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Musculoskeletal > Paediatric Orthopaedics > Flashcards

Paediatric Orthopaedics Flashcards

1
Q

what is the colloquial name for Osteogenesis Imperfecta?

A

brittle bone disease

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2
Q

what is osteogenesis imperfecta a defect of?

A

a defect of the maturation and organisation of type 1 collagen

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3
Q

what type of collagen accounts for most of the organic composition of bone?

A

type 1 collagen

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4
Q

what type of inheritance are the majority of osteogenesis imperfect cases?

A

autosomal dominant

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5
Q

what are the 4 main clinical signs/symptoms of autosomal dominant osteogenesis imperfecta?

A
  • multiple fragility fractures of childhood
  • short stature with multiple deformities
  • blue sclerae
  • loss of hearing
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6
Q

rarer cases of osteogenesis imperfecta are aurosomal recessive, how do these present?

A

either fatal in perinatal period
or
associated with spinal deformity

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7
Q

how do fractures tend to heal in a patient with osteogenesis imperfecta?

A

heal with abundant but poor quality callus

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8
Q

how are fractures in patients with osteogenesis imperfecta treated?

A

with splintage, traction or surgical stabilisation

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9
Q

what is the medical term for short stature?

A

skeletal dysplasia

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10
Q

what is skeletal dysplasia caused by?

A

abnormal development of bone and connective tissue

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11
Q

is skeletal dysplasia hereditary?

A

can be

can also be a sporadic mutation

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12
Q

what is a proportionate short stature compared to a disproportionate short stature?

A

proportionate: limbs and spine proportionally short
disproportionate: limbs proportionally shorter/longer than spine

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13
Q

what is the commonest type of skeletal dysplasia?

A

achondroplasia

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14
Q

what type of inheritance is achondroplasia?

A

can be autosomal dominant but most cases are sporadic

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15
Q

what are the 5 key features of achondroplasia?

A 
disproportionately short limbs (proximal limbs are short- rhizomelic disproportion)
prominent forehead
widened nose
lax joints
mental development is normal
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16
Q

what are congenital connective tissue disorders?

A

genetic disorders of mainly type 1 collagen synthesis found in bones, tendons and ligaments

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17
Q

what is the difference between osteogenesis imperfecta and connective tissue disorders in terms of what collagen is affected?

A

osteogenesis imperfecta- type 1 collagen of the bones affected

coonnective tissue disorders- soft tissues more than bone

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18
Q

what is the medical term for ‘double jointed’? (ie when a person has hypermobility of joints)

A

generalised (familial) joint laxity

[connective tissue disorder]

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19
Q

how is generalised (familial) joint laxity usually inherited?

A

autosomal dominant

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20
Q

what are people with generalised (familial) joint laxity more prone to?

A

soft tissue injuries (esp ankle sprains) and recurrent dislocations (esp shoulder and patella)

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21
Q

what type of inheritance is Marfan’s synrome? [connective tissue disorder]

A

autosomal dominant or sporadic

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22
Q

what gene is mutated in marfan’s syndrome?

A

fibrillin gene

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23
Q

what are the 3 main features of a patient with Marfan’s syndrome?

A

tall stature
disproportionately long limbs
ligamentous laxity

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24
Q

what are the 7 main associated features of Marfan’s syndrome? (ie on top of: tall stature, long limbs and laxity)

A
  • high arched palate
  • scoliosis
  • flattening of the chest (pectus excavatum)
  • eye problems
  • aortic aneurysm
  • cardiac valve incompetence
  • pneumothorax
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25
Q

what type of inheritance is Ehlers-Danlos syndrome? [connective tissue disorder]

A

often autosomal dominant

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26
Q

what macrostructures are abnormally formed in ehlers-danlos syndrome?

A

abnormal elastin and collagen formation

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27
Q

what are the 4 main features of ehlers-danlos syndrome?

A
  • joint hypermobility
  • vascular fragility (easy bruising)
  • joint instability
  • scoliosis
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28
Q

why can skin healing be poor in a patient with ehlers-danlos syndrome?

A

abnormal collagen and elastni causes stretched scars or wound dehiscence

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29
Q

what defect is involved in duchenne muscular dystrophy?

A

defect in dystrophin gene (involved in calcium transport)

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30
Q

when does death occur typically in duchenne muscular dystrophy?

A

early 20s

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31
Q

how is diagnosis of duchenne muscular dystophy confirmed?

A

raised serum creatinine phosphokinase

abnormalities on muscle biopsy

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32
Q

where is the growth plate of bones?

A

physis

-just above metaphysis (neck)

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33
Q

where does primary ossification occur and why?

A

occurs in diaphysis because this is where the blood supply first develops

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34
Q

where does secondary ossification occur and why?

A

occurs in the epiphysis

because a second blood supply starts to develop within the head

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35
Q

how do embryonic bones start off? (ie what are they made of?)

A

purely cartilage

-no ossification at all

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36
Q

compare the periosteum in children to adults?

A

children’s periosteum is very thick, becomes thinner in adults

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37
Q

why are children prone to get septic arthritis?

A

because the blood supply is quite sluggish in the blood vessels at the growth plate

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38
Q

what is the Heuter-Volkmann law?

A

the rate of the growth of a bone will be affected by pressures on it’s axis:
increased pressure inhibits growth, decreased pressure accelerates growth

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39
Q

what will fractures do to the growth of a bone?

A

stimulate growth

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40
Q

what will an increased blood supply do to a bone?

A

stimulate growth

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41
Q

what type of gait do children have?

A

broad-based gait

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42
Q

why do children have a broad-based gait?

A

legs are wider apart for increased support

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43
Q

at what age is an adult gait pattern established?

A

about 8 years old

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44
Q

when are flat feet abnormal?

A

when they are stiff or painful

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45
Q

what arch is lost in flat feet?

A

medial longitudinal arch

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46
Q

what tendon appears to be tight in flat-footed patients?

A

tight achilles tendon

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47
Q

what 2 muscles form the achilles tendon?

A

gastrocnemius and soleus tendons

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48
Q

what is normal median longitudinal arch development?

A

arch becomes increasingly developed as age increases (until after 30’s where foot becomes more flat again)

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49
Q

what are the 3 main causes of in-toeing?

A
  • femoral neck anteversion

- internal tibial torsion]- metatarsus adductus

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50
Q

what is femoral neck anteversion?

A

femoral neck is pointed forwards

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51
Q

what is internal tibial torsion?

A

inwards twisting of the tibia (knee cap in normal position)

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52
Q

what is metatarsus adductus?

A

front half of foot twisted inwards

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53
Q

what is the natural history of femoral neck anteversion, internal tibial torsion or metatarsus adductus?

A

usually all resolve with time

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54
Q

how do you assess a child for femoral neck anteversion?

A

get child to lie prone with knees flexed

check both internal and external rotation and note angles

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55
Q

when does femoral neck anteversion usually present?

A

after the age of 4

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56
Q

by what age should femoral neck anteversion have improved by?

A

age 12

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57
Q

when does internal tibial torsion usually present?

A

before the age of 4

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58
Q

how do you asses a child for metatarsus adductus?

A

draw a line between heel and mid foot- see which toes the line exits between

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59
Q

what are the benefits of slight in-toeing?

A

able to run faster

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60
Q

what tibial deformity causes infantile bow legs?

A

medial tibial torsion

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61
Q

when are bow legs normal?

A

below 2 years: normal

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62
Q

if a patient has bow legs after 2 years what should you consider?

A

skeletal dysplasia

-check if patient’s height is below 2nd standard deviation

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63
Q

when should you refer a patient with bow legs?

A

if:

  • assymetrical
  • not resolving (ie older than 2 years)
  • painful
  • height
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64
Q

when do knock knees usually peak?

A

3.5 years old

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65
Q

when do you refer for knock knees?

A
  • if asymmetrical

- if inter-malleolar distance is >8cm (when knees are together) at 11 years

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66
Q

the impingement of what nerve is most associated with adolescent anterior knee pain localised to the patella?

A

obturator nerve impingement at hip joint

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67
Q

what is clubfoot? (CTEV)

A

a congenital deformity of the foot where the foot is plantar-flexed and the forefoot is supinated and has a varus alignment
(stiff in thie position)

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68
Q

who is clubfoot common in-boys or girls?

A

boys

69
Q

what is more likely- unilateral or bilateral clubfoot?

A

50% either way

70
Q

what is postural talipes?

A

a congenital foot deformity which looks like clubfoot but foot easily doorsiflexes

71
Q

what is the treatment of postural talipes?

A

physiotherapy and stretching

72
Q

what is the natural history of club foot?

A

doesn’t improve

gets worse

73
Q

what is the treatment of club foot?

A

Ponseti splintage ASAP
plaster cast
+ boots and bar (23 hours per day for 3 months then nightly wearing until age of 4)
[most children also require a tenotomy of the achilles tendon]

74
Q

what is rocker bottom feet?

A

a congenital deformity of the foot where the foot appears externally rotated, very prominent calcaneus

(mirror opposite of club foot)

75
Q

what is cerebral palsy caused by?

A

an insult to the growing brain

ie an injury to the brain which occured before myelination

76
Q

what is spasticity?

A

abnormal rate-dependant increase in muscle tone/stiffness

antagonistic mechanisms can fail

77
Q

what are the 3 treatment options of spasticity?

A
  1. muscle relaxers (eg benzodiazepines, baclofen)
  2. botulinum toxin (paralyses muscle plates)
  3. selective dorsal rhizotomy
78
Q

what are the 3 types of gait problems in cerebral palsy?

A
  1. primary
  2. secondary
  3. tertiary
79
Q

what are primary gait problems in cerebral palsy?

A

gait problems directly due to the initial CNS injury

ie loss of selective muscle control/loss balance mechanisms/abnormal tone

80
Q

what are secondary gait problems in cerebral palsy?

A

gait problems indirectly due to the initial CNS injury- result from growth abnormalities
(ie scoliosis, hip sublaxation, torsion)

81
Q

what are the tertiary gait problems in cerebral palsy?

A

gait problems due to the coping response of the patient to the muscle abnormalities and the growth abnormalities

82
Q

the GMFCS (gross motor function classification system) is used to classify the degree of cerebral palsy, what does a higher GMFCS score mean?

A

higher risk of dislocation

83
Q

what can cerebral palsy patients with a GMFCS score of 1-3 do that patients with a GMFCS score of 4+ not do?

A

walk

84
Q

are cavus feet normal or pathological?

A

usually pathological

85
Q

what type of disorder is cerebral palsy?

A

neuromuscular disorder

86
Q

when is the onset of cerebral palsy?

A

before 2-3 years of age

87
Q

what are the 7 main causes of cerebral palsy?

A
  • genetic problems
  • brain malformation
  • hypoxia during birth
  • intrauterine infection in early pregancny
  • prematurity
  • intra-cranial haemoorhage
  • meningitis
88
Q

what are the 3 main causes of brachial plexus injury during vaginal delivery?

A
  • large babies
  • twin deliveries
  • shoulder dystocia
89
Q

what is shoulder dystocia?

A

difficult delivery of the shoulder after the head with compression of the shoulder on the pubic symphysis

90
Q

what is the commonest type of obstetric brachial plexus palsy?

A

Erb’s palsy

91
Q

what nerve roots are damaged in Erb’s palsy?

A

C5, C6

92
Q

In Erb’s palsy, what muscles lose their motor innervation?

A
  • deltoid
  • supraspinatous
  • infraspinarous
  • biceps
  • brachialis
93
Q

why is physiotherapy required in Erb’s palsy fairly early on?

A

to prevent contractures

94
Q

what is prognosis of Erb’s palsy predicted by?

A

the return of bicpes function within 6 months

95
Q

if there is no recovery of motor innervation, what is the treatment of Erb’s palsy?

A

surgical release of contractures

tendon transfers

96
Q

what nerve roots are damaged in Klumpske’s palsy?

A

C8 and T1

97
Q

what is Klumpske’s palsy (obstetric brachial plexus palsy) caused by?

A

foreceful adduction

98
Q

In Klumpske’s palsy, what muscles lose their motor innervation?

A

intrinsic hand mucles

+/- fingers, wrist flexors

99
Q

why might a patient with Klumpske’s palsy also have Horner’s syndrome?

A

due to disruption of the first sympathetic ganglion from T1

100
Q

In Klumpske’s palsy what position are the fingers typically in?

A

flexed

101
Q

which palsy has a better prognosis: Erb’s palsy or Klumpske’s palsy?
(ie more likely to recover motor function)

A

Erb’s palsy

102
Q

what is the natural progression of knee aligment in a child?

A

at birth, children have varus knees (bow legs) which become neutrally aligned at 14 months.
This progresses to valgus (knock knees) at 3 years and then slowly regresses

103
Q

what is in-toeing?

A

a child who, when walking or standing, have feet that point towards the midline

104
Q

why as age develops does the median longitudinal arch develop?

A

due to muscles developing

105
Q

what is flexible flat footedness related to?

A

ligamentous laxity

106
Q

what is the underlying bony abnormality that causes rigid flat footedness?

A

tarsal coalition

bones of the hindfoot connected by an abnormal bony or cartilaginous connection

107
Q

what is developmental dysplasia of the hip?

A

disclocation or sublaxation of the femoral head during the perinatal period
-this affects the subsequent development of the hip joint

108
Q

who more commonly gets developmental dysplasia of the hip- girls or boys?

A

girls

109
Q

which hip is more likely to be involved in developmental dysplasia of the hip?

A

left hip

110
Q

what are the 5 main risk factors for developmental dysplasia of the hip?

A
  • family history
  • breech presentation
  • first born babies
  • down’syndrome
  • other congenital disorders
111
Q

what happens to developmental dysplasia of the hip if left untreated?

A

acetabulum becomes very shallow,

in severe ases a false acetabulum occurs superior to the original one creating a shorter lower limb

112
Q

what 2 manoeuvres test the presence of developmental dysplasia of the hip?

A

ortolani’s test

barlow’s test

113
Q

what is ortolani’s test?

A

tests the presence of a dislocated hip by reducing the hip with abduction and anterior displacement
-if positive, a click/clunk noise should be made

114
Q

what is barlow’s test?

A

tests the presence of a dislocatable hip with flexion and posterior displacement
-if positive a click/clunk noise should be made

115
Q

what are the 3 main signs of developmental dysplasia of the hip?

A
  • shortening of limb
  • asymmetric groin/thigh creases
  • click/clunk with Ortolani or Barlow manoeuvres
116
Q

what is the investigation of choice for a suspected developmental dysplasia of the hip in a child below 4-6 months?

A

ultrasound

117
Q

what is the investigation of choice for a suspected developmental dysplasia of the hip in a child above 4-6 months?

A

x-ray

118
Q

why can x-rays not be used in the early diagnosis of developmental dysplasia of the hip?

A

femoral head is unossified

119
Q

how are mild cases of developmental dysplasia treated? (ie slightly shallow acetabulum, midly dislocatable but reduced hip)

A

close observation with serial examination and ultrasound to ensure hip remains reduced

120
Q

how are servere cases of developmental dysplasia treated? (ie dislocated or persistenly unstable hips)

A

reduced and held with a special harness (Pavlik harness)

121
Q

what position does a Pavlik harness keep the child in?

A

a comfortable flexion and abduction of the thighs

122
Q

what can over-flexing and abducting the hip causes?

A

avascular necrosis

123
Q

how are children with developmental dysplasia of the hip with persistent dislocation (even after Pavlik harness use) treated?

A

open reduction + osteotomy to shorten/rotate femur and deepen/re-orientate the acetabulum

124
Q

what is the most common cause of hip pain in childhood?

A

transient synovitis

125
Q

what is transient synovitis?

A

a self-limiting inflammation of the synovium of a joint

126
Q

what is the most common joint to get transient synovitis?

A

hip joint

127
Q

what does transient synovitis commonly occur shortly after?

A

an upper respiratory tract infection (usually viral)

128
Q

who tends to get transient synovitis?

A

boys between 2-10

girls are more rarealy affected

129
Q

what is Perthes disease?

A

a childhood disorder in which the blood supply to the femur head is transiently inadequate resulting in avascular necrosis and subsequent abnormal growth or collapse

130
Q

how do you exclude perthes disease when suspecting transient synovitis?

A

X-ray

131
Q

how do you exclude septic arthritis when suspecting transient synovitis?

A 
clinical picture (less pain and bigger R.O.M than septic arthritis)
lower CRP than septic arthritis
132
Q

what is the treatment of transient synovitis?

A

NSAIDs and rest

133
Q

what should be done if there is no resolution of suspected transient synovits within a few weeks?

A

look for another cause for the hip pain

134
Q

who tends to get Perthes disease?

A

boys aged 4-9

especially of short stature who are very active

135
Q

what 2 main factors determine the prognosis of subsequent remodelling of the femoral head in a child with Perthes disease?

A
  • age of onset (younger = better prognosis)

- amount of femoral head collapse

136
Q

how do children affected with transient synovitis of the hip present?

A

limp and reluctance to weight bear on affected side

137
Q

how do children with Perthes disease present?

A

pain and limp

138
Q

what is the first clinical sign of Perthes disease and how does this progress?

A

first sign- loss of internal rotation
followed by loss of abduction
followed by positive trendellenburgs test

139
Q

most cases of Perthes disease are unilateral, in a patient with bilateral disease what should you consider?

A

possible underlying skeletal dysplasia or thrombophilia

140
Q

what is the treatment of Perthes disease?

A

regular x-ray observation
avoidance of physical activity

occasionally osteotomy of femur or acetabulum if femoral head has subluxed

141
Q

who tends to get a slipped upper femoral epiphysis?

A

overweight pre-pubertal boys

142
Q

what 2 conditions may predispose to a slipped upper femoral epiphysis?

A

hypothyroidism

renal disease

143
Q

what is a slipped upper femoral epiphysis?

A

femoral head epiphysis slips inferiorly in relation to the femoral neck

144
Q

what are the types of slipped upper femoral epiphysis?

A

acute
chronic
acute on chronic

145
Q

where can pain be felt in a slipped upper femoral epiphysis?

A

pain in groin

pain in knee (might present purely as this)

146
Q

what is the predominant clinical sign of loss of slipped upper femoral epiphysis?

A

loss of internal rotations

147
Q

why must a lateral view x-ray of a suspected slipped upper femoral epiphysis be obtained?

A

to detect mild degrees of slip

148
Q

what is the treatment of slipped upper femoral epiphysis?

A

urgent surgery to pin the femoral head to prevent further slippage

149
Q

what is jumper’s knee?

A

patellar tendonitis

150
Q

what is the treatment for patellar tendonitis?

A

self-limiting

requires rest and possibly physiotherapy

151
Q

why is knee extensor mechanism pain fairly common in adolescence?

A

body weight increases

sporting activities increase

152
Q

who tends to get adolescnet nterior knee pain-M or F? (patellofemoral dysfunction)

A

girls

153
Q

what are the subtle skeletal predispositions to patellofemoral dysfunction- adolescent anterior knee pain?

A

genu valgum
wide hips
femoral neck anteversion

154
Q

what is chondromalacia?

A

softening of the hyaline cartilage of the patella

155
Q

in adolescent anterior knee pain what might have happened to the hyaline cartilage of the patella?

A

chondromalacia patellae

(softening of the patellar hyaline cartilage

156
Q

what is the treatment of adolescent anterior knee pain?

A

self-limiting
physiotherapy to rebalance msucles

resistant cases may require surgery to shift forces on patella (tibial tubercle transfer)

157
Q

what joints are affected in clubfoot? (CTEV)

A

joints between talus, calcaneus and navicular

158
Q

what are the 5 main risk factors for clubfoot?

A
  • family history
  • breech presentation
  • oligohydramnios (low amniotic fluid content)
  • skeletal dysplasia
  • male
159
Q

what are mobile/flexible flat feet?

A

medial arch reforms with dorsiflexion of great toe

160
Q

what are rigid flat feet?

A

arch remains flat regardless of load or great toe dorsiflexion

161
Q

if a flat foot is described as rigid, what is the most possible cause of the flat foot?

A

tarsal coalition

162
Q

in children with painful scoliosis, what urgent investigation should be done?

A

MRI

163
Q

how many cases of slipped upper femoral epiphysis are bilatera?

A

1/2

164
Q

if a flat foot is described as dynamic (ie present when the foot is weight-bearing only) what is the most possible cause?

A

underlying ligamentous taxity

165
Q

what pain may a SUFE solely present with?

A

pain in the knee

166
Q

what is a greenstick fracture?

A

a fracture where one side breaks and the other side only bends

167
Q

what is a torus fracture?

A

an incomplete fracture characterised by bulging of the cortex

also known as a buckle fracture

168
Q

what is plastic deformation?

A

when an incomplete fracture (ie greenstick fracture) bends and remains in this bowed position instead of returning to normal position

Musculoskeletal (16 decks)

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