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BRS YR2 > Children's Orthopaedics > Flashcards

Children's Orthopaedics Flashcards

1
Q

What are physis?

A

growth plates - areas from which long bone growth occurs post-natally

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2
Q

What are the 2 different types of bone development?

A
  • intramembranous
  • endochondral
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3
Q

What is formed by intramembranous bone development?

A

flat bones

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4
Q

What is formed by endochondral bone development?

A

long bones

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5
Q

What is intramembranous ossification?

A
  • mesenchymal cells in the central ossification centres differentiate into osteoblasts
  • secreted osteoid traps osteoblasts which become osteocytes
  • trabecular matrix and periosteum form
  • compact bone develops superficial to cancellous bone
  • crowded blood vessels condense into red bone marrow
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6
Q

Where does endochondral ossification occur?

A

primary and secondary ossification centres

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7
Q

What is primary ossification centres?

A

sites of pre-natal bone growth from the central part of the bone

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8
Q

What is secondary ossification centres?

A

occurs post-natal after the primary ossification centre and long bones often have several physes

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9
Q

What happens in primary endochondral ossification?

A
  • mesenchymal differentation at the primary centre
  • the cartilage model of the future bony skeleton forms
  • capillaries penetrate cartilage
  • calcification at the POC forms spongy bone
  • perichondrium transforms into periosteum
  • cartilage and chondrocytes continue to grow at the ends of the bone
  • secondary ossification centres develop at proxial and distal end
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10
Q

What is the difference between intramembranous and endochondral ossification?

A

in endochondral, the tissue that becomes bone is cartilage first

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11
Q

What happens in secondary endochondral ossification?

A
  • happens at physis
  • zone of elongation in long bone contains cartilage
  • proliferation of chondrocytes and calcification of the extracellular matrix into immature bone that is then subsequently remodelled
  • epiphyseal side: hyaline cartilage active and dividing to form hyaline catrilage matrix
  • diphyseal side: cartilage calcifies and dies and is then replaces by bone
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12
Q

How do children skeletons differ from adults?

A
  • bone is elastic
  • presence of physis
  • increased speed of healing
  • remodelling potential
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13
Q

Why are children’s bones more elastic than an adult?

A

increased density of haversian canals

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14
Q

What is the impact of the increased elasticity of bones?

A
  • plastic deformity (bends before it breaks)
  • buckle fracture
  • greenstick injuries (one cortex fractures but other side does not break)
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15
Q

When does growth stop?

A

when physis close

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16
Q

What impacts when physis close?

A
  • gradual physeal closure
  • puberty
  • menarche
  • parental height
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17
Q

When do physis typically close?

A

girls: 15-16
boys: 18-19

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18
Q

What is used to characterise physeal injuries?

A

Salter-Harris

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19
Q

What is the possible impact of physeal injury?

A
  • growth arrest
  • eventual deformity
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20
Q

What is the speed of healing and remodelling dependent on?

A
  • location of injury
  • age of patient (younger = quicker)
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21
Q

Which physes grow more?

A

Knees and extreme of upper limb

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22
Q

What are common congenital conditions?

A
  • developmental dysplasia of the hip
  • club foot
  • achondroplasia
  • osteogenesis imperfecta
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23
Q

What is developmental dysplasia of the hip?

A

a group of disorders of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum

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24
Q

What is the spectrum of developmental dysplasia of the hip?

A
  • dysphasia (2/100)
  • subluxation
  • dislocation (2/1000)
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25
Q

What are the risk factors of developmental dysplasia of the hip?

A
  • female
  • first born
  • breech
  • family Hx
  • oligohyraminos
  • native american/laplanders (hip swaddling)
  • rare in african american/asian
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26
Q

What examinations are done for developmental dysplasia of the hip?

A
  • usually seen on baby check
  • RoM of hip (limited hip abduction)
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27
Q

What investigations are done for developmental dysplasia of the hip?

A
  • US (birth-4months)
  • after 4 months - XR
  • measures the acetabular dysplasia and the position of the hip
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28
Q

What treatments are there for developmental dysplasia of the hip if reducible hip and < 6 months?

A

Palvik harness (92%)

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29
Q

What treatments are there for developmental dysplasia of the hip if failed Pavlik Harness or 6-18 months?

A
  • secondary changes to capsule and soft tissue
  • MUA + closed reduction and Spica
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30
Q

What is clubfoot?

A

Congenital deformity of the foot due to muscle contracture, often bilateral

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31
Q

What are the CAVE deformities of clubfoot?

A
  • Cavus: high arch
  • Adductus of foot
  • Varus
  • Equinous
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32
Q

What is the risk factors associated with clubfoot?

A
  • males
  • hawaiians
  • genetic (PITX1 gene)
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33
Q

What is the gold standard treatment of clubfoot?

A

Ponseti menthod

  • series of casts to correct deformity
  • many require operative treatment (soft tissue releases)
  • foot orthosis brace
  • some with require a further operative intervention
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34
Q

What is Achondroplasia?

A
  • G380 mutation of FGFR3 (autosomal dominant)
  • inhibition of chondrocyte proliferation in the proliferative zone of the physis
  • results in defect in endochondral bone formation
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35
Q

What is the resulting impact of Achondroplasia?

A

Rhizomelic dwarfism

  • humerus shorter than forearm
  • femur shorter than tibia
  • normal trunk
  • adult height: 125cm
  • normal cognitive development
  • significant spinal issues
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36
Q

What is osteogenesis imperfecta?

A
  • hereditary (autosomal dominant or recessive)
  • decreased Type 1 collagen due to decreased secretion or abnormal collagen production
  • insufficient osteoid production
37
Q

What is the impact of osteogenesis imperfecta?

A 
bones:
- fragility fractures
- short stature
- scoliosis
non-bones:
- heart
- blue sclera
- dentinogenesis imperfeccta (soft, brown teeth)
- wormian skull
- hypermetabolism
38
Q

How do you describe a pediatric fracture?

A
  • pattern
  • anatomy
  • intra-extra articular
  • displacement
  • salter-harris
39
Q

What are the possible fracture patterns?

A
  • transverse
  • oblique
  • comminuted
  • spiral
  • avulsion (pulled off by a ligament)
  • greenstick
  • buckle
  • plastic deformity (not a fracture)
40
Q

What is the possible anatomy of paediatric fractures?

A
  • distal 1/3
  • middle 1/3 (diaphysis)
  • proximal 1/3
41
Q

What is primary bone healing?

A
  • heals by direct union
  • no callus formation
42
Q

When is primary bone healing preferred?

A

in intra-articular fractures to minimise the risk of post traumatic arthritis

43
Q

What is secondary bone healing?

A
  • hematoma formation
  • fibrocartilaginous callus formation
  • bony callus formation
  • bone remodelling
44
Q

What are the different possible displacements of a fracture?

A
  • displaced
  • angulated
  • shortened
  • rotated
45
Q

What form of displacement is not handled well for remodelling?

A

rotation

46
Q

What is the Salter-Harris classification?

A

classification of physeal injury

47
Q

What is a Salter-Harris Type 1 injury?

A

physeal seperation

48
Q

What is a Salter-Harris Type 2 injury?

A

fracture transverses physis and exits metaphysis (above, towards middle of bone)

49
Q

What is a Salter-Harris Type 3 injury?

A

fracture transverses physis and exits epiphysis (below, towards end of bone)

50
Q

What is a Slater-Harris Type 4 injury?

A

fracture passes through the epiphysis, physis and metaphysis

51
Q

What is a Slater-Harris Type 5 injury?

A

crush injury to physis

52
Q

How does Salter-Harris classification relate to the risk of growth arrest?

A

the risk of growth arrest increases from 1-5

53
Q

What type of Salter-Harris injury is most common?

A

Type 2

54
Q

What can cause growth arrest?

A

Any injury to the physis

55
Q

What can injury to the whole physis cause?

A

limb length discrepency

56
Q

What can injury to the partial physis cause?

A

angulation as the non-affected side continues to grow

57
Q

What is the impact of physis injury dependent on?

A
  • location
  • time of injury (how much growth left?)
58
Q

What is the aim when treating growth arrest?

A

correct the deformity

  • minimise angular deformity
  • minimise limb length difference
59
Q

How is limb length correction done?

A
  • shorten the long side
  • lengthen the short side
60
Q

How is angular deformity correction done?

A
  • stop the growth of the unaffected side
  • reform the bone (osteotomy)
61
Q

What are the principles of fracture management?

A
  • resuscitate
  • reduce
  • restrict
  • rehabilitate
62
Q

What is the aim of reducing a fracture?

A
  • correct the deformity
    and displacement
  • reduce secondary injury to soft tissue/neurovascular structures
63
Q

What is a closed reduction?

A
  • Reducing a fracture without making an incision
  • E.g. traction and manipulation in A&E
64
Q

What is open reduction?

A
  • Making an incision
  • The realignment of the fracture under direct visualisation
65
Q

What is the aim of restricting a fracture?

A
  • maintain the fracture reduction
  • provides the stability for the fracture to heal
66
Q

What is the implication of the remodelling and huge healing potential?

A

that operative internal fixation often can be avoided

67
Q

What are external restrictions?

A

Splints and plasters

68
Q

What are internal restrictions?

A
  • Plates and screws
  • intra-medullary device
69
Q

Which restricition method is more common in child fractures?

A
  • external
  • due to remodelling and huge healing potential
70
Q

What form of rehabilitation is recommended for children?

A
  • play
  • stiffness not as big of a concern
  • children rehabilitate much quicker
  • move, use and strengthen
71
Q

What are the differentials of a limping child?

A
  • septic arthritis
  • transient synovitis
  • Perthes
  • SUFE
72
Q

What is septic arthritis?

A
  • an infection in the inter-articular space
  • orthopaedic emergency
73
Q

What is result of septic arthritis?

A

can cause irreversible long term problems

74
Q

What is used to assess the probability of a child having septic arthritis?

A

Kocher’s classification:

  • non-weight bearing
  • ESR>40
  • WBC>12,000
  • temperature >38
75
Q

What is needed to clear the infection causing septic arthritis?

A

a surgical washout of the joint to clear the infection

76
Q

What Hx needs to be taken when septic arthritis is suspected?

A
  • duration
  • other recent illness
  • associated joint pain
77
Q

What is transient synovitis?

A
  • a diagnosis after septic arthritis has been excluded
  • an inflamed joint in response to systemic illness
78
Q

What is the treatment of transient synovitis?

A

supportive treatment with ABx

79
Q

How can septic arthritis cause long term joint problems?

A
  • necrotic effect of proteases in the joint itself
  • pressure effect on the chondrocytes and the cartilages that comes from the oedema in a closed space
80
Q

What symptoms are associated with septic arthritis?

A
  • joint pain
  • rashes
  • diarrhoea
  • vomiting
81
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

82
Q

What is the risk factors of Perthes disease?

A
  • 4-8 years old
  • male
83
Q

How can you differentiate septic arthritis and Perthes disease?

A
  • no temperature and inflammatory markers in Perthes
  • Perthes tends to have a longer onset
84
Q

What must be done in order to diagnose Perthes disease?

A
  • exclude septic arthritis
  • plain film radiograph
85
Q

What is the treatment of Perthes disease?

A

supportive

86
Q

What is SUFE?

A
  • slipped upper femoral epiphysis
  • the proximal epiphysis slips in relation to the metaphysis
87
Q

When is SUFE commonly seen?

A
  • obese, adolescent male
  • 12-13 years old
  • hypothyroidism/hypopituitrism
88
Q

What needs to be done before a diagnosing SUFE?

A

exclude septic arthritis

89
Q

What is the treatment for SUFE?

A

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

BRS YR2 (67 decks)

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