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BRS MUSCULOSKELETAL > 1b// Children's Orthopaedics > Flashcards

1b// Children's Orthopaedics Flashcards

1
Q

How many bones are there in a child’s skeleton?

A

270

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2
Q

What are growth plates called, and what do they do?

A

physis

they are the areas from which long bone growth occurs postnatally

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3
Q

What are the types of bone development?

A

intramembranous mesenchymal cells» bone

endochondral mesenchymal» cartilage» bone

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4
Q

What type of bone do intramembranous mesenchymal cells lead to?

A

flat bones (cranial bones and clavicle)

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5
Q

What type of bone do endochondral mesenchymal cells make?

A

long bones (all other long bones)

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6
Q

What is the process called of making cranial bones and the clavicle?

A

intramembranous ossification

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7
Q

What is the process called of making all other long bones?

A

endochondral ossification

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8
Q

Describe the process of intramembranous ossification.

A
  1. Condensation of mesenchymal cells which differentiate into osteoblasts – Ossification centre forms
  2. Secreted osteoid traps osteoblasts which become osteocytes
  3. Trabecular matrix and immature periosteum form
  4. then angiogenesis between woven bone and trabecular, forming bone marrow
  5. Compact bone develops superficial to cancellous bone. Crowded blood vessels condense into red bone marrow
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8
Q

Where does endochondral ossification occur?

A

both primary and secondary ossification centres

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8
Q

What are primary ossification centres? And what part of the bone are they located?

A

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

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9
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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10
Q

What are the 2 types of endochondral ossification?

A

primary and secondary

e.g., endochondral primary ossification

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11
Q

Describe the process of endochondral primary ossification.

A

pre-natal growth through primary ossification centres

a) Mesenchymal Differentiation at the primary centre

b) The cartilage model of the future bony skeleton forms

c) Capillaries (via angiogenesis) 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

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12
Q

Where are primary ossification centres?

A

middle of diaphysis (shaft of bone)

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13
Q

Where do secondary ossification centres develop? And how are they developed?

A

at proximal and distal ends of long bone with their own blood supply

blood supply calcifies the previously uncalcified matrix into immature spongy bone, so cartilage at ends of bone become sites of secondary ossification

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14
Q

What is endochondral secondary ossification for?

A

long bone lengthening

post bone growth through secondary ossification centres
“the physis”

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15
Q

Describe endochondral secondary ossification.
- where does it occur
- what zone and where
- what does it contain
- and sides

A

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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16
Q

What are the epiphyseal and diaphyseal sides?

A

the diaphysis (shaft or primary ossification centre), metaphysis (where the bone flares), physis (or growth plate) and the epiphysis (secondary ossification centre).

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17
Q

Do these make sense?

A
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18
Q

How does a child’s skeleton differ to that of an adult? (4)

A

more elasticity

physis (constantly growing)

speed of healing is much faster (due to continuous growth)

remodelling potential

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19
Q

What does it mean by a child’s bone elasticity? And why is it more elastic?

A

Children’s bone can bend – more elastic than adult

due to increased density of haversian canals

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20
Q

What can increased density of haversian canals lead to? (3)

A

Plastic deformity:
– bends before breaks

Buckle fracture:
– Tarus like the column

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

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21
Q

Why do children have more haversian canals?

A

as their bones are more metabolically active

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22
Q

Describe growth of bones in children, e.g., where and speed? And when does growth stop?

A

Growth occurs at varying rates at varying sites

Growth stops as the physis closes

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23
Q

When does physeal closure occur?

A

Complete at girls: 15-16

boys= 18-19

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24
Q

What does physeal closure depend on?

A

puberty
menarche
parental height

gradual physeal closure

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25
Q

How are physeal injuries categorised?

A

salter-harris

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26
Q

What can physeal injuries lead to? And what can that lead to?

A

growth arrest

leads to deformity

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27
Q

What is the speed of remodelling and healing dependent on?

A

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

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28
Q

Who heals bones more quickly in the general population?

A

younger child

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29
Q

Which physis grows the most?

A

at the knee and at the extreme of upper limb

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30
Q

What the stages of healing/ remodelling? (3)

A

inflammation
repair/ callus
remodelling

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31
Q

What are common children’s congenital conditions (that you need to know)? (4)

A

Developmental Dysplasia of the Hip

Club Foot

Achondroplasia

Osteogenesis Imperfecta

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32
Q

What is developmental dysplasia of the hip? And what type of disorder is it?

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’

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33
Q

What is a packaging disorder?

A

occurs in utero, due to the way a child sits

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34
Q

What is the normal development of the hip dependent on?

A

the concentric
reduction and balanced forces through the hip

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35
Q

What is the spectrum of developmental dysplasia of the hip? (3)

A

dysplasia
or
subluxation
or
dislocation

Dysplasia 2: 100 Dislocation 2:1000

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36
Q

What are risk factors for developmental dysplasia of the hip? (6)

A

Female 6:1

First born

Breech

FHx

Oligohydramnios

Native American/Laplanders – swaddling of hip

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37
Q

How is developmental dysplasia of the hip examined?

A

Usually picked up on baby check – screening in UK

Range of motion 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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38
Q

What are the investigations for developmental dysplasia of the hip?

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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39
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 (manipulation under anaesthetic) + Closed reduction and Spica

40
Q

What is clubfoot?

A

Congenital deformity of the foot

packaging disorder

41
Q

What is the epidemiology of clubfoot?

A

1:1000
Highest in Hawaiians
M2:1F
50% are bilateral

42
Q

What is the risk factor of clubfoot?

A

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

CAVE

43
Q

What causes CAVE deformity?

A

due to muscle contracture

44
Q

What is CAVE deformity?

A

deformity of Clubfoot

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

45
Q

What is the treatment for clubfoot?

A

Ponseti Method
Gold standard

  1. First a series of casts to correct deformity
  2. Many require operative treatment
    - Soft tissue releases or tendon transfers (more extreme is tendon)
  3. Foot orthosis brace
  4. Some will require further operative intervention to correct final deformity.
46
Q

What is achondroplasia?

A

The most common skeletal dysplasia

47
Q

What is the pathophysiology of achondroplasia?

A

Autosomal Dominant

  • G380 mutation of FGFR3
  • inhibition of chondrocyte proliferation in the proliferative zone of the physis
  • results in defect in endochondral bone formation

affects secondary ossification

48
Q

What does achondroplasia lead to?

A

rhizomelic dwarfism

49
Q

What is a part rhizomelic dwarfism?

A

Humerus shorter than forearm

Femur shorter than tibia

Normal trunk

Adult height of approx.125cm

Normal cognitive development

Significant spinal issues

50
Q

What is osteogenesis imperfecta?

A

brittle bone disease

decreased type 1 collagen

51
Q

Why is there decreased collagen in osteogenesis imperfecta? And what does that lead to?

A

Decreased Type I Collagen due to:
- Decreased secretion
- Production of abnormal collagen

leading to insufficient osteoid production

52
Q

How do you get osteogenesis imperfecta?

A

hereditary- autosomal dominant or recessive

53
Q

What are the manifestations of osteogenesis imperfecta on bones? (3)

A

Fragility fractures
Short stature
Scoliosis

54
Q

What are the non-orthopaedic manifestations of osteogenesis imperfecta? (5)

A

Heart

Blue Sclera

Dentinogenesis imperfecta – brown soft teeth

Wormian skull

Hypermetabolism

55
Q

What is wormian skull?

A

abnormal fusion of cranial sutures

56
Q

What should you consider with paediatric fractures? (5)

A

Pattern
Anatomy
Intra/Extra-articular Displacement
Salter-Harris

57
Q

What does the pattern of the fracture reflect?

A

reflects the way the energy is dissipated

58
Q

What are the types of patterns in fracture?

A

comminuted= high E, more than 1 part fractured

59
Q

What should you consider with anatomy and fractures?

A

where on the bone the fracture is

60
Q

What are the 2 methods of bone healing?

A

primary and secondary bone healing

61
Q

Which method of healing is prefered for intra-articular fractures?

A

primary bone healing is the preferred healing pathway in intra-articular fracture as minimises risk of post traumatic arthritis

62
Q

What is primary bone healing?

A

heals by direct union

no callus formation

63
Q

What is secondary bone healing?

A

bone healing by callus

*but remember…
- if the fracture affects the physis it affects growth

64
Q

What are the steps of secondary bone healing?

A
  1. haematoma formation
  2. fibrocartilaginous callus formation
  3. bony callus formation
  4. bone remodelling
65
Q

What are the types of displacements in fractures? (4)

A

*remodelling potential gives more allowance for displacement for children

*rotated is not well tolerated

*can be multiple at the same time

66
Q

How are physeal injuries classified?

A

Salter Harris

67
Q

How does Salter Harris classify physeal injuries?

A

Classification of physeal injuries (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

68
Q

Which type of physeal injury is most common and least common?

A

2 most common

5 least common

69
Q

What do injuries to the physis possibly lead to?

A

growth arrest

70
Q

What is key in growth arrest>

A

the location and timing

how much potential growth is affects

diff parts of the skeleton grow at diff rates

71
Q

What are the types of physeal injuries? (2)

A

Whole physis – limb length discrepancy

Partial – angulation as the non affected side keeps growing

72
Q

What are the aims of treatment for growth arrest?

A

Aim is to correct the deformity

Minimise angular deformity
Minimise limb length difference

73
Q

How can you treat limb length?

A

shorten the longer side or lengthen the shorter side

74
Q

How can you treat angular deformity?

A

stop the growth of the unaffected side
or
reform the bone (osteotomy)

75
Q

What are the 4 Rs for fracture management?

A

Resuscitate Reduce Restrict Rehabilitate

76
Q

What does it mean by reduce, for fracture management?

A

Correct the deformity and displacement

Reduce secondary injury to soft tissue / NV structures

77
Q

What are the 2 types of reduction?

A

closed and open

78
Q

What is a closed reduction?

A

Reducing a fracture without making an incision

Such as traction and manipulation in A&E

79
Q

What is an open reduction?

A

Making an incision

The realignment of the fracture under direct visualisation

80
Q

Give an example of closed reduction.

A

gallows traction
- commonly used for long bone fractures

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

81
Q

What is restriction for?

A

Maintain the fracture reduction

Provides the stability for the fracture to heal

82
Q

What do children rarely have issues with when it comes to bone fractures? And what can they have issues with?

A

with bone not healing
- however can have issues with too much healing

83
Q

What are the 2 broad categories of restriction?

A

external and internal

84
Q

What are examples of external and internal restriction? (2 each)

A
85
Q

What type of restriction is commonly used in paeds? And why?

A

external
plasters and splints

Remodeling and huge healing potential means that operative internal fixation often can be avoided

86
Q

What do you do when operative intervention may be required for restriction?

A
87
Q

Do you have to rehabilitate children?

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!

88
Q

Is operation more or less likely in children?

A

less as children have quicker healing

89
Q

What are causes of the limping child? (4)

A

Septic Arthritis
Transient Synovitis
Perthes
SUFE

90
Q

What is septic arthritis? And what is so important about it?

A

presence of infection in intra-articular space

child orthopaedic emergency
- can cause irreversible long term problems in the joint (therefore needs surgical washing of the joint to clear the infection)

91
Q

What is the score used to find out the probability of a child having septic arthritis, and what is in it?

A

Kocher’s classification
- Non weight bearing
- ESR >40
- WBC >12,000
- Temperature >38

92
Q

What is the diagnosis if septic arthritis has been excluded?

A

Transient synovitis is 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

93
Q

What is key in septic arthritis? (3)

A

the history…
- duration
- other recent illness
- associated joint pain

94
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

95
Q

With who is perthes disease most common?

A

usually in those 4-8

male 4:1

96
Q

What must be done before diagnosis of Perthes and what is the treatment?

A

Septic arthritis needs to be excluded first

Treatment is usually supportive in the first instance
- once diagnosed they are referred to a specialist

97
Q

What would you not expect to see in Perthes, that you would see in septic arthritis?

A

raised temp and inflamm markers

98
Q

What is SUFE?

A

Slipped upper femoral epiphysis

The proximal epiphysis slips in
relation to the metaphysis

99
Q

In who is SUFE most common in?

A

Usually obese adolescent male
- 12-13 years old during rapid growth

100
Q

What is the treatment for SUFE?

A

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

  • Septic arthritis needs to be excluded
    first

BRS MUSCULOSKELETAL (12 decks)

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