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Year 2 MSK > Children's Orthopaedics > Flashcards

Children's Orthopaedics Flashcards

1
Q

What is the difference between an adult and children’s skeleton?

A

Child’s has 270 bones - in continuous change

Physis (growth plates)

Elasticity

Speed of healing

Remodelling

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2
Q

What are the two pathways of bone development?

A

Intramembraneous

Endochondral

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3
Q

What are the main features of intramembraneous ossification?

A

Mesenchymal cells –> bone

Flat bones

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4
Q

What are the main features of endochondral ossification?

A

Mesenchymal –> cartilage –> bone

Long bones

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5
Q

What are the stage of intramembraneous ossification?

A

mesenchymal cells in the central ossification centres differentiate first into preosteoblasts and then intoosteoblasts

These cells synthesize and secreteosteoidand the osteoblasts further differentiate into osteoclasts

These cells then collectively create the immature woven trabecular matrix and immature periosteium.

Angiogenesis occurs and Blood vessels incorporated between the woven bonetrabeculaewill form the future bone marrow.

Later, the woven bone is remodeled and is progressively replaced by mature lamellar bone.

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6
Q

What are the stages of primary endochondral ossification?

A

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.

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7
Q

What are primary ossification centres?

A

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

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8
Q

What are secondary ossification centres?

A

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

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9
Q

What is the role of the physis?

A

responsible for the further growth of bones ‘Secondary ossification sites’.

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10
Q

What happens if the physis are faulty?

A

Any congenital malfunction to this area or acquired insult – weather it is traumatic/infective or otherwise will therefore have a subsequent impact on growth of the child

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11
Q

What are the main features of children’s bone being more elastic?

A

Children’s bone can bend – more elastic than adult

Increased density of haversian canals

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12
Q

Why are there more Haversian canals in children’s bones?

A

More metabolically active as they are growing

Need more metabolites

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13
Q

What are the different injuries seen in children?

A

Plastic deformity
– bends before breaks

Buckle fracture
– Tarus like the roman column

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

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14
Q

When does growth stop?

A

When the physis close

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15
Q

What influences when growth stops?

A

Puberty, Menarche, Parental height

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16
Q

When does growth stop typically?

A

Complete at
Girls 15-16
Boys 18-19

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17
Q

What are the features of remodelling in children’s bone?

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

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18
Q

What are common children’s congenital conditions?

A

Developement dysplasia of the hip

Club foot

Achondroplasia

Osteogenesis Imperfecta

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19
Q

What is DDH?

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’

Occurs in utero and depends on how they sit in the womb

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20
Q

What does normal development of the hip result in?

A

The normal development relies on the concentric reduction and balanced forces through the hip

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21
Q

What are the different ways DDH presents?

A

Spectrum with
- dysplasia
– subluxation
– dislocation

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22
Q

What are risk factors of DDH?

A 
Female 6:1
First born
Breech
FH
Oligohydramnios
Native American/Laplanders – swaddling of hip
Rare in African American/
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23
Q

When is DDH usually picked up?

A

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

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24
Q

What investigations should be done for DDH?

A

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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25
Q

How is DDH treated?

A

Reducible hip and <6 months
Pavlik harness 92% effective
Holds femoral head in the acetabulum

Failed Pavlik Harness or 6-18 months

Secondary changes- capsule + soft tissue
MUA + Closed reduction and Spica

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26
Q

What is the aim of DDH treatment?

A

No prevent morbidity in infancy

but to allow for as normal hip development as possible to avoid problems in later life

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27
Q

What is congential talipes equinovarus?

A 
Congenital deformity of the foot 
1:1000
Highest in Hawaiians
M2:1F
50% are bilateral
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28
Q

What is the genetic aspect of club foot?

A

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

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29
Q

What are the presentations of club foot?

A

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

30
Q

What is the treatment of club foot?

A

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
  4. Some will require further operative intervention to correct final deformity.
31
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

32
Q

What results in achondroplasia?

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

Normal cognitive development
Significant spinal issues

33
Q

What are the bone effects of OI?

A

Fragility fractures
Short stature
Scoliosis

34
Q

What are the non-orthopaedic manifestations of OI?

A

Heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull - abnormal fusion of cranial sutures
Hypermetabolism

35
Q

How do we describe fractures?

A

Pain

Pattern
Anatomy
Intra/Extra-articular
Displacement

36
Q

What is used to classify fractures when it involves the physis?

A

Salter-Harris

37
Q

What is the pattern of fracture representative of?

A

How the energy was dissipated through the bones

38
Q

What does anatomy refer to?

A

Where in the bone

For example, long bones are split into thirds (proximal, middle, distal)

39
Q

What is meant by intra/extra articular?

A

Intra - primary bone healing

Extra - secondary bone healing

40
Q

What are different terms describing displacement?

A

Displaced
Angualted
Shortened
Rotated

41
Q

What displacement is not tolerated very well?

A

Rotated

42
Q

What does the slater harris classifcation?

A

Classifies physial injuries

43
Q

What are the 5 types in the Salter-Harris classification?

A

SALT

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

Risk of growth arrest increases from 1 -5

Type 2 injuries most common

44
Q

What are the main features of growth arrest?

A

Injuries to the physis can cause growth arrest

The location and timing is key

How much potential growth is left?

How much of the physis is affected?

45
Q

What are the outcomes that depend on how much of the physis is affected?

A

Whole physis – limb length discrepancy

Partial – angulation as the non affected side keeps growing

46
Q

What is the aim of treatment of growth arrest?

A

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

47
Q

How can limb length be corrected?

A

Shorten the long side

OR

Lengthen the short side

48
Q

How can angular deformity be corrected?

A

Stop the growth of the unaffected side

OR

Reform the bone (osteotomy)

49
Q

What are the four R’s of fracture management?

A

Resuscitate
Reduce
Restrict
Rehabilitate

50
Q

What is closed reduction?

A

Reducing a fracture without making an incision

Such as traction and manipulation in A&E

51
Q

What is open reduction?

A

Making an incision

The realignment of the fracture under direct visualisation

52
Q

What is common in paediatric fractures for reduction?

A

Closed

e.g. gallows traction

53
Q

What is Gallows traction?

A

Skin traction applied to the femur

Holding the skin, the long bones of the lower limb can be reduced

54
Q

What is the purpose of restricting a fracture?

A

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!

55
Q

What are external holding methods?

A

Plaster

Splints

56
Q

What are internal holding methods?

A

Plates
Screws
Intramedullary devices

57
Q

What are the features to consider with fixation in children?

A

Operative intervention may be required
Consider the ongoing growth at the physis
Metalwork may need to be removed in the future

58
Q

What are the main features of paediatric rehabilitation?

A

Children generally rehabilitate very quickly

Play is a great rehabilitator

Stiffness not as major issue as in adults

Use it, Move it and Strengthen!

59
Q

What can cause a limp in child?

A

Septic arthritis
Transient synovitis
Perthes
SUFE

60
Q

Why is septic arthritis important to always consider in a limping child?

A

Septic arthritis in a child is a orthopaedic emergency!

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

61
Q

What is Kocher’s classification?

A

Kocher’s classification can help score probability of septic arthritis

Non weight bearing
ESR >40
WBC >12,000
Temperature >38

62
Q

What is key in the history when considering septic arthritis?

A

Duration
Other recent illness
Associated joint pain

63
Q

What is transient synovitis?

A

diagnosis once septic arthritis has been excluded
Is a inflamed joint in response to a systemic illness
Supportive treatment with antibiotics is the treatment

64
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

65
Q

Who is Perthes disease seen in?

A

Usually in those 4-8 years old

Male 4:1 Female

66
Q

What need to be done first with Perthes?

A

Septic arthritis needs to be excluded first

67
Q

What is the treatment for Perthes?

A

Treatment is usually supportive in the first instance

68
Q

What is SUFE?

A

Slipped upper femoral epiphysis

The proximal epiphysis slips in relation to the metaphysis

69
Q

In who does SUFE normally occur?

A

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

70
Q

What need to be done first with SUFE?

A

Septic arthritis needs to be excluded first

71
Q

What is treatment of SUFE?

A

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

Year 2 MSK (9 decks)

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