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brs (phase 1b) > (msk) children's orthopaedics > Flashcards

(msk) children's orthopaedics Flashcards

1
Q

define physis

A

cartilaginous disc separating the epiphysis from the metaphysis

is responsible for interstitial bone growth of long bones

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2
Q

where are the physes found in children’s long bones?

A

two physes for each long bone: at the proximal and distal end

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3
Q

why are physes important?

A

site of interstitial bone growth needed for bone lengthening as children grow

(reserve, proliferative, hypertrophic and calcification zones)

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4
Q

differentiate between epiphysis, metaphysis, diaphysis and physis

A

epiphysis = wide end of long bones containing spongy, cancellous bone

diaphysis = tubular shaft of bone from distal to proximal end

metaphysis = region that connects the epiphysis to the diaphysis

physis = cartilagenous growth plate between epiphysis and metaphysis where interstitial bone growth for bone lengthening takes place

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5
Q

what are the two types of bone development?

A

intramembranous ossification

endochondral ossification

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6
Q

what type of bones is intramembranous ossification important for?

A

flat bones (e.g. clavicle, cranial bones)

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7
Q

what type of bones is endochondral ossification important for?

A

long bones

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8
Q

what is the main difference between endochondral and intramembranous ossification?

A

intramembranous = mesenchymal cells to bone

endochondral = mesenchymal cells to CARTILAGE to bone

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9
Q

describe the process of intramembranous ossification

A

mesenchymal cells differentiate into osteogenic cells and then osteoblasts = ossification centre forms

osteoblasts secrete osteoid and become trapped in the matrix as calcification occurs

when trapped, osteoblasts become osteocytes and bone formation occurs

in the central regions, the trabecular matrix develops forming spongy bone

blood vessels condense here and supply this region to form spongy red bone marrow

cortical bone develops superficial to the cancellous bone

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10
Q

how does spongy bone develop in intramembranous ossification?

A

trabecular matrix develops and blood vessels condense and supply this region
= spongy, cancellous bone

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11
Q

how does cortical bone develop in intramembranous ossification?

A

osteoblasts secrete osteoid and become trapped in the matrix as osteocytes during calcification, forming cortical bone

(occurs superficial to spongy bone formation)

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12
Q

what is the ossification centre in intramembranous ossification?

A

when osteoblasts, recently differentiated from mesenchymal cells, accumulate in a region prior to osteoid secretion

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13
Q

describe the process of endochondral ossification

A

1) mesenchymal cell differentiation
2) hyaline cartilage model with a lateral bony collar forms
3) interstitional and appositional growth of cartilage model
4) central matrix of cartilage model begins to CALCIFY as blood vessels condense to supply this region = forming the primary ossification centre + perichondrium converted into periosteum
5) spongy bone forms a the centre and extends proximally and distally - cartilage/chondrocytes develop
6) osteoclastic activity in the centre breaks down some bone and cartilage to form the medullary cavity
7) secondary ossification centres develop with its own blood vessel and calcification at the epiphyseal proximal and distal end – calcification of the matrix
8) some cartilage remains = articular cartilage, physis

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14
Q

describe the process of endochondral ossification

A

hyaline cartilage model with a lateral body collar forms

interstitional and appositional growth of cartilage model

central matrix of cartilage model begins to calcify as blood vessels condense to supply this region forming the primary ossification centre

spongy bone forms at the centre and extends proximally and distally

osteoclastic activity in the centre breaks down some bone and cartilage to form the medullary cavity

by birth, at the proximal and distal epiphyseal regions, blood vessels form and calcification occurs = secondary ossification centres

secondary centres = bone development in epiphyseal regions

but remnants = articular hyaline cartilage and epiphyseal growth plates (of initial hyaline cartilage model)

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15
Q

what is endochondral ossification divided into?

A

primary endochondral ossification

secondary endochondral ossification

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16
Q

what is primary and secondary endochondral ossification?

A

primary

  • pre-natal
  • involved formation of primary ossification centres & subsequent central bone growth

secondary

  • post-natal, adolescent
  • involves the development of epiphyseal secondary ossification centres
  • long bone lengthening at epiphyseal growth plates
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17
Q

what are primary ossification centres?

A

sites of pre-natal endochondral ossification in the central part of the bone

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18
Q

what are secondary ossification centres?

A

sites of post-natal endochondral ossification in the epiphyseal part of the bone

= interstitial bone lengthening occurs

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19
Q

where do primary ossification centres form in endochondral ossification?

A

in the central (diaphyseal) portion of the hyaline cartilage model

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20
Q

where and when do secondary ossification centres form in endochondral ossification?

A

when = post-natally, adolescent years

where = epiphyseal portion of long bone

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21
Q

why does osteoclast activity occur in endochondral ossification?

A

medullary cavity formation

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22
Q

why is the articular cartilage and epiphyseal growth plate important in endochondral ossification?

A

the only remnants of the initial hyaline cartilage model

  • articular cartilage = joint articulation
  • growth plate = sites of interstitial bone growth and lengthening
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23
Q

what happens at the physeal (epiphyseal growth) plate?

A

interstital bone growth

= chondrocytes proliferate, mature, hypertrophy and then form a calcified matrix to add to the ossified bone of the diaphyseal edges

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24
Q

differentiate between the epiphyseal and the diaphyseal side in interstitial bone growth

A

epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix

diaphyseal side – cartilage calcifies and cell death and then replaced by bone

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25
Q

what are four ways in which children’s bones differ primarily from adult bones?

A

physis

remodelling potential

elasticity

speed of healing

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26
Q

why are children’s bones more elastic than adult bones?

A

increased density of Haversian canals within children’s bones
to meet the increased metabolic demand

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27
Q

explain how the increased elasticity of children’s bones helps with bone growth

A

increased elasticity
= increased density of Haversian canals
= more dense blood supply
= increased bone growth

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28
Q

why do children have more Haversian canals in their bones?

A

to increase the vascular supply to the bone

as children’s bones are more metabolically active

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29
Q

what is the main consequence of the increased elasticity of children’s bones?

A

increased plastic deformity of the bones

i.e. likely to bend before they break

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30
Q

what is a Buckle fracture?

A

where only one side of the bone buckles/crumples but the other side of the bone is unaffected

(due to longitudinal force through bone cortex)

i.e. torus fracture

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31
Q

what is a Greenstick fracture?

A

when bone bends to the extent that one side breaks and the other side remains intact

(breaking twigs = the tough bark on one side will break but the bark on the other side remains intact)

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32
Q

what are Haversian canals?

A

microscopic tubes within cortical bone osteons housing the neurovascular supply to the bone

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33
Q

what is physeal growth?

A

(interstitial) bone growth at the epiphyseal growth plates at various sites at varying rates

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34
Q

which factors determine when growth at epiphyseal plates ceases?

A

puberty, menarche, parental height, genetic factors

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35
Q

in girls, when does physeal growth cease?

A

15-16

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36
Q

in boys, when does physeal growth cease?

A

18-19

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37
Q

what are two possible consequences of traumatic injuries to the physes?

A

1) growth arrest

2) deformity

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38
Q

how are physeal injuries categorised?

A

based on the Salter-Harris scale

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39
Q

how can physeal injury lead to growth arrest?

A

when the entirety of the physeal plate is injured, interstitial bone growth is significantly impaired

= growth arrest

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40
Q

how can physeal injury lead to deformity?

A

when a portion of the physeal plate is injured, interstitial bone growth continues in the intact region but stops in the injured region

= deformity

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41
Q

what three factors do the speed of healing and remodelling potential depend on?

A

1) location of injury
2) age of patient
3) GROWTH level at the site of injury

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42
Q

which group of patients heal most quickly?

A

young children

greatest growth = fastest healing

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43
Q

which region of the upper limb heals most quickly and why?

A

shoulders and wrist regions

areas of greatest growth = fastest healing

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44
Q

which region of the lower limb heals most quickly and why?

A

around the knee (distal femur, proximal tibia)

areas of greatest growth = fastest healing

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45
Q

why is the rate of healing accelerated in children?

A

children’s bones have very rapid growth rates

greatest, rapid growth rates = fastest healing + remodelling potential

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46
Q

how is healing linked to growth rate?

A

the more rapid the growth rate in a region, the faster the healing and the more the remodelling potential of the area

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47
Q

list four paediatric congenital orthopaedic conditions

A

developmental dysplasia of the hip (DDH)

club foot

achondroplasia

osteogenesis imperfects

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48
Q

what is developmental dysplasia of the hip?

A

disorder of the neonatal hip

where the head of the femur is unstable or incongruous in relation to the acetabulum

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49
Q

what does normal hip development require?

A

concentric reduction + balanced forces through the hip

= hip needs to sit in acetabulum so they can exert forces on each other to produce a normal hip joint

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50
Q

what happens if the hip develops outside the acetabulum?

A

if hip develops outside the socket, lack of force and pressure exertion on the acetabulum

= impaired acetabular development

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51
Q

what are the three types of DDH?

A

1) dysplasia
2) subluxation
3) dislocation

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52
Q

what is dysplasia in DDH?

A

hip lies in acetabulum BUT not centrally placed

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53
Q

what is subluxation in DDH?

A

hip lies in acetabulum but loosely

pops in and out of socket due to shallow acetabulum

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54
Q

what is dislocation in DDH?

A

hip never been inside acetabulum, develops outside

acetabulum very shallow

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55
Q

what are the risk factors for DDH?

A

female

firstborn

breech

family history

oligohydramnios

Native America/Laplanders (nature of swaddling the baby)

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56
Q

how is DDH diagnosed?

A

in the baby check (screening in the UK)

shows:

  • reduced range of motion
  • Barlow, Ortolani and Galeazzi tests show DDH
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57
Q

what are the findings in a baby check of a patient with DDH?

A

reduced RoM

Barlow, Ortolani, Galeazzi tests shows DDH

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58
Q

what is the primary method of investigation for DDH?

A

ultrasound (up till 4 months)

for 4+ months = usually X-ray

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59
Q

how is DDH treated?

A

reducible hip and <6 months = Pavlik harness

harness fails/6-18 months = surgical intervention (MUA, closed reduction, Spica cast)

60
Q

in patients where a Pavlik harness fails, how is DDH treated?

A

surgical intervention (MUA, closed reduction, Spica cast)

61
Q

why is ultrasound the preferred method of investigation for DDH?

A

shows hip positioning AND acetabular dysplasia/angles

62
Q

what is clubfoot?

A

congenital bilateral deformity of the foot

occurs in utero

63
Q

what are the risk factors for clubfoot?

A

male
(Hawaiian)
family history
genetics = PITX1 gene

64
Q

what is CAVE deformity in clubfoot?

A

deformity seen in clubfoot due to excessive muscle contracture

Cavus = high arch; intrinsic foot muscles, FDL, FHL

Adductus = tibialis anterior + posterior

Varus = tight tendinoachilles, tibilaise anterior + posterior

Equinous = tight tendinoachilles

65
Q

what causes the CAVE deformity in clubfoot?

A

muscle contracture

66
Q

how is clubfoot treated?

A

1) Ponseti method = series of casts to correct deformity (gold standard)

2) operative treatments
- soft tissue release
- foot orthosis brace

3) further operative intervention
- soft tissue release
- tendon transfers

67
Q

what is the gold standard treatment for clubfoot?

A

Ponseti method = series of casts to correct deformity

68
Q

what operative interventions are offered for clubfoot?

A

soft tissue release

foot orthotic braces

(maybe even tendon transfers)

69
Q

what is the most common skeletal dysplasia?

A

achondroplasia

70
Q

what kind of genetic abnormality is achondroplasia?

A

autosomal dominant

71
Q

how does achondroplasia manifest?

A

rhizomelic dwarfism

  • humerus < forearm
  • femur < tibia

(normal trunk + normal cognitive development BUT significant spinal issues)

72
Q

why does achondroplasia cause rhizomelic dwarfism?

A

achondroplasia
= inhibition of chondrocyte proliferation in the proliferative zone of the epiphyseal growth plates

= impaired secondary endochondral ossification
= impaired interstitial bone growth
= rhizomelic dwarfism

73
Q

what is the normal adult height for patients with achondroplasia?

A

approx 125cm

74
Q

what is osteogenesis imperfecta?

A

brittle bone disease due to impaired collagen production

autosomal dominant or recessive

75
Q

what happens to type I collagen in osteogenesis imperfecta?

A

1) quantitative problem = reduce synthesis of type I collage
2) qualitative problem = abnormal type I collagen produced

= both result in decreased osteoid secretion SO brittle bones

76
Q

what are the orthopaedic manifestations of osteogenesis imperfecta?

A

fragility fractures

short stature

scoliosis (spinal manifestation)

77
Q

what are the non-orthopaedic manifestations of osteogenesis imperfecta?

A

cardiac problems

blue scelera

dentinogenesis imperfecta (soft, brown teeth)

hypermetabolism (via PTH pathway)

Wormian skull (impaired fusion of skull sutures)

78
Q

what does a fracture pattern indicate?

A

the way the energy is dissapated through the bone

79
Q

children’s bones are more elastic - what is the implication of this?

A

more scope for plastic deformity

= more likely to be deformed than be fractured unless force of injury very high

80
Q

name some common fracture patterns

A 
simple
transverse
oblique
spiral
comminuted
avulsion
greenstick
buckle/torus
81
Q

what is an oblique fracture?

A

the break has a curved or sloped pattern

82
Q

what is a transverse fracture?

A

the broken piece of bone is at a right angle to the bone’s axis

83
Q

what is a spiral fracture?

A

the bone is broken with a twisting motion

84
Q

what is a comminuted fracture?

A

the bone breaks into several pieces

85
Q

what is an avulsion fracture?

A

when a fragment of bone is separated from the main mass

86
Q

what is the difference between open and closed fractures?

A

open = broken the skin (compound fracture)

closed = under the skin (simple fracture)

87
Q

how do you describe where in the bone the fracture has occurred?

A

proximal 1/3
middle 1/3 (diaphysis)
distal 1/3

88
Q

if in children, there is a fracture of the proximal or distal 1/3, why does the approach change?

A

in the proximal and distal 1/3s of children’s long bones
= secondary ossification centres AND epiphyseal growth plates
= must assess extent of damage to these

89
Q

define intra-articular and extra-articular fractures

A

intra-articular = fractures that extend into the joint

extra-articular = fractures that do not extend into the joint

90
Q

which is the preferred form of healing at intra-articular fractures?

A

primary (intramembranous) bone healing

91
Q

which is the preferred form of healing at extra-articular fractures?

A

secondary (endochondral) bone healing

92
Q

why is primary bone healing preferred for intra-articular fractures?

A

lack of callus formation prevents inflammation in the joint

= reduces the risk of post-traumatic arthritis

93
Q

what are the ways in which a bone can be displaced?

A

displaced
angulated
rotated
shortened

94
Q

which type of displacement is best tolerated by children’s bones?

A

in the angle of function

i.e. displaced, angulated, shortened but NOT rotated

95
Q

which type of displacement is tolerated least/not at all by children’s bones?

A

rotated fractures

not tolerated very well despite the huge remodelling potential of children’s bones

96
Q

how are physeal injuries classified?

A

Salter-Harris classification

97
Q

injuries to which part of the bone are most dangerous in children’s bones?

A

physis

98
Q

explain Salter-Harris classification

A

type I-V

risk of growth arrest increases with classification

based on SALT

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

99
Q

describe type I physeal injuries

A

physeal separation (S)

100
Q

describe type II physeal injuries

A

fracture goes through physis and metaphysis (above)

101
Q

describe type III physeal injuries

A

fracture goes through physis and epiphysis (lower)

102
Q

describe type IV physeal injuries

A

fracture goes through epiphysis, physis and metaphysis (all)

103
Q

describe type V physeal injuries

A

crush injury to physis

104
Q

how does the risk of growth arrest change with physeal classification?

A

risk of growth arrest increases from type 1 -5

105
Q

which type of physeal injuries are most common?

A

type II physeal injuries = above the physis i.e. physis + metaphysis

106
Q

why is type V physeal injury the most dangerous for children?

A

crush injury to the complete physis
= can significantly impair/inhibit secondary endochondral ossification
= impaired interstitial bone growth
= stunted long bone growth

107
Q

which two factors affect growth arrest in physeal injury?

A

location of injury

timing of injury

108
Q

how does timing affect growth arrest in physeal injury?

A

older bone
- closer to physeal closure = small amount of growth potential left to affect
= reduced growth arrest

younger bone
- physis very active = greater amount of growth potential affected
= more growth arrest

109
Q

how does location affect growth arrest in physeal injury?

A

whole physeal injury = limb length discrepancy

whole physeal injury = angular deformity

110
Q

why is there an angular deformity in partial physeal injury?

A

non-affected side keeps growing

111
Q

what are the two ways in which growth arrest can be treated?

A

1) minimise limb length discrepancy

2) minimise angular deformity

112
Q

how can limb length discrepancy be minimised in growth arrest?

A

shorten the long side (cross-nails to prematurely fuse physes)

lengthen the short side (limb-lengthening device)

113
Q

how can angular deformity be minimised in growth arrest?

A

stop growth on unaffected side

reform bone (surgical intervention, osteotomy)

114
Q

what are two ways growth arrest can manifest?

A

limb length discrepancy

angular deformity

115
Q

what are the four Rs of paediatric fracture management?

A

resuscitate, reduce, restrict/, rehabilitate

116
Q

when reducing the fractures, what must you also do?

A

assess neurovascular status (!!!!!)

= reduce secondary injury to soft tissue and neurovascular structures

117
Q

what is open reduction?

A

realignment of the fracture under direct visualisation

e.g. mini-incision, full exposure

118
Q

what is closed reduction?

A

realigning a fracture but without making an incision

e.g. traction, manipulation

119
Q

give examples of closed reduction in paediatrics

A

1) applying a plaster (A&E or MUA in theatre)

2) Gallows traction = skin traction applied to the femur to hold the long bones

120
Q

why do we restrict/hold fractures?

A

provides stability for the fracture to heal

121
Q

fracture holding can be fixation with metal or closed - which one is preferred in children and why?

A

remodeling and huge healing potential means that operative fixation (open holding) often can be avoided

= so tend to use plasters and splints to hold

122
Q

when may operative intervention/fixation be required to hold a fracture in children?

A

1) when the physis is compromised and there is an increased risk of growth arrest
2) fracture is beyond tolerance of remodelling

123
Q

what must happen in children if metal is used to fixate and hold the reduced fracture?

A

metalwork must be removed at a later date

124
Q

how does rehabilitation occur in children’s fractures?

A

use, move, strengthen, weight bear

physio not usually required

125
Q

what are the main differentials for a limping child?

A

1) septic arthritis (!!!!)

transient synovitis
perthes
SUFE

126
Q

what is septic arthritis?

A

presence of infection in intraarticular space

  • necrotic effect of proteases
  • pressure effect on the chondrocytes and cartilage due to oedema in the closed space

= irreversible, long-term damage in the joint

127
Q

how is septic arthritis treated?

A

surgical washout of the joint to clear the infection

128
Q

how is septic arthritis classified?

A 
Kocher's classification
- non-weight-bearing
- ESR > 40
- WBC > 12,000
- temperature > 38 (fever)
= NEWT

= more of the above features present, the more likely the diagnosis of septic arthritis is

129
Q

what are the key features of a septic arthritis history?

A

duration

other recent illness

associated joint pain & symptoms

130
Q

what in the history indicates septic arthritis in the child?

A

child was previously well BUT now, off food/drink

cannot move leg/hip

fever

= classic indicators of a septic arthritis kid

131
Q

what is the most likely diagnosis if not septic arthritis?

A

transient synovitis

diagnosis of exclusion

132
Q

what is transient synovitis?

A

inflammation of the joint in response to a systemic illness

= associated muscle pain

133
Q

how is transient synovitis treated?

A

supportive management

= fluids, antibiotics, observations

134
Q

what is Perthes disease and who does it affect the most?

A

idiopathic necrosis of the proximal femoral epiphysis

  • males > females
  • ages 4-8
135
Q

what must be excluded before diagnosing Perthes disease?

A

septic arthritis

136
Q

how is Perthes differentiated from septic arthritis?

A

Perthes

  • more chronic: goes on for longer
  • cannot see the temperature + inflammatory markers seen in septic arthritis
137
Q

what is the investigation of choice for Perthes disease?

A

plain film radiograph

138
Q

how is Perthes disease treated?

A

supportive treatment

referral to specialist for continuous observation and management

139
Q

what is SUFE?

A

slipped upper femoral epiphysis

= when the proximal epiphysis slips in relation to the metaphysis

140
Q

which group is affected most by SUFE?

A

obese adolescent male

12-13 year olds during rapid growth

141
Q

what are the risk factors for SUFE?

A

family history

endocrine underlying disorder (hypothyroidism, hypopituitarism)

overweight

male

142
Q

what must be excluded before diagnosing SUFE?

A

septic arthritis

143
Q

what are the classifications of SUFE?

A

acute

chronic

acute on chronic (history of limping in past but worse suddenly)

144
Q

how is SUFE treated?

A

operative internal fixation

1) to prevent further slippage
2) to minimise long term growth problems and reduce risk of growth arrest (as physis can be affected)

145
Q

how is SUFE differentiated from septic arthritis?

A

SUFE

  • not as acute as septic arthritis
  • cannot see the temperature + inflammatory markers seen in septic arthritis
146
Q

what is the main differential for a limping child?

A

SEPTIC ARTHRITIS (!)

= must be excluded before moving onto anything esle

147
Q

how are paediatric fractures described?

A 
P = pattern
P = pieces (simple/fragmented)
A = anatomy (where?)
I = intra/extraarticular
D = displacement, angulated, rotated, shortened
S = Salter-Harris

brs (phase 1b) (71 decks)

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