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Year 2 BRS MSK > Children's orthopaedics > Flashcards

Children's orthopaedics Flashcards

1
Q

LO:

A
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2
Q

Children’s MSK System

A

Differences:

  • Firstly there are more bones in a child skeleton, it has 270 compared to 206 in adult
  • Diagram on right demonstrates a child’s typical musculoskeletal system, and the blue lines you can see within the skeletal structure are the physis or growth plates, and these are the areas from which the long bone growth occur post-natally
  • So you can see that most long bones have 2 physis, one at the proximal end and one at the distal end. These are very important when discussing child MSK pathology, either via congenital conditions or trauma related to them.
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3
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Bone Development

A
  • Bone development can be broadly differentiated into 2 different pathways: Intramembranous and the other is endochondral.
  • Intramembranous ossification is the way that the cranial bones as well as the clavicle is formed
  • Endochondral bone development is responsible for the development of all the long bones of the body. This is particularly important in the paediatric skeleton.

YouTube Links for more information

Intramembranous ossification: https://www.youtube.com/watch?v=MZGRiUdg0RA

https://www.youtube.com/watch?v=gh6J2CHR_q4&t=52s

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4
Q

Intramembranous Ossificaiton

A

Intramembranous Ossification - Development of Flat Bones – cranium and clavicle

4 key stages

  • In intramembranous ossification, a group of mesenchymal cells in the central ossification centres differentiate first into preosteoblasts and then into osteoblasts.
  • These cells synthesize and secrete osteoid and the osteoblasts further differentiate into osteoclasts
  • These cells then collectively create the immature woven trabecular matrix and in turn the immature periosteium.
  • After this angiogenesis occurs and Blood vessels incorporated between the woven bone trabeculae will form the future bone marrow.
  • Later, the woven bone is remodeled and is progressively replaced by mature lamellar bone.
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5
Q

Intramembranous ossification:

A
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6
Q

Endochondral Ossification

A
  • During endochondral ossification, the tissue that will become bone is firstly formed from cartilage.
  • Responsible for development and growth of all the other long bones. This endochondral ossification occurs in 2 different ways, both at the primary and secondary ossification centres.
  • Primary Ossification Centres

Sites of pre-natal bone growth through endochondral ossification from the central part of the diaphysis of the bone.

  • Post natally, bone growth occur through the secondary Ossification Centres and these are what we referred to earlier as the physis, where usually each long bone has 2 physis, one at the proximal and one at the distal end of the bones respectively:

Occurs post-natal after the primary ossification centre and long bones often have several (the physis)

YouTube Links

Endochondral Ossification: https://www.youtube.com/watch?v=RpV1t9ZMSxY

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7
Q

Endochondral Primary Ossfication 1)

https://www.youtube.com/watch?v=RpV1t9ZMSxY

A

1) Perichondrium vascularised by blood vessels. These blood vessels start delivering nutrients that are going to stimulate those mesenchymal cells that remain there to differentiate into osteoblasts. Newly formed osteoblasts gather along the diaphysis wall (the outer edge of long bones) and start depositing osteoid to form a bone collar. Primary ossification centre is starting point for endochondral ossification.
2) Formation of the bone collar will cause chondrocytes that remain within that central cavity, to enlarge and send a signal to the surrounding cartilage to calcify. Calcified matrix causes an impermability of nutrients towards the inner portion of that developing bone. The cells in that area are therefore no longer receiving the nutrients they need for survival so causes cell death. Central clearing forms where cells have died (supported by bone collar). While this is all occuring at the primary ossification centre, there are still going to be healthy chondrocytes further distal towards the ends of the bone that are still producing cartilage matrix and are in charge of elongating of that structure.

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8
Q

Endochondral Primary Ossfication 2)

https://www.youtube.com/watch?v=RpV1t9ZMSxY

A

3) Periosteal bud invades cavity and causes the formation of spongey bone. The reason it does this is because the periosteal bud consists of an artery, vein, lymphatics, nerves, and it’s also going to deliver osteogenic cells (osteoclasts degrade cartilage matrix while osteoblast deposit new spongey bone. Bone continues to elongate elsewhere as have chondrocytes depositing new cartilage.
4) Primary ossification centre is going to continue to enlarge. Osteoclasts break down the newly formed spongey bone so that the early stages of the medullary cavity can form (where we store fat). Cartilaginous growth now only within epiphyses. Bony epiphyseal surface begins to form (as osteoblasts deposit osetoid here). Secondary ossification may appear after birth at one or both epiphyses of the developing bone (not going to start ossifying until after birth, so will remain as cartilage). Larger bones are more likley to have 2 secondary ossification centres. Short bones more likley to have 1 secondary ossification centre, irregular bones may have several.

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9
Q

Endochondral Primary Ossfication 3)

https://www.youtube.com/watch?v=RpV1t9ZMSxY

A

5) Cartilage now remains on bone surface eg articular cartilage and at epiphyseal plates (important for growth)

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10
Q

Endochondral
Primary Ossification

A

Pre-natal bone growth through primary ossification centres.

During endochondral ossification, the tissue that will become bone is firstly formed from cartilage

In primary endochondral ossification the ossification occurs at the primary centres, which is in the middle of the diaphysis of the shaft of the bone, and this occurs in the prenatal period.

The first site of ossification occurs in the primary center of ossification, which is in the middle of diaphysis of the bone - prenatal

a) Mesenchymal Differentiation at the primary centre
b) As this occurs you develop the cartilage model of the future bony skeleton forms
c) The through angiogenesis, capillaries penetrate this cartilage, and you create the primary ossification centre, and spongey bone forms from the middle of the shaft as we described.

Calcification at the primary ossification centre – spongy bone forms

Perichondrium transforms into periosteum

d) This spongey bone then continues to form up the shaft and as it does so cartilage and chondrocytes continue to grow at ends of the bone
e) Secondary ossification centres develop with its own blood vessel and calcification at the proximal and distal end of these long bones– calcification of the matrix (this blood supply then begins to calcify the previously uncalcified matrix into immature spongey bone)
f) So what your left with is cartilage at the proximal and distal ends of the bone and the epiphyseal growth plate, which will then be the point of secondary endochondral ossification in the postnatal period. (Cartilage remains at epiphyseal (growth) plate and at joint surface as articular cartilage.)

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11
Q

Endochondral
Secondary Ossification

A

YouTube Links

Endochondral Ossification: https://www.youtube.com/watch?v=rzuCav3xTyU&t=3s

Secondary Endochondral ossification

So by the time the fetal skeleton is fully formed and in the children’s skeleton ie by the time the child is born, cartilage remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate (aka physis)

It are these physis that is responsible for the futher growth of bones ‘Secondary ossification sites’.

The physis has various zones – and again the youtube link will describe secondary enchochondral ossification in more details’ but the zones each have a role in the growth of the long bones

This is again by the proliferation of chondrocytes and the subsequent calcification of the extracellular matrix into immature bone that is then subsequently remodelled.
What is key however is that it is the physis that is responsible for the skeletal growth of a child. So any congenital malfunction to this area or acquired insult – whether it is traumatic/infective or otherwise will therefore have a subsequent impact on growth of the child

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12
Q

Children’s Skeleton differs to that of an adult:

A

4 key ways: RESP

  1. The bone structure itself is different, in the material properties, principally that it is more elastic.
  2. Children’s musculoskeletal system is constantly developing and growing, particularly at secondary ossification centres, the physis.
  3. As a result of the continual growth, the speed of healing is vastly different in children compared with adults.
  4. As a result of the increased speed of healing there is a big difference in the remodelling potential, ie the amount of deformity that can be corrected as a result of the growth that the child is going through.
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13
Q

Elasticity

A
  • Children’s bones can bend more as have increased density of Haversian canals (microscopic tunnels within the cortex of the bones that circulate the blood supply).
  • Children have more Haversian canals, due to the fact that their bones are more metabolically active, at the virtue of them continuously growing.
  • As bones more elastic, get more plastic deformity, so when an energy is dissipated through the bone, it can bend more before it actually breaks, and this will give different types of fracture patterns when children sustain injuries.
    • One of these is known as a buckle fracture. So when a child may fall onto their outstretched hand, instead of the bone fracturing, it can actually buckle in on itself, and create this Torus like structure, which is named after the old Roman columns. Torus or buckle fracture: This occurs when only one side of the bone is compressed and buckles but does not break all the way through, creating a bulge.
    • Another way that children’s bones can be injured differently, is that they can be predisposed to getting Greenstick injuries. This is described like an immature tree, as if you find an immature sapling and try and break it, instead of being able to snap it in half, you’ll find that one side snaps, but the other side buckles.
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14
Q

Physis

A
  • Children have physis, adults don’t.
  • Closure of physis is dependent on various factors, these include: Puberty, Menarche in girls, Parental height and certain other genetic factors.
  • But generally speaking 15-16 years old for girls and 18-19 years old for boys.
  • Traumatic injuries of the physis can cause premature failure of growth. And the traumatic injuries are classified by the Salter-Harris classification.
  • If there is significant injury to the physis, it can cause growth arrest and the problem is growth arrest may not just across a whole physis itself, but part of it, and this can cause deformities. One part of the bone will continue to grow but the other will have stopped.
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15
Q

Speed and Remodeling

A
  • Dependent on age and location
  • Younger child is growing more rapidly and therefore they have the ability to heal more quickly than an older child and an adult.
  • Rate of growth at physis vary from site to site.
  • Eg in upper limb for instance, it’s extremes of the upper limb so the shoulder and the wrist that have the most growth, whereas in the lower limb it’s around the knee, so the distal femur and the proximal tibia grows more, as opposed to the proximal femur or the ankle itself.
  • So injuries where there is most growth, in the younger child has firstly the fastest healing, but secondly the largest modelling potential.
  • Here can see series of radiographs (X-rays) in a child, and they’ve sustained a midshaft humerus fracture, and as you can see, within 2 weeks, there’s huge amounts of new bone formation, and by 6 months you can barely notice that the child has had any injury at all. Now the rate of healing in these radiographs is much more accelerated than that of an adult and actually we know that children can tolerate huge amounts of angulation and deformity in most of the planes due to the fact that they are continuously healing so quickly.
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16
Q

Remodeling

A

Set of images demonstrating how significant remodelling potential in a child can be, that is simply not available in an adult:

  • This is a young girl age 9 who was involved in a road traffic incident and broke both of her proximal humeri. As you can see there is significant displacement of both the fractures.
  • But because this is an area of rapid growth, being at the proximal humerus, her age being favourable, you can see in the next series of radiographs at the bottom, that within 2 years, the fracture had fully healed and actually that significant deformity had fully remodelled, to the point where actually there was no visible deformity and no functional restrictions. And this was all as a result of being managed non-operatively and conservatively in a sling.
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17
Q

Common Children’s Congenital
Conditions

A

There are countless more examples, but these are the most common.

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18
Q

Developmental Dysplasia of the Hip (DDH)

A
  • Can think of this as a ‘packaging disorder’ as it occurs in utero, so when the child is in the mother’s womb, usually due to the way the child sits, it can affect the way that the hip sits within the acetabulum.
  • And the normal development of the hip in the acetabulum relies on this concept of concentric reduction and balanced forces. So in order for the hip to develop normally, and vice versa for the acetabulum to develop normally, the hip needs to sit within the acetabulum, and you need to have the normal forces going through the joint.
  • If the hip sits outside the acetabulum, not only would the hip not develop normally, but the acetabulum, because it doesn’t have those pressures going through it, will in turn not develop either.
  • This is a spectrum of a condition, so in the very mild cases you get what’s known as dysplasia, so the hip may be within the socket, but not quite centrically placed, therefore the socket does not develop into a nice cup.
  • More severe conditions have subluxation, where at times the hip is in the socket, but due to the shallow nature of the socket, the hip will pop in and out.
  • In very severe conditions you can have dislocation where the packaging disorder has been so severe that the hip has never been inside the socket and develops outside of it, and as a result, because the socket of the acetabulum has never had that pressure, it develops with a very shallow cup.
  • Now it is one of the most common conditions of the child and dysplasia can be as common as 2 in every 100 children, and dislocation in 2 in every 1000 children.
  • Risk factors
    • More common in females
    • First born
    • Breech position
    • Family history
    • As it is a packaging disorder, there are other risk factors sych as oligohydramnios (so not enough fluid within the amniotic sac)
    • More common in native Americans and Laplanders, due to the habbit of swaddling of the hip once a child is born, and this can actually worsen the condition after the child has been delivered. Swaddling is a traditional practice of wrapping a baby up gently in a light, breathable blanket to help them feel calm and sleep. Swaddling infants with the hips and knees in an extended position may increase the risk of hip dysplasia and dislocation.
    • Rarely seen in African American/ Asian population

YouTube Links

Hip Dysplasia: https://www.youtube.com/watch?v=twb_JeuWEug

19
Q

Developmental Dysplasia of the Hip

examination, investigation and treatment:

A
  • DDH usually picked up on baby check, which is a routine part of screening for all newborn children in the UK.
  • At the screen you examine the range of motion in the hip, and perform special tests known as Barlow and Ortalani’s.
  • The Galeazzi sign is elicited by placing the child supine with both hips and knees flexed. An inequality in the height of the knees is a positive Galeazzi sign and usually is caused by hip dislocation or congenital femoral shortening.
  • If there is any concern, then the investigation of choice is an ultrasound. This is effective and sensitive from birth to 4 months.
  • After 4 months, it’s typically preferable to perform an X-ray, but there is no benefit of X-ray prior to this, as the secondary ossification centres of the hip have not yet ossified.
  • The other thing to consider, is that sometimes you can find abnormal examinations in premature children, so this needs to be age adjusted when you factor this in, and the ultrasound can then give your measurements of the acetabular angles, as well as the position of the hip.
  • The treatment of DDH is normally by the means of a harness, so the image on the right you can see a baby in a Pavlik Harness. So the hips are flexed and abducted, and the aim of this is to hold the femoral head within the acetabulum, so that as the child grows, you get the concentric pressures through the hip joint, and this supports the further normal development.
  • If however the Palvik Harness fails, unfortunately the abnormalities picked up are too late for it to be effective, then it may warrant surgical intervention. A hip spica cast is a sort of orthopedic cast used to immobilize the hip or thigh. It is usedto facilitate healing of injured hip joints or of fractured femurs. A hip spica includes the trunk of the body and one or both legs.
  • Take home message: This is a condition that is progressive and it is about the normal development of te hip, so treatment at the infant age as you can see is not about preventing morbidity in age but it’s to give the child the most normal development of the hip as possible so that when the child is an adolescent and adult, they avoid any issues from a dysplastic hip in the future.
20
Q

Clubfoot

A
  • It’s again a packaging disorder, so it occurs in utero.
  • You’ll find an obvious clinical deformity in a child’s foot, and it is often bilateral.
  • It occurs in about 1 in 1000 children, with a predisposition towards boys, it’s highest in the Hawaiian population. There is a genetic link, it is the PITX1 gene, and it affects approx 5% of all future siblings.
  • The Cavus and Adductus deformities occur in the midfoot, while the Varus and Equinus deformities occur in the hindfoot.The deformity you will find can be remembered by CAVE:
    • Cavus foot with high arch and tight muscles: the intrinsic muscles, the flexor hallucis longus and flexor digitorum longus.
    • -Cavus in the midfoot is the first part of the deformity of clubfoot. The arch of the foot is higher than normal.as a result of the first metatarsal being plantarflexed in relation to the calcaneum and hindfoot.
    • Then the foot is held in adductus
    • -Adductus is movement towards the midline. Adductus is the second part of the clubfoot deformity. The forefoot is adducted towards the midline. This is the second part of the deformity of clubfoot. The navicular moves medially and starts to dislocate off the talus. The calcaneum also rotates medially under the talus as part of the adductus deformity.
    • In Varus. Varus means movement towards the midline. Varus of the hindfoot is the third part of the deformity of clubfoot. The heel is in varus in relation to the tibia.
    • And in Equinous. Equinus means an increase in the plantarflexion of the foot. The entire foot points downwards in relation to the tibia. Equinus of the hindfoot is therefore the fourth part of the clubfoot deformity.
21
Q

Clubfoot: treatment

A
  • Again clubbed foot is usually diagnosed on the usual baby check when the baby is newly born.
  • The gold standard treatment method is the Ponseti Method. So the child’s foot is placed in a series of casts to gradually correct the deformity, and the deformity is corrected as per the CAVE acronymn. A technique known as the Ponseti method is the main treatment for club foot nowadays. This involves gently manipulating your baby’s foot into a better position, then putting it into a cast. This is repeated every week for about 5 to 8 weeks.
  • It is typical to require some form of operative treatment, and usually it’s just in the form of a soft tissue release.
  • And once the child has has their sequential casting, then often they will require a foot orthosis brace, shown in image, and it looks like the child’s feet are placed on a skateboard.
  • For the most part this is sufficient to treat the deformity, but some children will require further operative intervention to give them the full functional return. And this can be in the form of further soft tissue releases, or unfortunately significant interventions such as tendon transfers.

YouTube Links

Ponseti Method: https://www.youtube.com/watch?v=1otnjPTsEXU

22
Q

Achondroplasia

A
  • Earlier it was mentioned that congenital deformities in children can occur if there are abnormalities within the physis themselves. One of these conditions is known as achondroplasia-most common skeletal dysplasia.
  • This occurs if there is an abnormality in the proliferation zone of the physis where the normal chondrocyte proliferation is no longer effective.
  • In achrondroplasia, this is autosomal dominant abnormality that is a G380 mutation of the FGFR3 zone. And unfortunately this result in a defect of normal endochondral bone formation effects secondary endochondral ossification.
  • The deformity in photo is typical of achondroplasia, so you get what’s known as a Rhizomelic dwarfism, where the humerus is shorter than the forearm and the femur is shorter than the tibia, but you get a normal trunk size. The final adult height is typically 125cm.
  • In terms of other manifestations, they tend to suffer from spinal issues which often require operative intervention, but they have normal cognitive development
23
Q

Osteogenesis Imperfecta

A
  • This is an abnormality that affects the collagen structure within the bone itself, and it can be either autosomal dominant or recessive.
  • It creates an abnormality in the type 1 collagen that you find in bone. This can be either a quantitative issue, or a qualitative issue of the type 1 collagen.
  • Again osteogenesis imperfecta is a spectrum of conditions, and there are many different manifestations. This is described by the sillence classification.
  • Essentially it can effect both the bones and there can also be non-orthopaedic manifestations-eg cardiac abnormalities, blue sclera-see pic (most common), you also hear of the Dentinogenesis imperfecta, so you get brown soft teeth and other features include a wormian skull due to the abnormal fusion of cranial sutures as well as hypermetabolism, typically effecting the parathyroid pathway.
  • In terms of the bones, most typically you get fragility fractures, as the bones are brittle and the patients are prone to multiple fractures. Some forms of osteogenesis imperfecta can result in the patient having a short stature and it is quite typical for the patient to have spinal manifestations such as scoliosis.
  • In 1979, Sillence et al. developed a classification of OI subtypes based on clinical features and disease severity: OI type I, mild, common, with blue sclera; OI type II, perinatal lethal form; OI type III, severe and progressively deforming, with normal sclera; and OI type IV, moderate severity with normal sclera.

YouTube Links

Osteogenesis Imperfecta: https://www.youtube.com/watch?v=JA5ap43iFrQ

24
Q

Previous slides gave insight into how different abnormalities can occur, both in utero as a packaging disorder or congenitally, either due to abnormalities within the physis or within the boney matrix itself.

Paediatric Fractures:

The way that we describe fractures doesn’t change for that of an adult

A

PAID

The other consideration we must have in the paediatric fracture, is that of the physis. So if the fracture affects the physis, then this can be described by the Salter-Harris classification.

25
Q

Pattern

A
  • Pattern can be described in same way as adult
  • The pattern is often reflective of how the energy is dissipated through the bones.
  • If there is a rotational torque pattern of injury, then you often get a spiral fracture.
  • In higher energy injuries, you can get a comminuted fracture where there is more than one part.
  • And if the bone has been pulled off by it’s ligamentous attachment, then you get the avulsion type fractures.
  • Now remember, as discussed previously, the paediatric skeleton has increased elasticity, and more scope for plastic deformity than the adult fracture, so sometimes whereas in the adult population you might see a fracture, it can be, in the paediatric population you simply get plastic deformity, as shown by image on right.
  • Otherwise you can get fracture patterns that you wouldn’t typically see in the adult population, such as the greenstick fracture, as well as the torus fracture.
26
Q

Anatomy

A

Now the anatomy is where in the bones the fracture is located. So typically the way we describe this is to split the long bones into thirds so you get the proximal third, the middle third or the diaphysis and the distal third. This is not dissimilar to that of an adult, but in the paediatric population, what we must be cognitant of is that in the proximodistal third, there is the secondary ossification centres for endochondral bone formation, the physis. And that is when the management of fractures and the consideration may differ from that of an adult.

27
Q

Intra/Extra-Articular

A

The ‘I’ in paid stands for intra or extra-articular.

Again, this is very important as it can affect and dictate the way we manage fractures. Remember, bone can heal in one of two ways, either by primary bone healing, which is by direct union without callus formation, or by secondary bone healing, which is bone healing by callus.

Again, we’ve got to remember that the child has a much faster healing potential, as well as remodelling potential. So, as shown in the previous radiographs, any extra articular fractures that would be managed typically by secondary bone healing, will heal much more quickly than that of an adult, with a significant scope for remodelling potential.

But what we’ve got to remember, again, is the physis. If a fracture affects the physis, which we’ll discuss in a short moment, then the worry is it can affect growth. So this needs special consideration, which is not an issue in the adult population.

28
Q

Displacement

A

So displacement is again discussed just like in the Adult fracture, so you can talk about whether it’s displaced, angulated, shortened or rotated, so a fracture can be one or many of the above.

When we discuss remodelling potential, the remodelling potential can give a significant amount of allowances for any level of displacement. There are some considerations for this, however, is that any displacement is best in the angle of function, and remodelling does not occur in any rotated fractures. So rotation is not tolerated very well, but angulation, shortening and displacement can be, when considering the potential remodelling the children have.

29
Q

Salter-Harris

A

So as I’ve alluded to, the key consideration in fractures in the child is the physis and the Salter-Harris classification is a way to classify physeal injuries. And the way that I find best to remember this is by the pneumonic of SALT.

There are five stages in this Salter-Harris classification. The first is type one, which is a physeal separation where the injury goes through the physis. The type two is where the fracture transverses a physis and exits above the physis or through the metaphysis, and that is the A insult. Type three is where the fracture transverses the physis and exits distal to this or lower, and through the epiphysis which is the L. Type four is a fracture that passes through both the epiphysis, the physis itself, and the metaphysis, and the T is through. And Type five is a crush injury to the physis which is relatively uncommon. So there are five different types in the classification of Salter-Harris. Type two is by far the most common and the risk of growth arrest increases from type one to type five.

30
Q

Growth Arrest

A

Now, the topic of growth arrest is a complex one, and is beyond the scope of this lecture to discuss in its entirety. However, the way you can think about growth arrest is, and any injury to the physis can cause growth arrest. As we now know, the Salter-Harris classification gives you an idea, an indication of how likely growth arrest is. The key, however, is the location of the injury and the timing. So as we’ve discussed previously, different parts of the skeleton grow at different rates, and the child also grows at different rates as they grow older. It’s mentioned if you are closer to physeal closure when the injury happens, you’ve got only a small amount of potential growth left. An injury to a physis that is a large part of that limbs growth at a younger age means that the potential for growth arrest is much greater.

The other thing to consider is how much of the physis is affected. Is it an injury to the whole physis, or is it an injury to just part of the physis? Because this is going to affect the way that the growth arrest occurs. If it’s a whole physis, then you’ll get a limb leg discrepancy as a primary outcome, such as the image on the right. As you can see, this child has had an unfortunate injury to their left femur in the past, and their left femur is therefore shorter than the right. However, this appears to have affected the whole physis as there’s not much of an angular deformity.

The image to the left shows an injury to again, the left ankle in a different child. But this has unfortunately developed more of an angular deformity as it’s been more the lateral aspect of the distal tibia physis that’s been affected. So the medial side has continued to grow, but the lateral distal tibia has failed to grow and therefore you’ve got this angular deformity.

So to recap, it’s about when the injury happens. how much potential growth is left to be affected, and where the injury happens, where in the skeletal structure is it? How much potential growth occurs in that area? and is across the whole or is it just part of the physis?

31
Q

Growth Arrest: treatment

A

Now, the treatment of growth arrest, the aim of it is to correct the deformity, to minimise the angular deformity and to minimise the limb length difference.

The way that this is addressed, again depends on patient factors. So, again, where has the injury occurred? When has the injury occurred? And how much growth is left? Broadly speaking, you have several ways to address it. If you’re trying to correct the limb length, one way is to actually shorten the long side, so prematurely stop the growth of the unaffected side to help balance that limb length correction.

The other way is of course to try and lengthen the short side. So in the image you can see here, you’ve got one image where the surgeon has prematurely fused the physis of the distal femur using these crossed screws. So the aim of it is to correct the deformity by shortening the unaffected side. The image below this has shown an intramedullary device that is a limb lengthening device.

If there’s an angular deformity, the principles are again, broadly the same. What you can try and do is stop the growth of the unaffected side-try and balance things out. Or if this is not possible, then to reform the bone, ie perform an osteotomy to surgically balance out the deformity. Now, these are very broad principles because as mentioned, the way and the type of correctional surgical procedure we would use, depends as mentioned again on where in the body the injury is, when it occurred ie how much growth is left, and of course, this is often a very difficult management choice and we need to consider the multidisciplinary team with the physiotherapists and of course the patient and also the family. But these are the broad principles that we can take to correct growth arrest and the deformity that goes with it.

32
Q

Fracture Management

“The 4 R’s”

A

Now, this brings us nicely onto the principles of fracture management as we know the principles of fracture management for any patient can be catergorised by the 4 R’s and a paediatric fracture is no different.

Now, as I mentioned, again, there are special considerations in the child that may alter or need to be taken to consideration. One of which is obviously potential for growth arrest, and we’ll discuss this in more detail now.

33
Q

Resuscitate

A

Of course, the first thing we need to consider in the management of any traumatic injuries is to resuscitate.

So in the case of a paediatric patient, this would be following the paediatric advanced trauma life support pathway.

34
Q

Reduce

A

Now, provided the patient is stable, the first thing we need to consider is reducing the fracture. And this is the principle of correcting the deformity and displacement. Now, as mentioned before, the paediatric skeleton is different from the that of an adult, because of the plastic deformity potential and the increased elasticity of the bones.

What you’ve got to consider therefore, is the soft tissue injuries and neurovascular structures that might be affected as the energy is dissipated through that fracture. However, the principles of reduction of that are the same of the adult. You’ve got close reduction techniques and open reduction techniques.

The other thing you must consider in the paediatric population is also the massive remodelling potential. So we know that paediatric fractures now heal more quickly than that of an adult. And due to this, and the potential remodelling, actually quite significant angular deformities can be tolerated as these will remodel out.

35
Q

Closed
Reduction

A

As a result, it’s quite common practice to manage paediatric fractures with close reduction alone. So closed reduction is a simple method of manipulation of the fracture to correct the deformity. And this can be as simple as applying a plaster in A and E, or sometimes a patient may need to go to theatre for manipulation and anaesthesia and application of plaster. So the series of radiographs you see below is a Salter-Harris Type 2 fracture of the distal radius in this skeletal image of an immature child. So we know that in a Salter-Harris type 2 fracture the energy goes through the physis and above it into the metaphysis. It’s the most common type of physeal injury, and relatively has a low risk of growth arrest. Now, this child had a visible deformity that you can perhaps appreciate from the lateral radiograph. And although the likelihood is that the child will remodel, the decision was taken to have a closed reduction. So the child was taken to theatre anaesthetised and a closed reduction under anaesthesia was performed and the child was placed in a moulded plaster.

Other treatment modalities more commonly used in the paediatric population, is traction. So here we’ve got a clinical picture of a child in Gallows traction. So there is skin traction applied to the femur with a weight, and this can help hold the long bones of the lower limb whilst the fracture heals. This is quite commonly used for long bone fractures in the younger child in the past, although it’s slightly less commonly used now. It’s still a perfectly reasonable way in theory of managing such an injury.

36
Q

Restrict

A

Once you have a satisfactory reduction of any fracture, the next principle is to restrict it or hold that fracture reduction in place. This provides stability for the fracture to heal. Now, contrary to adults, children rarely have an issue with bones not healing, their metabolic activity means that the bones are rapidly growing, they’re very highly vascularised, and generally speaking, they don’t have the patient risk factors that an adult patient may have to inhibit growth. In fact, in a younger child, there can be issues with too much healing or overgrowth, which can be a factor to consider when considering midshaft fractures in the long bones. And remember, the child’s fracture will heal much more quickly with their greater remodelling potential also.

Now, restriction of any fracture can be categorised into that of an external method or an internal method. Just like an adult, external methods include application of a splint or plasters, as we’ve already discussed. And an internal method will be formed intraoperatively. This can be in the form of plates and screws or intramedullary devices, just like that in an adult population.

(A cast wraps all the way around an injury and can only be removed in the doctor’s office. All casts are custom-made with fiberglass or plaster. A splint is like a “half cast.” The hard part of a splint does not wrap all the way around the injured area. It is held in place by an elastic bandage or other material)

37
Q

Restrict

External restriction methods:

A

Extenal restriction methods are commonly used in the paediatric fracture, as mentioned the ones used are plasters and splints. Because the child has a large amount of remodelling potential, as well as faster healing. It does tend to mean that operative interventions can be avoided more than the adult population. So here you’ve got a picture of a very young child in a Spica cast (remember for DDH). This is a special type of plaster that will hold the lower limbs in place. And then below you’ve got a very typical below albow plaster in a teenager’s forearm.

38
Q

Restrict

Internal restriction methods:

A

Now, occasionally, operative intervention may be required in the form of internal fixation. As said, this can be in the form of plate and screws or in the form of intramedullary devices. Often these operative intervention is utilised when the fracture affects the physis, and we need to correct any potential deformity to prevent growth problems in the future, or if the deformity as in the picture below, is not to the around the physis, but beyond the potential tolerance of remodelling.

What we must consider in the paediatric population is to avoid further trauma to the physis for the risk of growth arrest, and also any metal work that is put in, is more likely to be needed to be removed in the future again due to growth. So what you see on the picture, on the right is a child with a Salter-Harris type 3 fracture of the distal tibia, so a fracture that’s gone through the physis and is exiting distal to that. Now, we know this has a slightly increased risk compared to Salter-Harris type two of growth arrest, and also this is affecting the joints. So what we want to achieve is anatomical reducton of that fracture fragment, compression to allow for primary bone healing. So here we’ve got one single screw to compress that fracture fragment. And as you can see, it’s been carefully placed to avoid any direct trauma to the physis to avoid growth arrest.

In these radiographs of the forearm. You’ve got a paediatric forearm fracture with significant angulation both in the AP and in the lateral plane. This is obviously beyond the level of correctable remodelling. So this patient required a closed reduction in theatre and due to the fact that the fracture is unstable and likely to deform if place simply into a plaster, there had an intramedullary device inserted. These wires, a called flexible nails, they’re made of titanium and they are fed through the skin into the intramedullary canal. And the principles of it, is that they are slightly elastic and they help tension the forearm through the intraosseous membrane and hold the reduction in place. These wires and then bent and buried under the skin and then will require subsequent operation to remove them once the fracture has healed.

39
Q

Rehabilitate

A

Finally, just like in the adult population, once you’ve resuscitated, reduced and restricted the fracture, and the fractures healed. The final step is rehabilitation.

Children generally rehabilitate very quickly and don’t need any formal physiotherapy for the most part. For younger children, play is a great rehabilitator, and stiffness is not as major an issue as in adults. But just like in the adult population, the basic principles remain the same as using it, moving it and strengthening it.

Fracture management-4 Rs summary

So we’ve covered in broad principles the management of paediatric fractures by the 4 Rs, remember, resuscitate, reduce the fracture, hold the fracture and rehabilitate the fracture. The key ways in which the child’s musculoskeletal system differs from that of an adult is the fact that they heal more quickly, they have further remoulding potential. So generally speaking, operative intervention is not quite as commonly required for most fractures as in the adult population. The special consideration we must always consider is the physis in the risk of growth arrest. So if any intervention is required, then principles are to minimise any further trauma to the physis to minimise the risk of any future growth arrest.

Thankfully, as mentioned, children do rehabilitate very, very quickly and therefore formal physiotherapy is not often required, but it is something to consider nonetheless.

40
Q

The Limping Child

A

Now, this is a clinical conundrum often faced by those both in the primary care setting as well as in hospital. And the reason this is of any significance is, it can potentially have huge ramifications on the child’s functional outcome. The reason being is, is that one of the key differentials in any limping child must and will always be septic arthritis.

Septic arthritis is a condition we’ll discuss in more detail, but is effectively an infection in the joint and this can have catastrophic and irreversible damage to the joint that will unfortunately last with a child lifelong if it is to be missed.

The other differential diagnosis of any limping child is, of course, transient synovitis. And there are other conditions such as Perthes or SUFE (Slipped Upper Femoral Epiphysis), which will also discuss.

41
Q

Septic arthritis

A

Septic arthritis and a child is an orthopaedic emergency. It’s the presence of an infection within the intraarticular space. It can cause irreversible long term problems in the joints due to both the necrosing effect of the proteases that the organisms create within the joint itself, but also due to the pressure effect from the chondrocytes and the cartilage that occurs from the oedema within closed space.

The management of septic arthritis in is invariably surgical wash out of the joint to clear the infection. The problem is, is that septic arthritis can be sometimes challenging and difficult to diagnose, especially a younger child who may not give a thorough history. And if the history of the presenting complaint is not quite as clear. The history, however, is key. What you’ve got to identify is, what symptoms they are having, the duration of the symptoms and the chronicity and the acuteness, whether they’ve had any recent illnesses. Often coryzal symptoms, and these are very common in children and any other associated joint pains, rashes, diarrhoea, vomiting the child may have.

There is a classification system known as Kocher’s classification that can help score the probability of a child having septic arthritis. Now, the typical history of any child presented to you may be something along the lines of a young child who’s previously fit and well, who over the last 24, 48 hours has become off their food off their drink, and in the last twelve hours or so has become unwell with a fever and not wanting to move their knee and their hip. Kocher’s classification can help score the probability of this being septic arthritis. And it’s based on four markers:

  1. A child being non-weight bearing.
  2. Having a temperature over 38 or less than 36
  3. Biochemical markers: ESR raised above 40 or
  4. white cells more than 12.

The more of these criteria you have, the more likely it is to be septic arthritis.

As mentioned, septic arthritis is a surgical emergency. However, the key differentiatial diagnosis is transient synovitis and this is a common condition, secondary to often a coryzal illness. Any child can often have associated muscle pains related to it. However, transient synovitis is a diagnosis of exclusion once septic arthritis can be excluded. Transient synovitis can be treated with supportive measures such as fluids, observation and antibiotics. Whereas, as mentioned, septic arthritis needs an emergent surgical wash out of the joint to clear the infection. And failure, to identify this and treat this accordingly can cause irreversible damage to the joint and loss of function in the long term for the child.

This is why the limping child is always a concern for an orthopod and must be taken seriously. I’ve attached here a YouTube video that goes into that diagnosis management and history of a child with septic arthritis in more detail.

YouTube Links

Septic Arthritis: https://www.youtube.com/watch?v=90lNRlfTFAA

42
Q

Perthes Disease

A

Now, one of the less common differential diagnosis of a limping child is Perthes disease. This is an ideopathic necrosis of the proximal femoral epiphysis. It is usually found in those between four to eight years old, and is more common in boys than girls.

Remember, septic arthritis must be excluded first, but the presentation of a child with Perthes can be quite similar. It’s a child usually in the age group above who’s not walking with a limp. However, the key differentials is the chronicity. This will often be going on for a bit longer than in a child with septic arthritis, or transient synovitis. And again, you wouldn’t expect to see the temperatures and the inflammatory markers that you would in septic arthritis.

The key diagnostic test is a plane film radiograph. And you can see on the radiograph on the right that this child has perthes disease of the left hip where the epiphysis is not as symmetrical and well-formed as the other side.

Treatment is usually supportive in the first instance for children with Perthes Disease. And if diagnosed warrants a referral to the specialist for continued observation and management of the condition.

43
Q

SUFE

A

In the slightly older age group, usually between 12 and 13 years old, a differential for limping child is also SUFE or slipped upper femoral epiphysis. This is a condition where the proximal epiphysis slips in relation to metathesis and is usually found in those around, as mentioned 12-13 years old during a period of rapid growth.

Risk factors include a family history, underlying endocrine disorders, more common in males, and is found in those who are overweight.

Must exclude septic arthritis first in a limping child. The history again is more akin to perthes where the child may be complaining of a limp, it is not as acute typically as septic arthritis, and again you wouldn’t expect child to have temp or increased biochemical markers.

The presentation of SUFEs can be broadly classified into acute or chronic where sometimes you can get an acute on chronic presentation, where the child may have had episodes of hip pain and limping in past but it has suddenly got worse. There are special classification systems that can further differentiate it into whether the child is able to weight bear or not, and this will inturn affect the management.

Treatment

-If unstable slip, will usually be in the form of operative fixation, to prevent further slip, and to minimise further growth problems, because as you can appreciate, this is an injury that affects the physis and so can affect the growth of that hip.

Again if suspicious of SUFE, investigation is plane film radiograph, this is what’s known as a frogs leg view, that gives very good view of physis and can identify potential slips.

This again warrants referral to a tertiary specialist

44
Q

The Limping Child

A

But remember, the differential diagnosis for any limping child is septic arthritis, septic arthritis, septic arthritis and septic arthritis. You must exclude septic arthritis in any limping child. Transient synovitis is a diagnosis of exclusion and Perthes disease and SUFE, and there many other differential diagnosis of a limping child that they aren’t as common, certainly as transient synovitis. But you must exclude septic arthritis in the first instance.

Year 2 BRS MSK (12 decks)

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