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Pediatric Orthopedic Problems

Back pain in children. We generally think that back pain is the domain of the adult but there is an ever increasing amount of back pain seen in children. Up to 36% of school age children have back pain and up to 7% of these kids will seek medical attention for it. Unlike adults, back pain is usually organic in origin. There is very little secondary gain, drug seeking or disability behavior in children. So if they come to you with back pain, generally itís a real thing.

The four major categories that we see are spondylolysis and spondylolisthesis and that is just a slipping of one portion of the spine on another portion of the spine. Usually itís L5 on S1. Scheuermannís kyphosis is a hunchback type of deformity that we see in otherwise healthy adolescent children. Generally in very rigorous laborers, weight lifters and farm boys, we see this Scheuermannís kyphosis which is a common cause of back pain. An infection, diskitis or vertebral osteomyelitis that we see can cause back pain. Thereís a whole list of secondary things like tumors and leukemias and things like that and some metabolic things but spondylolysis/spondylolisthesis, Scheuermannís kyphosis and infection are about 

Spondylolisthesis. This is L5 and this is S1 and you can see here that the posterior margin of the vertebral column up to this point is pretty smooth in the three vertebral bodies you can see and then there is a step off. This is the front of the body and this is the back and you can see that the L5 has slipped forward on S1. We call that a spondylolisthesis or a slipping of the

Scheuermannís kyphosis. It is a sharp, angular forward bend of the spine. This is in the sagittal plane. This plane is youíre looking from the side and there has got to be at least three vertebral bodies that are angulated more than 5ļ. You see these little things here in

Examine the child. Take all the childís clothes off down to their underwear. Even with babies and young children I will take their underwear completely off. There is not much surface area so there is no reason to miss something because you didnít disrobe the child. Look for cachexia, pallor. If they just donít look right to you, then they are probably not right. If they have any gait abnormalities. Do they have ataxia? Do they have a lurch? Do they have what seems to be one leg longer than the other? Anything can be diagnostic of some sort of an intraspinal lesion. Do they have any abnormal skin lesions and midline defects or hair patches which would make you think that there is some sort of myelodysplastic process going on like spina bifida. Look at their spine. See if they have any scoliosis. Have them do a forward bend and we will go into that in a few minutes. Look at their kyphosis. Do they have an unusually hunched posture which can be postural round back, which is normal, or it can be Scheuermannís kyphosis? Do they have local tenderness when you palpate over their spine? It is important because that is very unusual in children. If they have local tenderness, then you have to think about a local process that is acting right there like a tumor. Or if it is low in the spine, possibly a spondylolisthesis. Do a complete

Here is a difference in looking at the kid. You can tell this kid has a little bit of a round back deformity. He has got postural round back and his mom keeps telling him to straighten up and put his shoulders back and if he does that it will go away. This kid, this is not a postural round back. This is a sharp angular curve that you see in Scheuermannís kyphosis and you canít mistake that for that. They are two different entities. He cannot straighten it out if he stands up straight. In fact, he canít even lay on his back because it hurts him to lay on the prominence of that. That probably will require surgical treatment because this is pretty far along but I thought it was a good picture for a demonstration of Scheuermannís kyphosis.

So what diagnostic studies should you get? This is a hair patch, in case you hadnít guessed, and underneath there there is spina bifida. There is a midline defect. You wonít see ones as pronounced as that. That is sort of one so you wonít forget what it looks like. But that

If the history is unclear, in other words they donít have a history of trauma, they wake up with it or they develop it over a couple of days, if there are minor physical examination findings, maybe some tight hamstrings, maybe you see a little bit of a curve, then I would suggest getting an AP and lateral of the spine standing. If you think that there is a little bit of tightness in the hamstrings, there may be a spondylolisthesis or a spondylolysis, you might need obliques of the lumbosacral spine to bring out that area of the spine which is

If you are looking for a spondylolysis or a spondylolisthesis and you are not going to treat it, donít get the x-rays. If they have an unclear history or minor physical examination findings, send them to an orthpod because that is when I would start to worry that this

Scoliosis. Weíre going to sort of move centrally down. It is defined as lateral curvature of the spine with rotation. A lateral curvature of the spine without rotation is not scoliosis. It has to be greater than 10ļ and that is as per the Scoliosis Research Society definition. There is no known etiology, thus the word idiopathic. We donít know. There is a female predominance of 5:1.

There are three types that we know: Infantile which occurs from birth to three years. This is the only one that has a male predominance seen in Great Britain for some reason more than in North America. It is very rare in North America and it is associated with

Scoliosis. This is curvature of the spine with rotation. That is scoliosis. There is a curve here and how do you know there is rotation? Because the ribs are twisted. If the ribs are twisted, there is rotation. If the ribs are not twisted, then there is no rotation and it is not

Developmental dysplasia of the hip. CDH is historic terminology. We donít use CDH anymore, we use DDH. The reason we do that is because some hips are stable at birth and develop instability afterwards so we think that it is not always congenital with birth. It sometimes is after birth. It is a complex disorder and it goes all the way from teratologic dislocations Ė dislocations that happened way before birth which are things like arthrogryposis that are horrible dislocations that are really hard to treat Ė all the way down to some late acetabular dysplasia where they have normal hips at birth and they get a little bit loose at three or four months and I canít explain that. So there is a wide spectrum probably because there is a wide inheritance pattern. The incidence is about 2.7 to 17 out of 100 live births. It is very common.

Multifactorial etiology. Ligamentous laxity. Usually it is an inherited condition thought to be more in males. It is thought to be autosomal dominant. Hormonal, which is when the baby gets the mom relaxin hormone in their circulation from the baby passing through the birth canal and their ligaments relax like the momís do when they pass the baby. It can be mechanical, both pre- and postnatal. The most

Clinical examination is the most helpful and to do that the baby must not be agitated. A crying baby can mask an unstable hip by tightening up their abdominal muscles. So the baby canít be crying. Do whatever you do. I will take a pacifier. I will put my pinky in the kidís mouth. I will do whatever to get the kid to stop crying so that I can examine and you have to do that. Examine one hip at a time. Donít try to examine both hips at one time. You canít do it. Look for metatarsus adductus, torticollis or knee dislocation. All of these things increase the incidence of DDH if they are present. The Barlow test is the first one that I do. It provokes subluxation and/or dislocation and we will go through that. The Ortolani test I do next and that provokes reduction. The reason I do the Barlow first and then the Ortolani is because B comes before O and I can remember it.

This is the Barlow test. This is the exact way your hand should be. Your thumb should be on the lesser trochanter. Your first web space should cradle the knee and your index finger should be over the greater trochanter. You give a gentle adduction and axial

This is the Ortolani test. It is abduction of the hip. Your hands are in exactly the same place. Your middle finger is over the greater trochanter, your first web space cradles the knee and your thumb is on the lesser trochanter. You gently push up with your middle finger trying to push the greater trochanter into the socket so that you can reduce the hip. If you push it out here and you can push it up there, then it is Barlow positive, Ortolani positive. If it is out and you canít get it back in, then it is a Barlow positive, Ortolani negative hip.

As far as descriptions, a "clunk" is the feel of translation of the femoral head either in or out of the acetabulum. It is pathological. It is a sign of dysplasia or instability. A "click" is a result of snapping of myofascial or ligamentous structures about the hip or the knee. It is a normal variant and is not related to instability. Of all the referrals for hip clicks, all those kids are normal. A click is normal. A click is a

Slipped capital femoral epiphysis is when the head of the femur becomes posteriorly displaced on the neck of the femur. It is fairly common, seen in 2 to 10 out of 100,000 patients. We see a lot of it. Boys 10 to 17 years. Twice as common in boys as in girls. Girls itís a little bit younger because girls mature faster. It is more common in blacks. Half the slips are over 95% percentile for weight. This

Legg-Perthes disease is another serious hip problem. It is an osteonecrosis of the femoral head. It involves the physis and metaphysis and we donít know what causes it. We have a theory that there are two embarrassments to the femoral neck blood supply through the circumflex system because there have been some experiments done where they clamp the medial circumflex once and no osteonecrosis happened. Then they clamp it again and the head started to die. So they call it a "double infarct" theory. But again it is only a theory. It happens in children from 4 to 10 years. It is more common in boys than girls and 10% may be bilateral but it is never symmetrical. In other words, you will see the same involvement of both hips at the same time. If there is you have to think about things like epiphyseal dysplasias or some sort of renal osteodystrophy or rickets or 

Tibial and femoral torsion. This is sort of the stuff that we will go through quickly but this is pretty important. It is rarely the cause of long term disability. It causes more anxiety in parents, relatives and doctors. It is caused by intrauterine molding. The thigh-foot angle. If you lay them prone, bend their knee up and look at the angle that their thigh makes and the angle that their foot makes, it will initially be

The natural history of tibial and femoral torsion is spontaneous improvement. The primary care doctors have to emphasize this to the parents. The orthopedic pep talks take up valuable clinic time that can be used to treat treatable things like Perthes disease. What we

Bowed legs and knock knees. Natural history consists of spontaneous resolution. The varus is worst at birth, neutral at 18 months and valgus at 30 and 36 months. That is what happens. This is by a group out of Sweden who documented a lot of kids with bowing and knock knees and this is the natural history. So you can put these up in your office and the kid comes in and has this much bowing at 1 year or 2 years and you know that it falls within a certain amount of standard deviations of normal. The alignment is usually adult by 4 to 5 years and x-rays of this are rarely necessary.

Reassurance is the key unless there are severe bowed legs or knock knees at 18 to 24 months which they should have already resolved. That you want to think about Blountís disease and rickets which are treatable and are severe if they are left alone. If a patient has significant short stature like metaphyseal chondrodysplasia and bowed legs, that is abnormal. If they have asymmetrical involvement, one leg really bows and one leg doesnít, then you want to think about these things like focal fibrocartilaginous dysplasia.

Club feet. Just quickly, it is forefoot adductus, hindfoot varus and ankle equinus. The incidence is 1 in 1,000 live births. Multifactorial etiology. Postural, congenital, syndromic such as Larsenís or arthrogryposis. This is a club foot. You canít miss that. That is pretty obvious when you see that in a newborn nursery. Initial treatment of all club feet is manipulation, casting and taping. I do casting. My

Metatarsus adductus. Very common. Caused by intrauterine molding. The forefoot is rotated medially. It has a convex lateral border. The hindfoot is not in equinovarus making this different from a club foot. If they have a medial crease, which will be right here, thatís a sign of a rigid metatarsus adductus which, again, is very rare. 85% of this improves without treatment. Usually the feet are