children's orthopaedics Flashcards

1
Q

how does the children’s skeleton differ from that of an adult?

A

The paediatric skeleton and musculoskeletal system is NOT a miniaturised version of an adult

A child’s skeleton has 270 bones (206 in adults) and is a system that is in continuous change

The physis (growth plates) are the areas from which long bone growth occurs post-natally

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2
Q

what are the different types of bone development?

A

intramembranous:
mesenchymal cells
->
bone

used for flat bones

endochondral:
mesencymal cells
->
cartilage
->
bone

used for long bones

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3
Q

what Is the process of intramembranous ossification?

A

eg. in clavicle and skull

condensation of mesenchymal cells which differentiate into osteoblasts - ossification centre forms

->

secreted osteoid traps osteoblasts which become osteocytes

->

trabecular matrix and periosteum forms

->

compact bone forms superficial to cancellous bone. crowded blood vessels condense into red bone marrow

->

immature woven bone is remodelled and replaced by lemellar bone

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4
Q

what is the process of endochondral ossification?

A

All other long bone formation
- At both the primary and secondary ossification centres

Primary Ossification Centres:
Sites of pre-natal bone growth through endochondral ossification from the central part of the bone

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

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5
Q

what happens in the pre-natal part of endochondral ossification (in primary ossification centres)?

A

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

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

a) Mesenchymal Differentiation at the primary centre

  • > b) The cartilage model of the future bony skeleton forms
  • >

c) Capillaries penetrate cartilage.
Calcification at the primary ossification centre – spongy bone forms
Perichondrium transforms into periosteum

  • > d) 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 – calcification of the matrix
  • >

f) Cartilage remains at epiphyseal (growth) plate and at joint surface as articular cartilage.
these become the secondary ossification sites

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6
Q

what happens In the secondary ossification centre part of endochondral ossification?

A

Post bone growth through Secondary ossification centres
“The Physis’

This is again by the proliferation of chondrocytes and the subsequent calcification of the extracellular matrix into immature bone that is then subsequently remodelled.

Long bone lengthening

Happens at the physis (physeal plate)
Zone of elongation in long bone
Contains cartilage
Epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix
Diaphyseal side – Cartilage calcifies and dies and then replaced by bone

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7
Q

what are the main ways in that the Childs skeleton differs from that of an adults?

A

elasticity:
children’s bones are more elastic

physis:
growth happens at the physes, adult bones don’t grow

speed of healing:
much faster

remodelling:
the amount of deformity that can be corrected is greater in children

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8
Q

how is bone elasticity different in children to adults?

A

Children’s bone can bend – more elastic than adult

children have an Increased density of haversian canals (more of them)
Therefore you can get:
Plastic deformity
– bends before breaks

Buckle fracture
– Torus like the column

Greenstick
– like the tree
One cortex fractures but does not break the other side

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9
Q

how is physis different in children than adults?

A

Growth occurs at varying rates at varying sites
Growth stops as the physis closes

Gradual Physeal closure, depends on, Puberty, Menarche, Parental height

Complete a:
Girls 15-16
Boys 18-19

Physeal injuries are catgorised by Salter-Harris

Physeal injuries can lead to growth arrest

Growth arrest can lead to deformity

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10
Q

how does the speed of healing and remodelling differ from children to adults?

A

The speed of healing and remodeling potential is dependent on the location and the age of the patient

Younger child heals more quickly

Physis at the knee grows more
Physis at extreme of upper limb grows more

the faster a bit grows (knee, shoulder, wrist) the faster healing, and the more remodelling potential

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11
Q

what are some common children’s congenital bone conditions?

A

developmental dysplasia of the hip

club foot

achondroplasia

osteogenesis imperfecta

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12
Q

what is developmental dysplasia of the hip?

A

Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum.
A ‘Packaging Disorder’
The normal development relies on the concentric reduction and balanced forces through the hip

Spectrum with:
dysplasia - hips is on socket but not quite right, so socket doesn’t form a nice cup
subluxation - hip in socket, but socket is shallow so hip pops in and out
dislocation - hip isn’t in socket at all, so acetabulum is very shallow

Dysplasia 2: 100
Dislocation 2:1000

risk factors:
Female 6:1
First born
Breech
FH
Oligohydramnios
Native American/Laplanders – swaddling of hip
Rare in AfricanAmerican/Asian
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13
Q

what examination and investigations are done for developmental dysplasia of the hip?

A

examination:

Usually picked up on baby check – screening in UK:
RoM of hip
Usually limitation in hip abduction
Leg length (Galeazzi)
In those 3 months or older Barlow and Ortalani are non-sensitive

investigations:
Ultrasound – birth to 4 months
After 4 months X-ray
If prior to 6 weeks needs to be age adjusted
Measures the acetabular dysplasia and the position of hip

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14
Q

what is the treatment for developmental dysplasia of the hip?

A

Reducible hip and <6 months -
Pavlik harness 92% effective

Failed Pavlik Harness or 6-18 months
Secondary changes- capsule + soft tissue
MUA + Closed reduction and Spica

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15
Q

what is club foot?

A

Congenital Talipes Equinovarus

Congenital deformity of the foot 
occurs 1:1000 people
Highest in Hawaiians
M2:1F
50% are bilateral

Genetic:
Approx. 5% likely of siblings
Familial in 25%
PITX1 gene

CAVE deformity due to muscle contracture
Cavus –high arch: tight intrinsic, FHL, FDL
Adductus of foot: Tight tib post and ant
Varus: Tight tendoachillies, tib post, tib ant
Equinous: tight tendoachilles

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16
Q

what is the treatment for club foot?

A

Treatment:

Ponseti Method
Gold standard

  1. First a series of casts to correct deformity
  2. Many require operative treatment
    Soft tissue releases
  3. Foot orthosis brace (looks like snowboard)
  4. Some will require further operative intervention to correct final deformity.
17
Q

what is achondroplasia?

A

The most common skeletal dysplasia
Autosomal Dominant:
G380 mutation ofFGFR3
inhibition of chondrocyte proliferation in theproliferative zoneof thephysis
results in defect in endochondral bone formation

Rhizomelic dwarfism:
Humerus shorter than forearm
Femur shorter than tibia
Normal trunk size
Adult height of approx. 125cm

Normal cognitive development
Significant spinal issues

18
Q

what is osteogenesis imperfecta?

A

Osteogenesis Imperfecta
Brittle bone disease

Hereditary – autosomal dominant or recessive
Decreased Type I Collagen due to:
Decreased secretion
Production of abnormal collagen

-> Insufficient osteoid production

Effects:
Bones -
Fragility fractures in some 
Short stature
Scoliosis 
Non-orthopaedic manifestations-
Heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull
Hypermetabolism
19
Q

how do we describe paediatric fractures?

A

same as adults

PAID
Pattern
Anatomy
Intra/extra-articular
Displacement

salter-harris - whether it effects the physis or not

20
Q

what are possible patters on fractures in children?

A

same as adults?

transverse
oblique
spiral
comminuted
avulsion (chunk of bone pulled off by its ligamentous attachment)

but unlike adults you can also get greenstick fractures or torus fractures
due to the increased elacticity

21
Q

what are the possible anatomical points for a fracture?

A

name the bone

then it is split into the proximal 1/3
middle 1/3
distal 1/3

proximal and distal contain the phases

22
Q

what does intra and extra articular mean?

A

primary bone healing:
heals by direct union
no callus formation
is the the preferred healing pathway in intra-articular fractures it minimises the risk of post traumatic arthritis

secondary bone healing:
bone healing by callus

23
Q

what are the possible displacements of fractures?

A

displaced
angulated
shortened
rotated

the improved remodelling potential in children means that there is more leeway with the extent of displacement

but remodelling can’t really happen with rotation

24
Q

what is the salter-harris classification?

A

Salter-Harris

Classification of physeal injuries (SALT)

  1. physeal Separation
  2. Fracture traverses physis and exits metaphysis (Above)
  3. Fracture traverses physis and exits epiphysis (Lower) (end of bone)
  4. Fracture passes Through epiphysis, physis, metaphysis
  5. Crush injury to physis (uncommon)

Risk of growth arrest increases from 1 -5

Type 2 injuries most common

25
Q

what is growth arrest?

A

Growth Arrest:

Injuries to the physis can cause growth arrest

The location and timing is key. different parts of the skeleton grow at different rates. so if injury is closer to the time of physis closing, then there is less damage to be done

Whole physis – limb length discrepancy

Partial – angulation as the non affected side keeps growing

26
Q

how do you treat growth arrest?

A

Aim is to correct the deformity
Minimise angular deformity
Minimise limb length difference

limb length correction:
shorten the long side
lengthen the short side

angular deformity:
stop the growth of the unaffected side
reform the bone (osteotomy)

27
Q

that are the general methods of fracture management?

A

the 4 R’s

resuscitate:
make sure patient is stable

reduce:
Correct the deformity and displacement

Reduce secondary injury to soft tissue / NV structures

closed - reducing a fracture without making an incision, such as traction and manipulation in A&E
open - making an incision. realignment with direct visualisation

restrict:
Maintain the fracture reduction
Provides the stability for the fracture to heal
Children rarely have issues with bone not healing
Can have issues with too much healing!

But remember the child’s quicker fracture healing times and remodeling potential

external - splints, plaster (commonly used in paediatrics)
internal - extra medullary plate and screws, intramedullary device. (consider more when there is damage to the physis)

rehabilitate:
Children generally rehabilitate very quickly
Play is a great rehabilitator
Stiffness not as major issue as in adults
Use it, Move it and Strengthen!

28
Q

what are the differential diagnoses for a limping child?

A

septic arthritis!!!!!!
transient synovitis
perthes
SUFE (slipped upper femoral epiphysis)

29
Q

what is septic arthritis?

A

Septic arthritis in a child is a orthopaedic emergency!

presence of infection in the intra-articular space

Can cause irreversible long term problems in the joint
Therefore needs surgical washout of the joint to clear the infection

Kocher’s classification can help score probability:
the child is Non weight bearing on affected side
ESR >40
WBC >12,000
Temperature >38

The history is key:
Duration
Other recent illness
Associated joint pain

30
Q

what is transient synovitis?

A

Transient synovitis is a diagnosis once septic arthritis has been excluded

it Is a inflamed joint in response to a systemic illness

Supportive treatment with antibiotics is the treatment

common condition, often secondary to a coryzal infection

31
Q

what is Perthes?

A

more uncommon

Idiopathic necrosis of the proximal femoral epiphysis

Usually in those 4-8 years old
Male 4:1 Female

Septic arthritis needs to be excluded first

Treatment is usually supportive in the first instance

usually goes on fro longer than septic arthritis or transient synovitis. also no temperature and inflammatory markers

key diagnostic test is a plain radiograph

32
Q

what is SUFE?

A

Slipped upper femoral epiphysis

The proximal epiphysis slips in relation to the metaphysis

Usually obese adolescent male:
12-13 years old during rapid growth
Associated with hypothyroidism/hypopituitrism

Septic arthritis needs to be excluded first

Treatment is operative fixation with screw to prevent further slip and minimise long term growth problems