region. Here in Osteomyelitis, a bone infection is much less likely to discharge into the epiphysis. And this is important for the types of pattern that we see in infancy with bone infection. One of the reasons why in infants and in young Children, bone infections is much more common. Um is it's a relatively immune deficient area around here. There's there's relatively low flow. There are these sinusoidal vessels, there's a very high blood supply coming to the growth plate itself. And these sinusoidal vessels and this sluggish blood flow uh in a relatively immune deficient area means that a shower of bacteremia that can happen for a whole host of conditions. It could be a, it could be a scratch which cause some mild infection somewhere else in the body causing a shower of bacteremia. Um Sometimes the child might be malnourished, which will also mean they're less able to fight off the infection um can result in a localized uh abscess of the bone. Um And we can see this here. So what is the difference between acute bone infection, acute osteomyelitis and chronic osteomyelitis. So, we just shown in the previous slide that you have a high blood supply coming to the meta region of the bone. These sinusoidal vessels, a relatively immune deficient area, you can get a localized abscess of the bone. Uh This area here, I hope you can see my cursor. Um And so you get an infection of the bone, a localized abscess within the bone that in the infant of course, can travel across the growth plates and infect the epiphysis. Um But even if it doesn't, what then happens is the the bone, the abscess of the bone continues to grow and then can discharge into the subperiosteal area. So you can see the periosteum, the lining of the bone here and it discharges into the periosteum. Now, the initial findings for acute osteomyelitis is what you'd expect would be localized pain and redness and tenderness around the area. Now, the hope is that the child or the adult will present at this stage um and that they will be um attending hospital um and then it'll be diagnosed that they've got what is most likely an acute bone infection. Uh We'll be looking in a moment and some of the x-rays and some of the signs of that. Now, in the very earliest stages, IV intravenous antibiotics can be successful for this. Um in the later stages. When it's, it's becoming more developed, then it may be necessary to incise this subperiosteal pocket of pus and to release that. Now, if that acute bone infection is not managed, chronic Osteomyelitis will supervene. And what happens is that the blood supply on the inside of the cortex, the so called endosteal blood supply that of course gets stripped off. And so you end up with a loss of endosteal blood supply because the pressure effects of the abscess has caused the um has caused the blood supply to um to um to stop and then the subperiosteal collection strips off the blood supply from the periosteum. Now, the periosteum is typically a very rich environment, strong blood supply there. But if that is then peeled off the bone, you can imagine at this stage, you have the blood supply stripped from the endosteal, the inside blood supply and the periosteal blood supply. So you've got an area of bone here that has no blood supply. Now, the two important terms that we need to know are sequestrum and involucrum. Now, the sequestrum is dead bone, sequestrum is this dead area of cortex that um it has has resulted in the stripping off the blood supply, which is dead bone. Now, what will then happen is the body will try to lay down new bone in most situations. Now, the new bone formation is called the involucrum and the involucrum forms because the periosteum has uh lots of mesenchymal cells that can differentiate into osteoblasts and lay down new bone and we'll show some x-rays of this. So, what are the radiological changes with acute Osteomyelitis? Well, initially, you may not see anything at all. You'll have a patient with some localized redness and tenderness uh around the area. If you did blood tests, you would find up high white cell count and a raised sr and crp. Um But the initial radiographs may not show anything at all. If you did an MRI scan. If that was available, you would see some high signal in the meta area that might confirm your diagnosis. Now, over the course of the next week, you can see some rar application of the area around the acute Osteomyelitis. You'll see some bone changes that are forming and this is really signs of this intraosseous bone abscess that is causing an erosion of the localized metas or bone. Another week on that area of osteomyelitis is discharged across the cortex. You've got a disruption of the endosteal blood supply. The periosteum has been lifted off. We start to see some early new bone formation and this is very early involucrum that is forming and this is really where we're coming from acute osteomyelitis starting to form chronic osteomyelitis. Now, and in more extreme examples, you have situations you may well have seen in your practice and in your studies when you're visiting the hospitals, whereas this is left untreated. Then you have a situation where the bone itself. This is the sri this is dead bone which is trying to discharge yourself through the skin. This large secretion can sometimes involve the entire bone itself. And you can see on the x-rays here, this area here is the sequestrum. This was the original tibial shaft that is sequestered because the entire region of the diaper area of the tibia has become dead bone because the blood supply has been stripped off both inside and outside. Um And this whole tibial shaft is extruding out through the bone, which is the seru. Um And this would be in time gradually fall out by itself, but we would do surgery to pull that out. The important thing to note, of course, is that this three year old child has had an incredible involucrum formation. All of this bone around here is new bone which is involucrum formation. And of course, in this situation, the initial surgery is relatively easy. It just needs us to pull out this dead bone here to clean out this area. Um And you can see after that bone is being pulled out, uh you still got a very structurally sound to be your shaft. Now, in time, there may be some destruction of the growth plates or there may this growth plate may close and so there may be ongoing issues. But this child has been um fortunate in the direction of the chronic osteitis in that there's been a very good structural involucrum that has formed. Now, if you look at another case, this is the, of course, the proximal humerus where you've got a very severe Osteomyelitis here where you've got a nubbin here of the humeral head is the elbow down here, the radius and the ulnar. Um And you can see what has happened over the course of the following six months or so. Is that the entire humeral shaft is sequestered? So this is all dead bone around here. But, but remarkably, you can see how the body forms, this rather beautiful involucrum which comes round is spiraling around the humerus. Now, we're very careful to allow this to develop into something structural. To remove the sequestrum at this stage would be catastrophic because you'd pull out the dead bone, which would result in removal of the infection because this child will have chronic purulent pus drainage coming out, you'd remove this, but then you would lose the structural integrity of the bone. And if you're able to wait for some three months, even six months, then gradually this involucrum reforms and becomes stronger and stronger to a point that you're more confident to remove the sequestrum. So at this point here, here is the sequestrum, the dead humeral shaft which can then be removed. You can see it here has been removed to allow ongoing formation of the involucrum. Um And it's important to try to wait for this. So, in chronic osteomyelitis, there will be chronic discharge, there will be a little sinus, maybe several sinuses, the pus draining out, but it's a relatively steady state. The patient's not in any way sick. And the key thing to do then is not so much antibiotics because you've got an area of dead bone which won't be sterilized by the antibiotics, but will be to focus on the nutritional um situation of the adult or of the child to help them have enough nutritional cata bolic um uh ability in order to sorry uh anabolic activities, you're really building them up, helping them with their protein supplementation. And like, so they can actually build this inuk and then when the time is right, remove the sequestrum and then um uh and then hopefully deal with the underlying infection. Um The Squeo chronic osteomyelitis can be multiple, particularly in the growing child. Um as we've learned in the young child, you can have disruption from the metaphyseal area across into the epiphysis of the bone. And that can discharge into the joint and cause as septic arthritis. Uh even if the metas of Osteomyelitis um doesn't discharge into the epiphysis. It can often disrupt the growth plates and you can end up with a growth arrest or a file closure that you've seen in this proximal tibial here where the growth plate to the fibula, you can see but the growth plate to the tibia is disrupted. So now there's total closure of that proximal tibia if the sequestrum um is discharged or is removed before structural involucrum forms. And sometimes the involucrum doesn't form and the tibia is probably the commonest place where sometimes it does not form, then you end up with a large bone gap and that represents its own issue. So, bone loss due to a poor structural involucrum can often occur, you can of course get angular deformities, sometimes a differential growth arrest around the growth plate. If you had a bony bar across this side of the growth plate, the leg would become very bowlegged or you would get severe genu vera with an angular deformity. Of course, you can get recurrence of the infection. And in some areas like here, round down by the ankle, you can get joint destruction. Now, I won't dwell on this too much. But some of you may have heard of um areas of the body where there's an intracapsular metastasis where the end of the bone is actually inside the joint capsule. And one of these areas of the bone is the distal fibula. So, if you have infection around the distal fibula, which sits inside the capsule of the ankle joint, the metastasis can discharge directly into the joint. Um and uh and you can see that's resulted in in destruction of the ankle joint as well. Now, um the um the sequelae of the chronic osteomyelitis can also cause infection. So it can also cause um dislocation. So, if you have meta osteomyelitis here, it can discharge into the joints. The proximal femur is also one of the places where the metastasis sits inside the capsule of the hip joint. And that can discharge into the joints and then the building up of pressure within that hip joint can cause capsular laxity and can push that joint to be dislocated. So, joint dislocation is another is another sequelae. So on one side, the proximal femoral Osteomyelitis cause the joint to dislocate And on the other side is cause catastrophic avascular necrosis where it's just eroded away the pa at the head of the femur. So, joint dislocation and avascular necrosis uh can be another sequelae. And of course, the importance of this is to really highlight the effective care of acute osteomyelitis and acute septic arthritis to try to avoid getting into the chronic stage. So we'll move on to rickets. Now, rickets is a metabolic condition. Um It's due to a defect of mineralization of the bone matrix at the growth plate and it's due to abnormalities of the metabolism or the ingestion of calcium phosphate and vitamin D. Now, there are many different forms of rickets, but probably the most common is vitamin D, deficient rickets. Um for my last 10 years of practice working in Sub Saharan Africa, Central Africa, sometimes we'll have patients coming in with something like club foot, but maybe they've been kept inside um because of some societal stigmatization and sometimes they will turn up with rickets because they've been kept inside. They haven't er had um a regular sunlight and sunlight is critical for the metabolism of the active form of vitamin D and they can come in with sometimes with very profound rickets. Now, there are other forms of rickets, sometimes hereditary um where um there can be a lack of um um phosphate reabsorption through the kidneys. Um and sometimes that might need phosphate supplementation as well, but probably the most common form of rickets would be the vitamin d deficient rickets. And you can see this here. What are the main signs of rickets that you will see? You'll often see swelling around the wrist. Uh You can see this child's hand x-ray here and this is the growth plate. It's a really very broad growth plate with lots of osteopenia around the metastasis. We get this cupping around the metaphysis around here and you feel the breadth, you feel the width of this child's wrist. Um and what's happening is there's a failure of osteoid formation around the provisional zone of calcification. So of the growth plate here and this is a histological slide of this area. Here, you have all these wonderful columns of chondrocytes that are gradually apoptosis and then becoming um calcified and forming bone. But because there's not the vitamin D or the calcium absorption and metabolism, this area here does not form bone. And so the so the growth plate looks very, very broad. Now, in vitamin D deficient rickets, you can take intramuscular vitamin D or oral vitamin D. Um and then the result can be remarkable. So with vitamin D um supplementation in three months, you can have remarkable changes. No surgery, of course happened here. This is just with vitamin D supplementation. And in three months, even six months, the feces can then narrow the width of the vices shrinks down. The child who might have been very, very listless and unable to run around and play sometimes with severe Acular deformities. Um then um then starts to run around has no more bone pain and is a very different child. Indeed. So uh the diagnosis, the management of the rickets is, is a very, very rewarding thing. Uh and the same child of the knee. So you can see here the distal very broad cut flare meta tose regions and just three months after vitamin D treatment. Now it's resolved. Now, the deformities of R is can be very, very severe. Um And it's important to initially medically treat these Children before you'll manage these deformities. Because as an orthopedic surgeon, it's possible to get these bones straight. But when the bone is so thin and fragile, the medical management must come first. Um And we see Children sometimes who come in. This little girl here has got a skin condition called ichthyosis. Um But the point of this was that she was kept inside. I think there was concern about the skin condition within the society. Um But she could barely walk. She had to hold on the two hands to get to the other side of the room. And you can see how broad her growth plates are here, how osteopenic she is now by treating her just with vitamin D, you can see how the bones, how the hips. Now you can start to see the hip joints. And so she's walking well now just following vitamin D supplementation. But of course, she's got a waddling gait. Now, her feet are very externally rotated. But at this stage, surgery can be done in order to correct the hip deformities, they're not tipping in so much. And so her hip muscles, her abductor muscles are working better. And then after the medical treatment, you can do the surgical management. Now, the bones are that much stronger and you can effectively cut the bone reposition them to deal with the underlying deformity. And then a child who needed help to walk across the room with initial medical management followed by surgical management. It's transformative and so the medical management comes first and whatever the result and deformity is maybe six months, nine months a year later can then be addressed with surgery. Uh Pretty show two slides before sir uh before the gate. Oh I'm sorry, sorry. Say then these ones here. Uh No, before, before the child was walking, there was a slider uh even be even before then. Uh huh the, the initial, the, the initial one here this x-ray uh y yes, one more, one more before this. Um this one. Yes, sir. Thank you. So, so, so this child, this is a different child. Um But this child actually has a another condition called hypophosphatemic rickets. It's another form of rickets where there's a failure of absorption of phosphate through the renal tubules. Uh and this child needs to have treatment with phosphate. Um I think the details of rickets would merit in second separate talk. Um but suffice to say that whether it's there's the phosphates, it's the vitamin D or it's the calcium. Um that would be part of the underlying initial workup. And the initial workup for Rics would be to look at the serum calcium levels, the serum vitamin D levels and the serum phosphate levels. Um in addition to that, doing an alkaline phosphatase will be very, very high because of this ongoing bone turnover. But by doing the serum calcium phosphate and vitamin D, that can start to give an indication about what the underlying deficit is for the individual child to help guide management. Um Thank you for the question. The um and then, um and then after the ricin has been treated, another example here. So you've got a child with very severe bow legs at this stage here where the um where there's significant tibial vera as well as distal femoral varus as well. Um And we generally will treat Children like these with an intramedullary rod to plate these where you've got multiple areas of, of deformity. Here is a harder thing to do. But by putting a rod down the inside of the bone and cutting the bone to get the rod down, it's much more reliable. And you can see we've been careful to come perpendicular to the top of the bone. We've made an osteotomy around the proximal diaphysis around the distal diaphysis and passed a rod down. So a bone that was very curved has now become straight and they're repeating the same for the femur as well of just sending down an intramedullary rod in order to straighten the bones. And so this would be after the medical management to get the child straight again, so we'll move on to feet. Um And you're very welcome to interrupt me anytime. Um I really welcome any questions that, that you may have or we can take some at the end. Um So clubfoot um is a very, very common condition and um otherwise known as congenital Talipes, a Rena varus. So Talipes being or congenital, of course, being from birth, Talipes being the foot aquino being a equinus with a foot pointing down uh with the ankle pointing downwards and varus being an inward tilt of the heel. Now, the mainstay of treatment for this, you may have come across is called the Ponti technique. And over the last century, many different techniques have been tried and popularized. Um But the world's really come together in a very unusual way you can show Poncet um died not so long ago, but really was a remarkable Italian immigrant who was working in Ira in the United States and pioneered this technique of using a didactic series of casting and manipulations of the foot to gradually swing the foot around into a normal position. So it's a weekly manipulation of the foot where you stretch the foot around centering on the head of the talus, which is very prominent in this condition and you use the prominent bone, the prominent head of the talus as a fulcrum, pacing your thumb across the head of the talus and gradually stretching the foot around on a week by week basis. So you've corrected the deformity. Now, the um the, the deformity, I, I think I've got a slide on the no, here we are. Sorry. Let me just come back here. So the deformity can be. Um you can, you can remember what the deformity is by using the an Aron cave cave. Now, the C is Cavus. Cavus is the plant a flexion of the first ray of the foot. So it's the, it's the medial arch. You've got an excessive medial arch with a first metatarsal pointing downwards a lot more. That's Cavus which is plant flexion of the first ray C A is a deduction and you can see how the forefoot is severely AUC um coming towards the midline. The V is the varus. So the varus implies an inwards tilt of the hindfoot or of the Calcaneus. So the hindfoot is tilted inwards as well. So you've got inwards direction of the forefoot, which is the ad duction and inwards tilting of the hindfoot, which is the varus. Um And finally, e the cavee is a cous, you can see the foot and the hind foot is pointing downwards. So cavus adductus varus and a quin cavus of the first ray of the forefoot adduction of the midfoot varus of the hind foot and a quus of the ankle cave. Um And so through this didactic series of casts, um the foot is gradually corrected on a week by week basis. Typically requiring around five casts. You replace the soft roll, you place the plaster pas on and you use your thumb as a fulcrum to gradually stretch and correct the foot. Um At the end of the first cast, the feet may look like this after the initial cavus is starting to be corrected. Um Now, once the middle part of the foot is stretched out and corrected, what is left is persistent Aquinas, the e of cave. Um and, and for the persistent Aquinas, we just do a very simple achilles tenotomy. So we put some local anesthetic in with a needle around the achilles tendon on the inside of the achilles tendon, we take a knife and we make a little percutaneous stab. Now, in a child who's under the age of two, this is an outpatient clinic procedure. It's very safe. We do a localized sterile preparation with Betadine or chlorhexidine and the knife is placed just medial to the achilles tendon. We're very aware that all the blood vessels run anterior to the achilles tendon here. And so it's important to become posterior to that. And we make a little percutaneous knife cut. We rotate the blade posteriorly, we divide the achilles tendon and you can see a child who's got who's residual Aquinas, then you can dorsiflex the foot around 15 degrees or so. So after the tenotomy has been done, you place them in the final cast and you can see where the foot was twisted inwards. Now, the foot is outwards. And then after the, the final tenotomy cast, we wait three weeks and then we place the child into these boots and bars and we call this a foot abduction brace, the foot, uh, both feet are around the level of the shoulder on either side and the feet are externally rotated. And you can see this bar is bent and the feet themselves are dorsiflexed to stretch out that achilles tendon and that's typically maintained full time for three months. So the child has the sti casting, which typically takes around five weeks different cast fi uh for each week to correct the middle part of the foot. But you've still got the persistent Aquinas. And then you do the achilles tenotomy under local anesthetic. You put on the final, the sixth cast. Um, and then after three weeks, you place the child in these boots and bars and these boots and bars are typically full time for three months and then we just use them at night time and at nap time until the age of four. And I think recurrence is, is a big problem with club foot and often it's, um, it's an issue, maybe it's a parental compliance because they're not able to access the brace. Sometimes it may be that the foot wasn't fully corrected in the first place and the child can't fit into the brace, but it is important to maintain these braces until the age of four. Otherwise recurrence can occur. Now, um, we often see walking age Children with clubfoot and you can see here for both feet, probably the right side is the worst. You can see how that child um has got um severe forefoot, ad duction and the hindfoot, varus um and walking just on the side of the foot and really struggling. And for these, even these older Children, we do exactly the same. We do the Ponti technique in order to gradually stretch out the foot to correct uh that deformity to stretch the foot around. And then we'll do the achilles tendon, the achilles tenotomy or in older Children, we lengthen the achilles tendon, but we'll do a tibialis anterior tendon transfer as well. So for Children over the age of three or four who have never been treated will take off the, the tibialis anterior which is the tendon on the inside of the foot and we transfer it to the outside of the foot because it enables the that foot to be pulled up in a more neutral fashion. So we tend to do a tendon transfer. I think it goes beyond the bounds of this particular talk about the techniques. But a tendon transfer of the tibias anterior is an effective way to improve that child's walking. And you can see this child here who was, I hope you can see the videos, but you can see the difference of this child after the Ponti technique and after they've had a tendon transfer, um, a child at this age, they can't go into boots and bars, er, they're just too big and they won't tolerate them. And so that's why we tend to do the tendon transfer, which is like an internal splint and another child. Here again, you see on the left, um, severe untreated club foot and then by correcting the foot using the Ponti technique and then doing a tendon transfer cause this is an older child. Um, you get a very effective correction. So, for the infant, we use bracing for the older child, we tend to use a tendon transfer to help balance the foot. So, uh, we'll move on now to bone tumors. Now. It's, it's another big topic. Uh, and I just wanted to highlight a couple of things. One would be the difference between when it's a benign tumor and when you might be looking at a malignant tumor and we're talking about bone tumors here. Of course, you'll be dealing with cancer for all your different specialties you're working through. Um, and then primary versus metastatic. So, um, a primary tumor, a primary brain tumor is a tumor that grows from the bone. A metastatic bone tumor is one that comes from somewhere else. So you might have a lung cancer or a colon cancer. And the result of that can be that, that, that cancer will then metastasize to a bone. It may metastasize to another part of the body, but that would be a metastatic tumor. Now, how do we differentiate between a benign versus malignant tumor? And probably the most useful way or the most uh the easiest way to start to, to consider this is what we call the zone of transition. Now, you can see this picture on the left, this happens to be called a fibrous cortical defect. But the the it's it's not. So I don't so much want to highlight the the nature of the tumor. This this this fibrous cortical defect more just to highlight the difference between something benign and something malignant. Now, this you see the zone of transition is very, very sharp. I could take a pen and I could draw on the x-ray, a very clear line around the outside of the tumor just drawing it around here because it's got a very narrow zone of transition. And the narrow zone of transition implies a relatively slow growing tumor. You can see there's been osteoid formation just around the edge of it. Maybe it's the pressure effect, but it's a slow growing tune with a very narrow zone of transition which often will indicate benign pathology when you've got a situation on the right here where you've got a lesion here where it's harder to draw a line directly around. It's not so crisp and clear. Um, you're, you're getting some elevation here of the periosteum. I don't know if you can see there's just some elevation here and we call this onion skinning like the skin of an onion and this periosteal elevation, um, combined with a relatively permeated um unclear lesion indicates that this might be a malignant lesion. Now, of course, sometimes things like Osteomyelitis can also um have the appearance of what could be a bone tumor. And if there's doubt, we'll often get further imaging. If that's possible, we'll do a biopsy to see whether or not this could be cancer or could it be infection? And then on this side here, you can see all of this area around here, this so called osteoid new bone formation. And around here, this new bone formation, which is very, you can't really draw a line around it. You've got what we call this sunburst sign. You've got this periosteal elevation, this new bone formation and this is a malignant tumor. Um but you can see the difference, this zone of transition, I think is a very helpful way of trying to help understand what might be a benign lesion and what might be a malignant lesion. Now, a common lesion, probably the commonest bone tumor is an osteochondroma otherwise known as an exostosis. And you can see this here, you know, this is a benign bone lesion which is growing up from the metastasis. It originally starts at the growth plate and it's an area of some extra um osteoblasts being laid down with a, with a chondral cap. So the chondrocytes from the um uh from the growth plate, differentiate into osteoblasts. But it's an, it's an additional benign bone lesion that you can see is a continuation of the cortex and it's got a very well-defined uh edge to it. Um Now, if you, if they're symptomatic, if the child find has frequent pain from that, when you open it up, you find there's a cartilage cap looks like a little mushroom coming from the bone and we just remove these. So these are very common. Um We don't take them all out. We just take out ones which are symptomatic and are causing pain or if we're concerned that maybe um we're not sure if it is indeed a benign lesion. So this would be an exostosis and sometimes Children have many of them, multiple hereditary exostosis is uh a condition you'll sometimes see where there's a genetic problem um where they will have many, many of these exostosis around. But this is a benign lesion. We'll often still take these ones out when they're causing problems. Um But this is a benign condition. Now, a malignant bone, um a malignant um bone cancer. Probably the commonest one in Children um is an osteosarcoma and, and these will typically happen in adolescents and also in the elderly, they can also have an osteosarcoma and they are very, very aggressive. It's a bone forming tumor. They do metastasize to the lungs um and all too frequently in the areas where we work. They present late um and often amputation is frequently required. Now, it needs a combination of surgical care and chemotherapy. You can see this um this skull here has got huge swelling around the distal point of the femur. The skin is stretched over the top. The child is having a huge amount of pain, can't sleep at night because the pressure affects of the bone. And this is clinically a very late presentation of an osteosarcoma. But the important thing is the diagnosis initially and you can see this job the same x-rays. Um There's a huge amount of new bone formation. It's a hugely expansile lesion where it's eroded out from the the margins of the bone. It's laying down a huge amount of bone formation. Um and it is pushing into all of the soft tissues around here. And this front view, you can see how permitted and destructive it is. Um you might be able to have an MRI scan. It's not the best MRI um slice, but you get the idea the way that this soft tissue effect is actually eroding up into um into all the soft tissues is causing massive expansion, broken out through the margins of the bone is eroding into the soft tissues. Um and a child coming presenting this late will often have metastases to the lungs. Now, in this child, she did need an amputation. There wasn't a good limb sparing option because the blood vessels were um were right up against the tumor and there wasn't a limb sparing option. So a high above knee amputation was required in this case. Um But it's not always necessary to do an amputation. And I just want to show another picture of a, of a different child. Um Well, it is possible to do limb sparing surgery. Um Now, that would be the uh I'm just thinking all the environments where we work an amputation is a catastrophe pre for, for any patient. But of course, life has to come ahead. Um But sometimes limb sparing surgery is possible and sometimes you can do a very aggressive resection of these tumors. Um And um and then you can even do a replacement. So um it is possible to have a distal femoral replacement, effectively a knee replacement to remove the tumor and put in a distal femoral replacement. And that can, that can spare, can spare life and can spare limb. Um, a child we had in Ethiopia where, where we did like this. But it's of course, and it's an expensive device. There are companies trying to reduce the price of these in order to see whether or not we can make these more widely available. But there are other ways, even for some of these very aggressive tumors to prevent amputation, I must say that all too often the Children do present very late and that is necessary. Um OK, we're gonna move on to hip dysplasia. So, Children who were born with dislocated hips, this is a three dimensional ct you can see of the left hip here being dislocated and out of joint. And um it's probably one of the more more common um children's conditions um but often presents late in many countries around the world. There are screening techniques in order to identify these Children at a young age, but often they present late. Um I'll just play these videos again just as we're talking through them. You can see the child on the left looking at this x-ray, the left hip is dislocated, the child in the middle, both hips are dislocated. This femoral head should be sitting in the acetabulum down here and you can see the child in the middle has got this waddling gate and the child on the the right, the young adult on the right presents very late with a high left hip dislocation and a leg length discrepancy as a result. And the question is, what can we do for these Children um in some countries. Um It's very, very common in other countries less so. Um but what can we do for these Children? It is much more common in females. It's much more common. Um when there's a family history and if a child is born breech breach, when the bottom is coming out first, uh the hips are not forming in a safe stable position and that child themselves can end up with a hip dislocation. So the three commonest risk factors all over the world would be a female child. Often the first born where there's um relative oligohydramnios, there's a lot more of a packaging issue, the child being squished together. Um But with family history and a breech presentation, um these are significant risk factors for hip dysplasia. Um and we can assess this in the young child. We can do tests to see whether or not that hip is dislocated. Um And then probably the the commonest test we do is the auto Laney test, which is a hip, which is a test where we take a dislocated hip. The child's hip is often dislocated out the back and we abduct or we swing the leg out and we can feel that hip joint clicking, we feel a click of reduction. Um and this would be the auto Laney test. Sometimes the child's hip is very unstable, it can click in and out of joints. And we use the so called barlows test to a duck the hip to bring the hip into the midline and to push backwards and you feel the click of the hip dislocating out the back of the joint. So the auto Laney test takes a hip that is dislocated and you click it back in and the Barlow's test, you take a hip that is in joint but is unstable and you can click it out and you can feel this in Children under six months of age as part of the physical exam to see is this hip dislocated or not? Um Now, ideally an ultrasound scan is done. And if an ultrasound and sounds scan is available, you can screen this hip and see is this hip in or out. And these pictures, it's impossible to really look at an ultrasound scan unless you're doing it to actually see if these hips are in or out. It's a harder thing to see. But an ultrasound scan is the classic way of seeing this round ball here, is it sitting inside the socket and these for Children under six months of age. And if the hip is sitting inside the socket, the ideal treatment is something called a Pablo haris. And it's a set of straps that holds the hip in a flexed position and abducted to allow this hip to reenter back into the socket. And this would be um applied for maybe two or three months um with frequent monitoring on the ultrasound to see if that hip is sitting in joint. So this is the Pavlo harness. So for the infant under six months of age, we would try to do an ultrasound scan to see is the hip in or is it out? And then we would use a Pavlo harness to put, to hold this hip in a stable position and very quickly in the young child that hip can then stabilize in the majority of cases. Now, if that child comes along late and that can often be the case, then quite big surgery is needed. You can see on this side here, this is the thigh up, here is the back of the child. And you can see here, we've got a say we got a situation where we've got a dislocated hip. We've come through the front of the hip joint and this ball is the hip that is sitting out of socket and just down this deep dark hole here is the ace table where the hip should be going in. And so that hip needs to be pushed back into the socket. And often when we're doing this, we also need to reposition the femur into a femoral osteotomy, often taking a little piece of bone out to take the tension off the hip. And also to deepen the ace table itself. Often the ace tab in the cup is very shallow and we have to deepen this. So these older Children will often have to do an open hip reduction with a femoral osteotomy to cut the femur to take some tension off as well as an acetabular osteotomy as well to deepen the cup. So it's big surgery. Um And so you can see there's one of this child with a bilateral hip dislocations. That hip should be sitting in the socket down here. But the hip, the child waddles, the child can walk. They don't have any pain early in life gradually. In adolescence, these hips can become very, can become painful, they can start to erode up against the iliac wing and the um, and back pain can develop. Um, so we do try to treat these Children earlier and you can see this child is now two years on or a year on or so. Um, but you can see the waddling git has gone, the hips which were out of joint are now sitting nicely in joints after femoral and pelvic osteotomies and that child's walking. Well. So, um, uh yeah, the preference is trying to identify these Children earlier, um to avoid surgery. But if they come along a bit later, then we can do these open hip reductions with femoral and pelvic osteotomies really until the child is around eight, after the age of eight. it's, it's too late for surgery. There hasn't been enough formation of the, the ace table in the cup of the pelvis to allow a safe reduction. Um Now what can happen if this child ends up with, um, with not being treated, um, or if they have been treated even over the years, you can get gradual arthritis and this might have been due due to hip dysplasia, say of the hip, which was put back in, but it still went on to arthritis maybe after 20 or 30 years. Um Sometimes it might be due to infection. Of course, this is an x-ray of an adult 50 year old patient who's developed over the years, progressive loss of the cartilage. And so you can see a situation here where the joint surface is narrower. You see a big lipping, what we call an osteophyte, this extra bone formation coming around and this patient is now walking in pain, they can get across the other side of the room, but they have developed osteoarthritis, a lack of cartilage around the joint surface, joint space, narrowing, new bone formation, and so called osteophyte formation. Um And then what do we do in this situation? Um in an ideal play ti place you may be able to um offer a hip replacement. Um And what is a hip replacement? Uh A total hip replacement is replacing both sides of the joint where you have a femoral stem, a metal femoral stem that you put down inside the femur, you have a plastic liner and you have an acid tablet component that you fit into the cup. Um And this total hip replacement is a very effective orthopedic operation to relieve pain and stiffness from osteoarthritis. Um And it's probably one of the most successful orthopedic operations for reliability of outcome. And you can see this patient here who's had a severely worn out hip on the left with an ace tablet procedure and also some bone augmentation to improve the cup. Um This, um, this is the femoral component here, uh very effectively relieves pain and stiffness to give this um, patients a very normal function. Um These can last maybe 20 years and after 20 years or so, they'll often have to be replaced. But hip osteoarthritis can be managed in a multiple um different ways. But a total hip replacement is, is is a fairly standard way to manage these these patients. Um I just spend a few minutes on neuromuscular condition. So, cerebral palsy and spina bifida and I think after this, we'll stop and I'll just take some questions. Um And I really, I just bring these up because I think I'll just be really helpful for you to understand the difference between the two. So cerebral palsy spina bifida. Now, cerebral palsy is a condition affecting the brain. Now, often there's been a child who's born premature, say at 30 weeks of age and a relatively um uh relatively fragile cerebrovascular system where there can be an intraventricular intraventricular hemorrhage. Um maybe a child who um had obstructed labor was a full time child. There's a lack of maternal health care and then this child had a degree of anoxia lack of oxygen at the time of a traumatic prolonged delivery, maybe some shoulder dystonia. And so maybe the cord was around the neck and that will cause an area of infarct or hemorrhage around the developing brain that will cause uh issues with the legs and the arms um to um failure to be um working properly due to the neurological issue in the brain. Now, in spina bifida, it's not the brain issue. It's actually the spinal issue where there's been a failure formation of the lower points of the spinal cord, sorry, lower points of the of the vertebra where you get this, this dysraphism, you end up with a a situation where you've got um the outpouching of the nerves coming out the back of the spine and you can end up with a very um thin membrane over the top of these nerves. And this is a myelo meningocele form spina bifida. So um so different Children here walking with um I'll just turn off this sound, walking with spine a bit with walking with cerebral palsy. So cerebral palsy when the Children are walking, they may be affecting one leg. So called hemiplegia may be affecting both legs. And I'm sure you've seen many Children walking in and even adults walking this type of pattern where they've often got a lot of stiffness, affecting their muscles, spasticity, affecting their muscles. Um and it's all due to an injury to the immature brain and it's a permanent disorder of movement and posture to the immature brain. Now, the lesion does not change over time, but as the child is growing rapidly, you can end up with a lot of muscle tightness that causes the bone to twist. And depending on the severity can cause problems for that child walking and even gaining independence. And it will happen either before bo before birth due to infections, um can happen during birth or sorry before birth, due infections or even prematurity can happen during birth because of um cerebral anoxia or it can happen the first two years after birth. And typically we see this happening in the first two years of life, prenatally, perinatal or two years, postnatally often due to something like malaria, encephalitis or meningitis and the brain injury will often cause spasticity and tightness of the muscles. Um the muscles don't grow properly and then you can have twisting of the bones due to the abnormal muscle control over them. And eventually some of the more affected Children can have severe joint deformity and even develop arthritis. Now, in cerebral palsy, often the parent will come and saying, will my child walk? Well, you can have independent sitting by the age of two. So typically you'd expect a child to be sitting by six months of age. But if a child has got developmental delay and they can sit by two, that's quite predictive of them walking as an adult. Um and a lot of our work is then to say, what can we do to improve this child walking. Now, they can have patterns of, they can be hemiplegic, affecting one side of the body. Diplegic, affecting both legs and quadriplegic where they're severely involved and affecting all parts of the body. Um And so a child with CP diplegia, you can see both legs are affected, he's struggling, his both legs are very stiff. Um, and he's using sticks to walk. Whereas a child here with hemiplegia walking better just affecting the right side of the body. You can see the right arm is um is held in position of pronation and elbow flexion. And he's in a qunu, he's not able to touch his foot down flat to the ground contrast to spina bifida, which is a spinal issue with these outpouching, the lower points of the spine with these nerves um sitting just under these very thin level of arachnoid down here. Now that and neurosurgeon will typically close this area to make sure that this doesn't break down and causing infection around this area, which can be catastrophic and even travel to the brain causing a meningitis and encephalitis. I mean, sometimes it can be very mild, sometimes you just see a little scar at the base of the spine without any nerve outpouchings. And that can be a sign of a very mild spina bifida. Um And it's all due to the fact in in the embryo that the invagination of the neural groove fails to happen. And the key thing I think, which I'll just finish it with, this would be, it's often due to a lack of folate and folate is just a huge issue for spina bifida to make sure that parents and mothers are taking enough folate. And this has been shown to be one of the highest causes of spina bifida will be a lack of folate consumption, particularly if there's a child born with spina bifida. The um the amount of folate consumption which they must be having, they must be taking more folate for the next pregnancy. Um I'm going to stop that. The there's always a lot more to be talking about. I'm realizing I'm coming to the end of my time here. Um um But I just wanted to say thank you for your time. I hope that this has been a, an introduction of orthopedics and, and I hope as your curriculum develops, we'll be able to unpack these conditions more. But I hope this has been a, a fruitful time just to give an understanding of all the things that we can do for these Children and adults. Um And we'll lead on to further discussions about this, but I'm really very grateful to your time. I know you're from all over the world. And um uh and thank you for this opportunity. Thank you very much, Doctor for this pleasant lecture, really appreciated it. Um I'm so sorry, we cannot take any questions right now because we've run out of time. But I'm sure whoever's questions can accumulate it for the next lecture whenever you're gonna give it. And I thank you again for this amazing presentation. Hope you have a lovely day. Yeah. Thank you. Thank you. You too. Goodbye. Bye bye.