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Year 2 - BRS > 8.2 - Children's orthopaedics > Flashcards

8.2 - Children's orthopaedics Flashcards

1
Q

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

A

270 bones and is a system in continuous change

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2
Q

What do the bones of a child feature (that adult bones do not)?

A
  • the physis (growth plates) that are areas from which long bone growth occurs post-natally
  • most long bones have 2 physes - one at proximal and one at distal end
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3
Q

What are the two kinds of bone development and what bones use these methods?

A
  • intramembranous ossification (mesenchymal cells –> bone) = flat bones e.g. cranial, clavicle
  • endochondral ossification (mesenchymal cells –> cartilage –> bone) = long bones
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4
Q

Describe the steps 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 periosteum form
  4. compact bone develops superficial to cancellous bone; crowded blood vessels condense into red bone marrow
  5. immature woven bone remodelled and progressively replaced by mature lamellae bone
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5
Q

Where does long bone formation occur?

A

At both the primary and secondary ossification centres (diaphysis and epiphyses)

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6
Q

What are the primary and secondary ossification centres?

A
  • primary ossification centre: sites of prenatal bone growth through endochondral ossification from the central part of the bone
  • secondary ossification centre: occurs post-natal after the primary ossification centre, and long bones often have several (physis)
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7
Q

Describe the steps of primary ossification.

A
  1. mesenchymal differentiation at the primary centre (diaphysis/centre)
  2. cartilage model of future bony skeleton forms (chondroblasts and perichondrium)
  3. capillaries penetrate cartilage; calcification at primary ossification centre to form spongy bone; perichondrium transforms into periosteum
  4. cartilage and chondrocytes continue to grow at ends of bone
  5. secondary ossification centres develop at distal and proximal ends of bone (epiphysis) with its own blood supply which begins to calcify matrix into immature spongy bone
  6. cartilage remains at epiphyseal (growth) plate (site of secondary endochondral ossification postnatal) and at joint surfaces as articular cartilage
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8
Q

Describe the steps of secondary ossification (long bones lengthening)

A
  • by the time the child is born, the cartilage remains at the joint surface as articular cartilage and in between diaphysis and epiphysis as epiphyseal plate (AKA physis)
  • these physes are responsible for elongation of long bone
  • epiphyseal side (ends) - hyaline cartilage active and dividing to form hyaline cartilage matrix
  • diaphyseal side (centre) - cartilage calcifies and dies and then replaced by bone
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9
Q

What happens to chondrocytes in each of the growth plate zones?

A
  • metaphysis/zone of ossification - primary and secondary spongiosa
  • calcified matrix - cell death
  • maturation and hypertrophy - lipids, glycogen and alkaline phosphatase accumulate; matrix calcifies
  • proliferative zone - mitosis
  • reserve zone - matrix production
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10
Q

What are the four ways a child’s skeleton differs to that of an adult?

A
  • elasticity
  • physis
  • speed of healing and remodelling potential
  • remodelling
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11
Q

How does elasticity of a child’s skeleton differ to that of an adult?

A
  • children’s bone can bend - increased elasticity than adults
  • increased density of Haversian canals (tunnels in bone cortices that circulate the blood supply) due to child’s bones being more metabolically active since they continually grow
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12
Q

What does increased elasticity lead to in child bones? (3)

A
  • plastic deformity - bends before breaks
  • buckle fracture - Tarus structure like the column
  • greenstick - like the tree - one side snaps/fractures but other side buckles instead of breaking
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13
Q

How does physis of a child’s skeleton differ to that of an adult?

A
  • growth occurs at varying rates at varying physis sites
  • growth stops as physis closes:
    • girls 15-16
    • boys 18-19
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14
Q

What can influence physis to close? (4)

A
  • gradual physeal closure
  • puberty
  • menarche
  • parental height
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15
Q

What can physeal injuries lead to?

A

Growth arrest which can lead to deformity - one part of bone continues to grow, but other has stopped

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16
Q

How are physeal injuries classified?

A

Salter-Harris classification

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17
Q

How do speed of healing and remodelling potential of a child’s skeleton differ to that of an adult?

A
  • speed of healing and remodelling potential is dependent on the location and the age of the patient
  • younger child heals more quickly
  • physis at knee grows more (distal femur and proximal tibia)
  • physis at extremes of upper limb grows more (around shoulder and wrist)
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18
Q

How does remodelling of a child’s skeleton differ to that of an adult?

A

Remodelling potential in a child is a lot higher than in an adult e.g. proximal humerus fracture in a 9 year old completely remodelled in two years to show no visible deformity or functional restriction

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19
Q

What are some common children’s congenital conditions affecting bones? (4)

A
  • developmental dysplasia of the hip (DDH)
  • congenital talipes equinovarus / club foot
  • achondroplasia
  • osteogenesis imperfecta (brittle bone disease)
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20
Q

What is developmental dysplasia of the hip?

A
  • group of disorders of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
  • a ‘packaging disorder’
  • normal development of hip and acetabulum relies on the concentric reduction and balanced forces through the hip
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21
Q

Describe the spectrum of developmental dysplasia of the hip.

A
  • dysplasia (mildest) - hip may be within socket but not centrally placed so socket does not develop into a cup
  • subluxation - hip may be in socket but socket is shallow so hip can pop in and out
  • dislocation (severe) - hip develops outside of socket and socket develops as very shallow cup
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22
Q

How common is dysplasia and dislocation in developmental dysplasia of the hip?

A
  • dysplasia 2:100
  • dislocation 2:1000
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23
Q

What are the risk factors for developmental dysplasia of the hip? (7)

A
  • female 6:1
  • first born
  • breech position
  • family history
  • oligohydramnios (not enough fluid in amniotic sac)
  • native American/Laplanders (due to swaddling of hip)
  • rare in African American/Asian
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24
Q

How is developmental dysplasia of the hip examined?

A
  • usually picked up on baby check - screening in UK
  • range of motion of hip checked
    • usually limitation in hip abduction
    • leg length (Galeazzi)
  • special tests Barlow and Ortalani in those three months or older are non-sensitive
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25
Q

How is developmental dysplasia of the hip investigated?

A
  • ultrasound - birth to 4 months
    • after 4 months X-ray (US not sensitive after 4 months)
    • X-ray not useful before 4 months as secondary ossification centres of hip not ossified
    • if prior to 6 weeks needs to be age adjusted since premature children can have abnormal results
  • measures the acetabular dysplasia and the position of hip
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26
Q

How is developmental dysplasia of the hip treated?

A
  • Pavlik harness 92% effective in a reducible hip and <6 months
  • if Pavlik harness fails or baby is 6-18 months: surgery - MUA + closed reduction and Spica
  • aim is to give child normal development of hip as DDH is progressive, avoid issues in adolescence
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27
Q

What is congenital talipes equinovarus (clubfoot)?

A

Congenital deformity of the foot

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28
Q

Which groups is congenital talipes equinovarus (clubfoot) more common in?

A
  • 1 in 1000
  • highest in Hawaiians
  • M:F 2:1
  • 50% bilateral
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29
Q

How is congenital talipes equinovarus (clubfoot) caused?

A
  • genetic
  • approximately 5% likely to affect future siblings
  • familial in 25%
  • PITX1 gene
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30
Q

What are the deformities present in congenital talipes equinovarus (clubfoot)?

A
  • CAVE deformity due to muscle contracture
  • Cavus - high arch - tight intrinsic, FHL (flexor halluces longus), FDL (flexor digitorum longus)
  • Adductus of foot - tight tibialis posterior and anterior
  • Varus - tight tendonachillies, tibial post and tibial ant
  • Equinous - tight tendoachilles
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31
Q

What is the gold standard treatment for congenital talipes equinovarus (clubfoot)?

A

Ponseti method

  1. first a series of casts to correct deformity
  2. many require operative treatment e.g. soft tissue releases
  3. foot orthosis brace
  4. some will require further operative intervention to correct final deformity
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32
Q

What is achondroplasia a form of?

A

The most common skeletal dysplasia

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33
Q

What causes achondroplasia?

A
  • autosomal dominant
  • G380 mutation of FGFR3
  • causes inhibition of chondrocyte proliferation in the proliferative zone of the physis
  • results in defect in endochondral bone formation
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34
Q

How does achondroplasia present? (1 + 6)

A
  • Rhizomelic dwarfism
    • humerus shorter than forearm
    • femur shorter than tibia
    • normal trunk
    • adult height approx. 125cm
    • normal cognitive development
    • significant spinal issues
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35
Q

What is the heredity of osteogenesis imperfecta like?

A

Autosomal dominant or recessive

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36
Q

What does osteogenesis imperfecta cause a problem in?

A
  • decreased type I collagen due to:
    • decreased secretion
    • production of abnormal collagen
  • leads to insufficient osteoid production
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37
Q

How does osteogenesis imperfecta manifest in bones? (3)

A
  • fragility fractures
  • short stature
  • scoliosis
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38
Q

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

A
  • heart issues
  • blue sclera
  • dentinogenesis imperfecta - brown soft teeth
  • Wormian skull
  • hypermetabolism
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39
Q

What acronym can we use to describe paediatric (and adult) fractures?

A
  • PAID
  • Pattern
  • Anatomy
  • Intra/Extra-articular
  • Displacement
40
Q

What is the pattern of a fracture reflective of?

A

The way the energy was dissipated

41
Q

What different types of fracture patterns are there? (6)

A
  • transverse
  • oblique
  • spiral - rotational torque pattern of injury
  • comminuted - high energy injuries with >1 part
  • avulsion - bone pulled off by its ligament
  • in children - plastic deformity / buckle fracture / greenstick fracture
42
Q

What does the anatomy of a fracture mean?

A

Where in the bone the fracture is located

43
Q

How does the anatomy of a fracture differ between adults and children?

A

In children, the proximal and distal 1/3 have secondary ossification centres for physis - management differs from adult

44
Q

What are the two ways bone healing occurs?

A
  • primary bone healing - heals by direct union, no callus formation
  • secondary bone healing - bone healing by callus
45
Q

What kind of fracture is primary bone healing more common in and why?

A

Preferred healing pathway in intra-articular fractures as it minimises risk of post-traumatic arthritis

46
Q

What kind of fracture is secondary bone healing more common in and why?

A

Extra-articular fractures - they also heal much quicker in children due to extensive healing and remodelling potential

47
Q

What are the different types of displacement in a fracture? (4)

A
  • displaced
  • angulated
  • shortened
  • rotated
48
Q

Which kinds of displacement can be tolerated by remodelling?

A
  • displacements are best in angle of function - so displaced, angulated and shortened fractures can be tolerated by remodelling
  • remodelling does not occur in rotated fractures
49
Q

What is the Salter-Harris classification?

A

Classification of physeal injuries

50
Q

What are the stages in the Salter-Harris classification using the SALT acronym?

A
  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
51
Q

How does risk of growth arrest change as you go through the 5 types in the Salter-Harris classification?

A

Risk of growth arrest increases from type 1-5

52
Q

Which Salter-Harris classification type is most common?

A

Type 2

53
Q

What can cause growth arrest?

A

Injuries to physis can cause growth arrest - location and timing is key

54
Q

How can location of injury affect growth arrest?

A
  • if injury happens to whole physis you get limb length discrepancy
  • if there is partial physis injury there is angulation as the non-affected side keeps growing
55
Q

How does timing of injury affect growth arrest?

A
  • different parts of skeleton grow at different rates
  • if closer to physeal closure when injury occurs, only small amount of growth potential left
  • if injury to physis when younger, it is larger part of limb’s growth so potential for growth arrest is much greater
56
Q

What are the aims of growth arrest treatment?

A
  • aim is to correct the deformity:
    • minimise limb length difference
    • minimise angular deformity
57
Q

How do we minimise limb length difference?

A
  • shorten the longer side (prematurely stop growth of unaffected side e.g. fuse physis by crossed screws)
  • lengthen shorter side (lengthening device)
58
Q

How do we minimise angular deformity?

A
  • stop growth of unaffected side
  • reform the bone (osteotomy)
59
Q

What are the four Rs of fracture management?

A
  • Resuscitate
  • Reduce
  • Restrict (hold)
  • Rehabilitate
60
Q

What does ‘resuscitate’ mean (paediatric fracture management)?

A

Following the paediatric advanced trauma life support (ATLS) pathway

61
Q

What does ‘reduce’ mean (paediatric fracture management)?

A
  • correct deformity and displacement + bring ends together
  • want to reduce secondary injury to soft tissue and neurovascular structures, especially since children have plastic deformity potential and increased elasticity
62
Q

What closed reduction techniques are there? (Children’s orthopaedics)

A
  • reducing a fracture without making an incision e.g. traction and manipulation in A&E
  • Gallow’s traction - holding skin, the long bones of lower limb can be reduced
63
Q

What open reduction techniques are there?

A
  • making an incision
  • the realignment of the fracture under direct visualisation
64
Q

What type of reduction is often used in children and why?

A

Closed reduction - remodelling potential in children is more significant so even more significant angular deformities can be tolerated compared to adults

65
Q

What does ‘restrict’ mean (fracture management)?

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

Why do children rarely have issues with bone not healing?

A
  • metabolic activity means bones rapidly growing and are highly vascularised
  • do not have risk factors of older adult
  • they can have issues with too much healing (especially when considering midshaft fractures in long bones)
67
Q

What external methods of restricting fractures are there? (2)

A
  • splints
  • plaster
68
Q

What internal methods of restricting fractures are there? (2)

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

What type of restriction is more common in paediatric patients and why?

A
  • external restriction (plaster, splints) - child remodelling and healing potential therefore operative internal fixation can often be avoided
  • operations may be needed - when physis affected (to avoid growth problems), when fractures beyond the potential tolerance of remodelling
70
Q

What do we have to consider when doing operative intervention to treat fractures in paediatric patients? (2)

A
  • consider the ongoing growth at the physis - avoid further trauma (growth arrest risk)
  • metalwork may need to be removed in future due to child growing
71
Q

How does ‘rehabilitate’ work in children (fracture management)?

A
  • children generally rehabilitate very quickly
  • play is a great rehabilitator
  • stiffness is not a major issue as in adults
  • ‘Use it, Move it and Strengthen it!’
72
Q

What are the four key differentials for a limping child?

A
  • septic arthritis
  • transient synovitis
  • Perthes
  • SUFE
73
Q

What is septic arthritis?

A

Presence of infection within intra-articular space - medical orthopaedic emergency!!

74
Q

What can septic arthritis lead to?

A

Irreversible long term problems in joint due to necrosing effects of proteases created by the organism, but also pressure of oedema in closed space on chondrocytes and cartilage

75
Q

How do you clear the infection in septic arthritis?

A

Surgical washout of the joint

76
Q

What classification system can we use to help score probability of septic arthritis?

A

Kocher’s classification

77
Q

What are the four parts of Kocher’s classification for septic arthritis?

A
  • non weight-bearing
  • ESR >40
  • WBC >12000
  • temperature >38
78
Q

What parts of the history are key in the diagnosis of septic arthritis? (3)

A
  • duration
  • other recent illness (and coryzal/cold symptoms)
  • associated joint pain, rashes, diarrhoea, vomiting
  • (can be hard as younger child may not be able to give a thorough history)
79
Q

When is transient synovitis considered?

A

Once septic arthritis has been excluded

80
Q

What is transient synovitis?

A

An inflamed joint in response to a systemic illness

81
Q

What is the treatment for transient synovitis?

A

Supportive treatment with antibiotics

82
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

83
Q

What ages does Perthes disease usually occur in and what is the M:F ratio?

A
  • usually in 4-8 year olds
  • M:F 4:1
84
Q

What other disease needs to be excluded before Perthes disease can be diagnosed?

A

Septic arthritis

85
Q

How is the presentation of Perthes disease different to septic arthritis or transient synovitis? (2)

A
  • key differential is chronicity - Perthes’s more chronic
  • would not see temperatures and inflammatory markers that you would see in septic arthritis
86
Q

What is the key diagnostic test for Perthes disease?

A

Plain film radiograph (epiphysis on one femur may not be as symmetrical and well-formed as other side)

87
Q

What is the treatment for Perthes disease?

A
  • usually supportive in first instance
  • if diagnosed, specialist referral for continued observation and management occurs
88
Q

What does SUFE stand for?

A

Slipped upper femoral epiphysis

89
Q

What is SUFE?

A

Proximal epiphysis slips in relation to metaphysis

90
Q

Which paediatric patient groups is SUFE most common in?

A
  • usually obese adolescent males
  • around 12-13 years old during rapid growth
91
Q

What other health issues is SUFE associated with?

A

Hypothyroidism or hypopituitarism

92
Q

What other disease needs to be excluded first before SUFE diagnosis?

A

Septic arthritis

93
Q

How do we distinguish between SUFE and the other differentials?

A
  • history is akin to Perthes’ where child complains of limp
  • not as acute as septic arthritis
  • no temperature/raised biochemical markers
94
Q

How can the presentation of SUFE be classified?

A
  • acute or chronic
  • sometimes acute on chronic where child may have had episodes of pain and limping in past where it has suddenly gotten worse
  • special classification system to further differentiate if child can weight bear or not
95
Q

What is the treatment for SUFE?

A

Operative fixation to prevent further slip and minimise long term growth problems

96
Q

Which differential diagnosis of a limping child is most important?

A

Septic arthritis!! Must exclude septic arthritis first in any limping child (transient synovitis diagnosis of exclusion, Perthes’ and SUFE are not as common)

Year 2 - BRS (84 decks)

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