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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
  • condesation of mesenchymal cells that differentiate into osteoblasts, forming the ossification centre
  • 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 through endochondral ossification 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 (the physis)

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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
  • 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
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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
  • at physis
  • zone of elongation in long bone
  • containsn cartilage
  • 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 (tarus like the column)
  • greenstick (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

the 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

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21
Q

What are common congenital conditions?

A
  • dysplasia of the hip
  • club foot
  • achondroplasia
  • osteogenesis imperfecta
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22
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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23
Q

What is the spectrum of developmental dysplasia of the hip?

A
  • dysphasia (2/100)
  • subluxation
  • dislocation (2/1000)
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24
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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25
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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26
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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27
Q

What treatments are there for developmental dysplasia of the hip?

A

if: reducible hip and <6 months
- Palvik harness (92%)
if failed Plavik harness or 6-18 months:
- secondary changes: capsule + soft tissue
- MUA + closed reduction and spica

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28
Q

What is clubfoot?

A

CAVE deformity due to muscle
Cavus - high arch, tight intrinsic RHL, FDL
Adductus of foot - tight tib posterior and anterior
Varus: tight tendoachillies, tib post, tib ant
Equinous: tight tendoachilles

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29
Q

What is the risk factors associated with clubfoot?

A
  • males
  • hawaiians
  • genetic (PITX1 gene)
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30
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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31
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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32
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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33
Q

What is osteogenesis imperfecta?

A
  • hereditary (autosomal dominant or recessive)
  • decreased Type 1 collagen due to: decreased secretion, abnormal collagen production
  • insufficient osteoid production
34
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
35
Q

How do you describe a pediatric fracture?

A
  • pattern
  • anatomy
  • intra-extra articular
  • displacement
  • salter-harris
36
Q

What are the possible fracture patterns?

A
  • transverse
  • oblique
  • comminuted
  • spiral
  • avulsion (pulled off by a ligament)
  • greenstick
  • buckle
  • plastic deformity
37
Q

What is the possible anatomy of paediatric fractures?

A
  • distal 1/3
  • middle 1/3 diaphysis
  • proximal 1/3
38
Q

What is primary bone healing?

A
  • heals by direct union

- no callus formation

39
Q

When is primary bone healing preferred?

A

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

40
Q

What is secondary bone healing?

A
  • hematoma formation
  • fibrocartilaginous callus formation
  • bony callus formation
  • bone remodelling
41
Q

What are the different possible displacements of a fracture?

A
  • displaced
  • angulated
  • shortened
  • rotated
42
Q

What form of displacement is not handled well for remodelling?

A

rotation

43
Q

What is the Salter-Harris classification?

A

classification of physeal injury

44
Q

What is a Slater-Harris Type 1 injury?

A

physeal seperation

45
Q

What is a Slater-Harris Type 2 injury?

A

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

46
Q

What is a Slater-Harris Type 3 injury?

A

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

47
Q

What is a Slater-Harris Type 4 injury?

A

fracture passes through the epiphysis, physis and metaphysis

48
Q

What is a Slater-Harris Type 5 injury?

A

crush injury to physis

49
Q

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

A

the risk of growth arrest increases from 1-5

50
Q

What type of Salter-Harris injury is most common?

A

Type 2

51
Q

What can injury to the whole physis cause?

A

limb length discrepency

52
Q

What can injury to the partial physis cause?

A

angulation as the non-affected side continues to grow

53
Q

What is the impact of physis injury dependent on?

A
  • location

- time of injury (how much growth left?)

54
Q

What is the aim when treating growth arrest?

A

correct the deformity

  • minimise angular deformity
  • minimise limb length difference
55
Q

How is limb length correction done?

A
  • shorten the long side

- lengthen the short side

56
Q

How is angular deformity correction done?

A
  • stop the growth of the unaffected side

- reform the bone (osteotomy)

57
Q

What are the principles of fracture management?

A
  • resuscitate
  • reduce
  • restrict
  • rehabilitate
58
Q

What is the aim of reducing a fracture?

A
  • correct the deformity
    and displacement
  • reduce secondary injury to soft tissue/neurovascular structures
59
Q

What is the aim of restricting a fracture?

A
  • maintain the fracture reduction

- provides the stability for the fracture to heal

60
Q

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

A

that operative internal fixation often can be avoided

61
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
62
Q

What are the differentials of a limping child?

A
  • septic arthritis
  • transient synovitis
  • Perthes
  • SUFE
63
Q

What is septic arthritis?

A

an infection in the inter-articular space

64
Q

What is result of septic arthritis?

A

can cause irreversible LT problems

65
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
66
Q

What is needed to clear the infection causing septic arthritis?

A

a surgical washout of the joint

67
Q

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

A
  • duration
  • other recent illness
  • associated joint pain
68
Q

What is transient synovitis?

A
  • a diagnosis after septic arthritis has been excluded

- an inflamed joint in response to systemic illness

69
Q

What is the treatment of transient synovitis?

A

supportive treatment with ABx

70
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

71
Q

What symptoms are associated with septic arthritis?

A
  • joint pain
  • rashes
  • diarrhoea
  • vomiting
72
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

73
Q

What is the risk factors of Perthes disease?

A
  • 4-8 years old

- more so in males

74
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

75
Q

What must be done in order to diagnose Perthes disease?

A
  • exclude septic arthritis

- plain film radiograph

76
Q

What is the treatment of Perthes disease?

A

supportive

77
Q

What is SUFE?

A
  • slipped upper femoral epiphysis

- the proximal epiphysis slips in relation to the metaphysis

78
Q

When is SUFE commonly seen?

A
  • obese, adolescent male
  • 12-13 years old
  • hypothyroidism/hypopituitrism
79
Q

What needs to be done before a diagnosing SUFE?

A

exclude septic arthritis

80
Q

What is the treatment for SUFE?

A

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

BRS YR2 (70 decks)

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