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msk + rheum > 1B children orthopaedics > Flashcards

1B children orthopaedics Flashcards

1
Q

How many bones in a child skeleton?

A

270

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2
Q

What are the blue lines?

A
  • The physis (growth plates) that are the areas from which long bone growth occurs post-natally
  • Each long bone usually has 2- one at proximal and one at distal end
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3
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 vessels condense into red bone marrow

5) Immature woven bone remodelled and progressively replaced by mature lamellae bone

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4
Q

What bones use intramembranous ossification?

A

Flat cranial bones and clavicle

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5
Q

Describe endochondral ossification in terms of what the ossification centres do

A
  • Primary ossification centres
    • Sites of pre-natal bone growth through endochondral ossification from the central part of the bone
  • Secondary ossification centres
    • Occurs post-natal after the primary ossification centre and long bones often have several (the physis)
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6
Q

Describe primary ossification steps

A

1) Mesenchymal differentiation at the primary centre (in the diaphysis or middle of the shaft of bone) in the prenatal period

2) Cartilage model of future bony skeleton forms

3) Capillaries penetrate cartilage and calcification occurs to form spongy bone which forms up the shaft. Perichondrium transforms into periosteum

4) Cartilage and chondrocytes continue to grow at ends of the bone

5) Secondary ossification centres develop at proximal and distal ends of long bones with its own blood supply which begins to calcify matrix into immature spongy bone

Left with cartilage at distal and proximal ends of bone with epiphyseal growth plate which will be point of secondary endochondral ossification in post natal period

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7
Q

Describe secondary ossification steps

A
  • By the time the child is born the cartilage remains at the front surface as articular cartilage and in between diaphysis and epiphysis as the epiphyseal plate (aka physis)
  • These physes are responsible for elongation of the long bone
  • Epiphyseal side- hyaline cartilage is active and dividing to form hyaline cartilage matrix
  • Diaphyseal side- cartilage calcifies and dies and then replaced by bone
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8
Q

What are the 4 ways a child’s skeleton differs to that of an adult?

A
  • Elasticity
  • Physis
  • Speed and remodelling potential
  • Remodelling
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9
Q

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

A
  • Children’s bones have increased elasticity than adults
  • This is due to increased density of Haversian canals (tunnels in bone cortices that circulate the blood supply) due to child bones being more metabolically active since they continually grow
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10
Q

What does increased elasticity lead to in child bones?

A
  • Plastic deformity- bends before breaks
  • Buckle fracture- Torus structure like columns
  • Greenstick- like the tree- one side snaps and other side buckles instead of breaking
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11
Q

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

A

Growth occurs at varying rates at different physis sites

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12
Q

Growth stops as physis closes- what influences this to happen?

A
  • Gradual physeal closure
  • Puberty
  • Menarche
  • Parental height
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13
Q

What age does physis close?

A
  • Girls 15-16
  • Boys 18-19
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14
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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15
Q

How are physeal injuries classified?

A

Salter-Harris

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16
Q

How is a child’s skeleton speed and remodelling potential different from an adults?

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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17
Q

How is a child’s remodelling skeleton different from an adults?

A

Remodelling potential in a child is way more than in an adult e.g. below proximal humeruses are very broken in a 9 year old child but in 2 years (below image) it has completely remodelled to show no visible deformity or functional restriction

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18
Q

What are some common children’s congenital conditions?

A
  • Developmental dysplasia of hip
  • Congenital Talipes Equinovarus
  • Achondroplasia
  • Osteogenesis Imperfecta aka brittle bone disease
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19
Q

Define developmental dysplasia of 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
  • A ‘packaging disorder’
  • The normal development of hip and acetabulum relies on the concentric reduction and balanced forces through the hip
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20
Q

Describe the spectrum of developmental dysplasia of hip

A
  • Dysplasia (mild cases)- hip may be within socket but not centrally placed so socket doesn’t 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 a very shallow cup
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21
Q

How common is dysplasia?

A

2:100

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22
Q

How common is dislocation?

A

2:1000

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23
Q

What are risk factors of developmental dysplasia of hip?

A
  • Female children 6:1
  • First born
  • Breech position
  • Family history
  • Oligohydramnios (abnormally low level of amniotic fluid)
  • Native American/Laplanders due to habit of swaddling of hip once child is born
  • Rare in African American and Asian populations
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24
Q

What is oligohydramnios?

A

Not enough fluid in amniotic sac

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25
Q

How is developmental dysplasia of the hip investigated?

A

Ultrasound from birth to 4 months

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26
Q

What investigation for developmental dysplasia of the hip is used for premature babies/ babies older than 4 months and why?

A
  • After 4 months X-ray done since US isn’t sensitive after 4 months
  • If prior to 6 weeks you need to age adjust the test since you can find abnormal results in premature children
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27
Q

How is developmental dysplasia of the hip treated?

A

Pavlik harness

92% effective in a reducible hip and <6 months

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28
Q

What do we do if Pavlik harness fails or baby is 6-18 months (so DDH picked up late)?

A

Surgery- MUA + closed reduction and Spica

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29
Q

What is the aim of developmental dysplasia of the hip treatment?

A

It’s not about preventing morbidity but to give child normal development of hip because DDH is progressive so when adolescent the patient has no issues

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30
Q

What is clubfoot/ congenital talipes equinovarus?

A

Congenital deformity of the foot

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31
Q

Which groups is clubfoot more common in?

A
  • 1 in 1000
  • Highest in Hawaiians
  • M:F is 2:1
  • 50% are bilateral
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32
Q

How is clubfoot caused?

A
  • Genetic- PITX1 gene
  • Approx 5% likely to affect future siblings
  • Familial in 25% of cases
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33
Q

What are the deformities present in clubfoot?

A
  • CAVE deformity due to muscle contracture- described as club foot overall
  • Cavus- high arch- tight intrinsic, FHL (flexor halluces longus), FDL (flexor digitorum longus)
  • Adductus of foot: tight tibia posteriorly and anteriorly
  • Varus: tight tendoachilles, tibial post and tib ant
  • Equinous: tight tendoachilles
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34
Q

What is the gold standard for treatment of clubfoot?

A

1) Gold standard is the Ponseti method: a series of casts are used to correct deformity

2) Many require operative treatment e.g. soft tissue releases

3) Foot orthosis brace (bottom pic)

4) Some will require further operative intervention to correct final deformity

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35
Q

What is achondroplasia a form of?

A

The most common skeletal dysplasia

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36
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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37
Q

How does achondroplasia present?

A

Rhizomelic dwarfism

  • Humerus shorter than forearm
  • Femur shorter than tibia
  • Normal trunk
  • Adult height of approx 125cm
  • Normal cognitive development
  • Significant spinal issues
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38
Q

What is the heredity of osteogenesis imperfecta like?

A

Autosomal dominant or recessive

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39
Q

What does osteogenesis imperfecta cause a problem in?

A

Decreased Type I collagen due to either:

  • Decreased secretion (quantity of collagen)
  • Production of abnormal collagen (quality of collagen)
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40
Q

How does osteogenesis imperfecta manifest in bones?

A
  • Fragility fractures
  • Short stature
  • Scoliosis
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41
Q

What non-orthopaedic manifestations are there for brittle bone disease?

A
  • Heart issues
  • Blue sclera
  • Dentinogenesis imperfecta- brown soft teeth
  • Wormian skull due to abnormal fusion of cranial sutures
  • Hypermetabolism- typically affecting parathyroid pathway
42
Q

How do we describe fractures in both adults and kids?

A

PAID

  • Pattern
  • Anatomy
  • Intra/Extra-articular
  • Displacement
43
Q

What is pattern in fractures reflective of?

A

The way that the energy is dissipated

44
Q

What different types of fracture patterns are there?

A
  • Transverse
  • Oblique
  • Spiral- rotational torque pattern of injury
  • Comminuted- in high energy injuries with >1 part
  • Avulsion- if bone has been pulled off by its ligament
  • In kids you might get plastic deformity too or greenstick fracture (not seen in adults)
45
Q

What does the anatomy in a fracture mean?

A

Where in the bone the fracture is located

46
Q

How does anatomy in a fracture differ between adults and kids?

A

In kids in proximal and distal 1/3 there are secondary ossification centres for physis which is when management of fractures differs from adult

47
Q

What are the two ways that bone healing occurs?

A
  • Primary bone healing
  • Secondary bone healing
48
Q

Describe primary bone healing

A
  • Heals by direct union
  • No callus formation
49
Q

Which of intra or extraarticular fractures is primary bone healing more common in and why?

A

It’s the preferred healing pathway in intraarticular fractures as it minimises risk of post traumatic arthritis

50
Q

Describe secondary bone healing

A

Bone heals by callus

51
Q

Which of intra and extraarticular fractures is secondary healing more common in?

A
  • Extra articular fractures
  • They heal much more quickly in children as well compared to adults due to extensive healing and remodelling potential in kids
52
Q

What different displacements in fractures are there?

A
53
Q

When can remodelling not allow for displacement?

A
  • Displacements are best in the angle of function- so displaced, angulated and shortened fractures can be tolerated by remodelling
  • Remodelling doesn’t occur in rotated fractures
54
Q

What is the Salter-Harris classification?

A

A classification of when the physis is injured. Uses the SALT algorithm.

55
Q

What does SALT stand for?

A

There are 5 stages of Salter-Harris:

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 and metaphysis

5) Crush injury to physis

56
Q

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

A

Risk of growth arrest increases from type 1-5

57
Q

Which type is most common in the Salter-Harris classification?

A

Type 2

58
Q

What can cause growth arrest?

A

Injuries to physis can cause growth arrest

59
Q

What affects growth arrest?

A
  • Location of injury
  • Timing
60
Q

How does location of injury affect growth arrest?

A
  • If injury happens to whole physis you get limb length discrepancy (right pic)
  • If there’s a partial physis injury there’s angulation as the non-affected side keeps growing (left pic)
61
Q

How does timing affect growth arrest?

A
  • different parts of skeleton grow at different rates and child grows at different rates as they get older
  • so if you’re closer to physeal closure when injury happens there’s only a small amount of growth potential left
  • If you get injury to physis when you’re younger, it’s a larger part of the limb’s growth so potential for growth arrest is much greater
62
Q

What are the aims of growth arrest treatment?

A

To correct the deformity by:

  • Minimising limb length difference
  • Minimising angular deformity
63
Q

How is limb length difference minimised?

A
  • Shorten the longer side- prematurely stop growth of unaffected side (left pic shows premature fusing of physis of distal femur by crossed screws)
  • Lengthen the shorter side (right pic shows lengthening device)
64
Q

How is angular deformity minimised?

A
  • Stop the growth of the unaffected side
  • Reform the bone (osteotomy)
65
Q

What are the 4 R’s of fracture management?

A
  • Resuscitate
  • Reduce
  • Restrict
  • Rehabilitate
66
Q

What is resuscitation?

A

Following paediatric advanced trauma life support pathway

67
Q

What is the point of reduction of a fracture?

A

Correcting the deformity and displacement

68
Q

What do we have to consider especially in kids when reducing a fracture?

A

We want to reduce secondary injury to soft tissue and neurovascular structures especially since kids have plastic deformity potential and increased elasticity

69
Q

What closed reduction techniques are there?

A
  • Reducing a fracture without making an incision
  • Such as traction and manipulation in A&E
70
Q

Why are closed reduction techniques used often in kids?

A

Remodelling potential in kids is more significant so even more significant angular deformities can be tolerated compared to adults

71
Q

What is a Gallow’s traction?

A

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

72
Q

What open reduction techniques are there?

A
  • Making an incision
  • The realignment of the fracture under direct visualisation
73
Q

What is the point of restricting a bone fracture?

A
  • Maintain the fracture reduction
  • Provides stability for fracture to heal
  • Children have quicker fracture healing times and remodelling potential
74
Q

Why do kids rarely have issues with bones not healing?

A
  • Their metabolic activity means bones are rapidly growing and are highly vascularised + don’t have patient risk factors of older adult
  • There can actually be issues with too much healing- especially when considering midshaft fractures in long bones
75
Q

What external methods of restricting fractures are there?

A
  • Splints
  • Plaster
76
Q

Why are external methods more common?

A

Because of child remodelling and huge healing potential, operative internal fixation can often be avoided

77
Q

What internal methods of restricting fractures are there?

A
  • Plate and screws
  • Intra-medullary device
  • Surgery
78
Q

When is surgery done for internal methods of restricting fractures?

A
  • When fracture affects physis and we need to correct deformity to prevent growth problems in future
  • When fractures are beyond the potential tolerance of remodelling (below shows significant angulation in this radial + ulnar fracture and had intramedullary nails used → they’re slightly elastic and help tension the forearm through interosseus membrane and hold reduction in place- are removed when fracture is healed)
79
Q

What do we have to consider when doing operative intervention in kids?

A
  • To avoid further trauma to physis for risk of growth arrest
  • Metalwork may need to be removed in future due to child growing
80
Q

How does rehabilitation work in kids?

A
  • Children generally rehab very quickly
  • Play is a great rehabilitator
  • Stiffness is not a major issue as in adults
  • Principle of ‘Use it, move it and strengthen’
81
Q

What are 4 key differentials for the limping child?

A
  • Septic arthritis
  • Transient synovitis
  • Perthes Disease
  • SUFE
82
Q

What is septic arthritis?

A

Presence of infection within intraarticular space

83
Q

What issue can septic arthritis cause and how?

A

Can cause irreversible long term problems in joint due to necrosing effects of proteases the organisms create in joint but also pressure of the oedema in the closed space on the chondrocytes and cartilage

84
Q

What does septic arthritis need to clear the infection?

A

A surgical washout of the joint

85
Q

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

A

Kocher’s classification:

  • Non weight bearing
  • ESR >40
  • WBC >12,000
  • Temp >38
86
Q

What parts of the history are key for diagnosis of septic arthritis?

A
  • Duration
  • Other recent illness and coryzal symptoms (cold symptoms like cough, sore throat, malaise, rhinorrhoea)
  • Associated joint pain, rashes, diarrhoea, vomiting
  • What can be hard about taking a history?Younger child may not be able to give a thorough history and if presenting complaint isn’t clear
87
Q

When is transient synovitis diagnosis considered?

A

When septic arthritis has been excluded

88
Q

What is transient synovitis?

A

An inflamed joint in response to a systemic illness

89
Q

What is the treatment for transient synovitis?

A

Supportive treatment with antibiotics is the treatment

90
Q

What is Perthes Disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

91
Q

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

A
  • Usually in 4-8 year olds
  • M:F is 4:1
92
Q

How is the presentation of Perthes’ different to septic arthritis or transient synovitis?

A
  • Key differential is chronicity- Perthes’ will have gone on longer than the other 2
  • You don’t expect to see temperatures and inflammatory markers in Perthes’ that you would in septic arthritis
93
Q

What is the key diagnostic test for Perthes’?

A

Plain film radiograph (in below pic the epiphysis on the right femur isn’t as symmetrical and well-formed as the other side)

94
Q

What is the treatment for Perthes’?

A
  • Usually supportive in first instance
  • If diagnosed, specialist referral for continued observation and management occurs
95
Q

What does SUFE stand for?

A

Slipped upper femoral epiphysis

96
Q

What is SUFE?

A

Slipped upper femoral epiphysis

Proximal epiphysis slips in relation to metaphysis

97
Q

Which kid patient groups does SUFE happen usually in?

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

Associated with hypothyroidism/hypopituitarism

98
Q

How is SUFE and other diseases distinguished?

A
  • History is akin to Perthes’ where child is complaining of limp
  • It’s not as acute as septic arthritis and you don’t find temperature or raised biochemical markers
99
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’s suddenly gotten worse
  • There is a special classification system to further differentiate if the child can weight bear or not
100
Q

What is the treatment of SUFE?

A

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

101
Q

Which of the four differentials of a limping child is most important/common?

A
  • The differential for any limping child is SEPTIC ARTHRITIS
  • Must exclude septic arthritis first in any limping child
  • Transient synovitis is diagnosis of exclusion
  • Perthes’ and SUFE are there and aren’t as common as transient synovitis (and ofc septic arthritis)

msk + rheum (5 decks)

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