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BRS 1b > 9.3 Children's Orthopaedics > Flashcards

9.3 Children's Orthopaedics Flashcards

1
Q

How many bones does a child’s skeleton have?

A

270

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2
Q

Where does long bone growth occur postnatally?

A

the physis (growth plate)

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3
Q

What are the two types of ossification?

A

Intramembranous

Endochondral

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4
Q

What bones are formed from intramembranous ossification?

A

flat bones

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5
Q

What bones are formed from endochondral ossification?

A

long bones

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6
Q

What is the difference between intramembranous and endochondral ossification?

A

intramembranous:
mesenchymal cells –> bone

endochondral:
mesenchymal cells –> cartilage –> bone

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7
Q

What are the four stages of intramembranous ossification?

A
  1. In central ossification centers, differentiation of mesenchymal cells –> pre-osteoblasts, –> osteoblasts.
  2. osteoblasts synthesis and secrete osteoid. differentiation of osteoblasts –> osteoclasts
  3. cells become trabecular matrix and periosteum
  4. angiogenesis –> blood vessels incorporated and become red bone marrow. Compact bone develops superficial to cancellous bone
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8
Q

What two places does endochondral ossification occur?

A

primary and secondary ossification centers

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9
Q

What are the primary ossification centers?

A

Sites of prenatal bone growth at central part of the bone (through endochondral ossification)

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10
Q

What are the secondary ossification centers?

A

The physis

Long bones often have several and bone growth only occurs here postnatally, after the primary ossification centres.

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11
Q

What are the 5 stages of endochondral primary ossification?

A
  1. mesenchymal differentiation
  2. cartilage model of the future bony skeleton forms
  3. capillaries penetrate cartilage, calcification at primary ossification center - spongy bone forms, perichondrium transforms into periosteum
  4. cartilage and chondrocytes continue to grow at the end of the bone
  5. secondary ossification centers (the physis) develop
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12
Q

What are the two sides of the physis?

A

epiphyseal side and diaphyseal side

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13
Q

What happens at the epiphyseal side?

A

hyaline cartilage divides and grows to form hyaline cartilage matrix

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14
Q

What happens at the diaphyseal side?

A

cartilage calcifies and dies and then is replaced by bone

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15
Q

What are 4 ways that a children’s skeleton is different from an adults?

A

Elasticity
Physis
Speed of Healing
Remodeling

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16
Q

Why are childrens bones more elastic than an adults?

A

Increased density of haversian canals (microscopic tunnels)

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17
Q

Because of the increased elasticity in children’s bones, what are 3 types of fractures we see in children that we don’t usually see in adults.

A

Plastic deformity - bends before breaks
Buckle fracture - tarus like column
Greenstick - one cortex fractures but does not break other side

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18
Q

How does growth at the physis stop, when does this usually occur?

A

Growth stops gradually as the physis closes
Girls: 15-16
Boys: 18-19
Can be affected by parental height

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19
Q

What is the speed of healing and remodelling potential dependent on?

A

location and age of patient

younger children heal more quickly, different physis’ grows at different speed (knee more than hip etc.) but fractures near the physis heal more quickly

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20
Q

What is developmental dysplasia of the hip?

A

‘packaging’ disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum

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21
Q

What is required for normal development of the hip?

A

concentric and balanced forces through the hip

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22
Q

What is the difference between dysplasia and dislocation of hip?

A

on spectrum
dysplasia –> subluxation –> dislocation

dysplasia much more common than dislocation

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23
Q

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

A 
female
first born
breech
family history
oligohydramnios - not enough fluid in amniotic sac
native american/lapanders
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24
Q

How is developmental dysplasia of the hip screened and what do they check for?

A

usually picked up on baby check - screening in the UK

  • range of motion
  • usually limitation in hip abduction
  • leg length discrepancy
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25
Q

How is developmental dysplasia of the hip investigated?

A

birth to 4 months: ultrasound

4 months +: x-ray

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26
Q

How is developmental dysplasia of the hip treated?

A

reducible hip and <6 months: pavlik harness
failed pavlik harness or 6-18 months: manipulation under anesthetic (MUA) and spica cast (this is because of secondary changes to the capsule and soft tissue)

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27
Q

What is congential talipes equinovarus?

A

club foot

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28
Q

What are the risk factors for congenital talipes equinovarus?

A

male
hawaiian
family history (there is a very large genetic component, 5% chance if siblings, familial cause in 25% of cases)

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29
Q

What gene is mutated in congenital talipes equinovarus?

A

PITX1 gene

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30
Q

How is clubfoot characterised?

A 
congenital talipes equinovarus consists of four deformities (all four present) = CAVE
Cavus
Adductus of the foot
Varus
Equinous
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31
Q

What is the C in CAVE caused by ?

A

Cavus - high arch, tight intrinsic flexor hallucis longus, flexor digitorum longus

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32
Q

What is the A in CAVE caused by?

A

Adductus of foot - tight tib post, tib ant

33
Q

What is the V in CAVE caused by?

A

Varus - tight tendoachillies, tib post, tib ant

34
Q

What is the E in CAVE caused by?

A

Equinous: tight tendoachilles

35
Q

How is clubfoot treated?

A

Ponseti Method - gold standard

  1. A series of casts to correct deformity
  2. Many require operative treatment - soft tissue releases
  3. Foot orthosis brace (skateboard)
  4. Some might require further operative intervention to correct final deformity
36
Q

What is Achondroplasia?

A

An autosomal dominant condition that results in rhizomelic dwarfism.

Causes the inhibition of chondrocyte proliferation in the proliferative zone of the physis. –> Effects secondary endochondral ossification.

The most common skeletal dysplasia conditions

37
Q

What is the mutation that causes Achondroplasia?

A

G380 mutation of FGFR3

38
Q

What are the characteristics of rhizomelic dwarfism? (6)

A 
humerus shorter than forearm
femur shorter than tibia
normal trunk
adult height of approx. 125cm
significant spinal issues
normal cognitive development
39
Q

What is oesteogenesis imperfecta?

A

Hereditary disease (AD or AR)
Decreased Type 1 collagen due to:
- decreased secretion
- production of normal collagen

which results in insufficient osteoid production.

40
Q

What are the orthopaedic manifestations of OI? (3)

A

fragility fractures
short stature
scoliosis

41
Q

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

A 
heart problems
blue sclera
dentinogenesis imperfecta - brown soft teeth
wormian skull
hypermetabolism
42
Q

What are the 5 things we need to know about for paediatric fracture classification.

A 
Pattern
Anatomy
Intra/Extra articular
Displacement
Salter - Harris
43
Q

Give 5 examples of fracture pattern?

A 
Comminuted
Oblique
Spiral
Transverse
Avulsion

=COSTA

44
Q

What do we have to think about when classifying the anatomy of a fracture?

A

Where in the bone
proximal 1/3
middle 1/3 (diaphysis)
distal 1/3

45
Q

What is an intra-articular fracture?

A

A fracture that crosses a joint surface. (could involve cartilage damage)

46
Q

What is an extra-articular fracture?

A

A fracture that occurs outside or somewhere other than a joint

47
Q

What is the difference between primary and secondary bone healing?

A

Primary - heals by direct union

Secondary - bone healing by callus formation

48
Q

For intra-articular fractures, which type of bone healing is preferred?

A

Primary as this minimises risk of post-traumatic arthiritis

49
Q

What are the four types of fracture displacment?

A

displaced
angulated
shortened
rotated

50
Q

What is the salter harris classification, list all 5 types?

A

Classification of physeal injuries (SALT)

  1. Physeal separation
  2. Fracture transverses physis and exits metaphysis (above)
  3. Fracture transverses physis and exits epiphysis (lower)
  4. Fracture passes through epiphysis, physis, metaphysis
  5. Crush injury to the physis
51
Q

According to the salter harris classification, which type has the highest risk of growth arrest?

A

5

Risk of growth arrest increases from 1-5

52
Q

Which type of physeal injury according to the salter harris classification is the most common?

A

Type 2

53
Q

What are the type types of growth arrest?

A

whole physis - limb length discrepancy

partial - angulation as the non affected side keeps growing

54
Q

What two things affect the severity of growth arrest caused by injury to the physis?

A

location

timing (age)

55
Q

How is growth arrest causing limb length discrepancy, treated?

A

shorten the long side

lengthen the short side

56
Q

How is growth arrest causing angular deformity, treated?

A

stop the growth of the unaffected side

reform the bone (osteotomy)

57
Q

What are the 4 things to consider in fracture management?

A

resuscitate
reduce
restrict
rehabilitate

58
Q

what is reduce in fracture management?

A

correct the deformity and displacement

reduces secondary issue to soft tissue and neurovascular structures

59
Q

What is closed reduction?

A

reducing a fracture without making an incision

such as traction and manipulation in A&E

60
Q

What is open reduction?

A

making an incision

the realignment of a fracture under direct visualisation

61
Q

What is gallows traction?

A

Type of closed reduction where that by holding the skin, the long bones of the lower limb can be reduced

62
Q

What does restrict involve in fracture management?

A

maintain the fracture reduction

provides the stability required for the fracture to heal

63
Q

What are the two types of restriction, give examples for both.

A

External - splints, plaster

Internal - plates, screws, intra-medullary device

64
Q

What type of restriction is more commonly used in paediatric fractures, why?

A

External (plaster and splints) as remodelling and healing potential means that operative internal fixation can often be avoided

65
Q

What are the two things to consider for paediatric internal fracture restriction (plates, screws)?

A

ongoing growth at the physis

metalwork may need to be removed in the future

66
Q

What does rehabilitation involve for paediatric fractures?

A

play
children generally rehabilitate very quickly and don’t usually need physio, stiffness is also not as a major issue as in adults

67
Q

When is Kocher’s classification used?

A

to help score probability of septic arthritis

68
Q

What is Kocher’s classification?

A

Non-weight bearing
ESR >40
WBC >12,000
Temp >38

69
Q

Why is septic arthritis an orthopaedic emergency?

A

because it can cause irreversible long term problems in the joint

70
Q

How is septic arthritis treated?

A

surgical washout

antibiotics

71
Q

What are other symptoms of septic arthritis?

A

24-48 hr off food and drink
last 12 hours is unwell
doesn’t want to move joint

72
Q

What is transient synovitis?

A

Similar symptoms but only diagnosed once septic arthritis is excluded
Is an inflamed joint secondary to systemic (secondary) illness
Much more common

73
Q

How is transient synovitis treated?

A

Antibiotics and supportive treatment

74
Q

What is perthes diseases?

A

idiopathic necrosis of the proximal femoral epiphysis

75
Q

What are the demographics of most perthes disease patients?

A

4-8 years old

male 4:1 female

76
Q

What is SUFE?

A

Slipped upper femoral epiphysis

The proximal epiphysis slips in relation to the metaphysis

77
Q

What does a typical SUFE patient look like?

A

obese adolescent male
12-13 years old during rapid growth
associated with hypothyroidism/hypopituitarism

78
Q

What is the treatment for SUFE?

A

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

79
Q

Before diagnosing Perthes disease, transient synovitis, SUFE what needs to be excluded first?

A

Septic arthritis

BRS 1b (25 decks)

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