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BRS MUSCULOSKELETAL > 1b// Children's Orthopaedics > Flashcards

1b// Children's Orthopaedics Flashcards

1
Q

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

A

270

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2
Q

What are growth plates called, and what do they do?

A

physis

they are the areas from which long bone growth occurs postnatally

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3
Q

What are the types of bone development?

A

intramembranous mesenchymal cells» bone

endochondral mesenchymal» cartilage» bone

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4
Q

What type of bone do intramembranous mesenchymal cells lead to?

A

flat bones (cranial bones and clavicle)

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5
Q

What type of bone do endochondral mesenchymal cells make?

A

long bones (all other long bones)

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6
Q

What is the process called of making cranial bones and the clavicle?

A

intramembranous ossification

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7
Q

What is the process called of making all other long bones?

A

endochondral ossification

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8
Q

Describe the process 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 immature periosteum form
  4. then angiogenesis between woven bone and trabecular, forming bone marrow
  5. Compact bone develops superficial to cancellous bone. Crowded blood vessels condense into red bone marrow
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8
Q

Where does endochondral ossification occur?

A

both primary and secondary ossification centres

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8
Q

What are primary ossification centres? And what part of the bone are they located?

A

Sites of pre-natal bone growth through endochondral ossification from the central part of the bone

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9
Q

What are secondary ossification centres?

A

Occurs post-natal after the primary ossification centre and long bones often have several (the physis)

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10
Q

What are the 2 types of endochondral ossification?

A

primary and secondary

e.g., endochondral primary ossification

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11
Q

Describe the process of endochondral primary ossification.

A

pre-natal growth through primary ossification centres

a) Mesenchymal Differentiation at the primary centre

b) The cartilage model of the future bony skeleton forms

c) Capillaries (via angiogenesis) penetrate cartilage.
Calcification at the primary ossification centre – spongy bone forms
Perichondrium transforms into periosteum

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

e) Secondary ossification centres develop

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12
Q

Where are primary ossification centres?

A

middle of diaphysis (shaft of bone)

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13
Q

Where do secondary ossification centres develop? And how are they developed?

A

at proximal and distal ends of long bone with their own blood supply

blood supply calcifies the previously uncalcified matrix into immature spongy bone, so cartilage at ends of bone become sites of secondary ossification

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14
Q

What is endochondral secondary ossification for?

A

long bone lengthening

post bone growth through secondary ossification centres
“the physis”

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15
Q

Describe endochondral secondary ossification.
- where does it occur
- what zone and where
- what does it contain
- and sides

A

Happens at the physis (physeal plate)

Zone of elongation in long bone

Contains cartilage

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

Diaphyseal side – Cartilage calcifies and
dies and then replaced by bone

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16
Q

What are the epiphyseal and diaphyseal sides?

A

the diaphysis (shaft or primary ossification centre), metaphysis (where the bone flares), physis (or growth plate) and the epiphysis (secondary ossification centre).

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17
Q

Do these make sense?

A
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18
Q

How does a child’s skeleton differ to that of an adult? (4)

A

more elasticity

physis (constantly growing)

speed of healing is much faster (due to continuous growth)

remodelling potential

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19
Q

What does it mean by a child’s bone elasticity? And why is it more elastic?

A

Children’s bone can bend – more elastic than adult

due to increased density of haversian canals

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20
Q

What can increased density of haversian canals lead to? (3)

A

Plastic deformity:
– bends before breaks

Buckle fracture:
– Tarus like the column

Greenstick:
– like the tree
One cortex fractures but does not break the other side

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21
Q

Why do children have more haversian canals?

A

as their bones are more metabolically active

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22
Q

Describe growth of bones in children, e.g., where and speed? And when does growth stop?

A

Growth occurs at varying rates at varying sites

Growth stops as the physis closes

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23
When does physeal closure occur?
Complete at girls: 15-16 boys= 18-19
24
What does physeal closure depend on?
puberty menarche parental height gradual physeal closure
25
How are physeal injuries categorised?
salter-harris
26
What can physeal injuries lead to? And what can that lead to?
growth arrest leads to deformity
27
What is the speed of remodelling and healing dependent on?
The speed of healing and remodeling potential is dependent on the location and the age of the patient
28
Who heals bones more quickly in the general population?
younger child
29
Which physis grows the most?
at the knee and at the extreme of upper limb
30
What the stages of healing/ remodelling? (3)
inflammation repair/ callus remodelling
31
What are common children's congenital conditions (that you need to know)? (4)
Developmental Dysplasia of the Hip Club Foot Achondroplasia Osteogenesis Imperfecta
32
What is developmental dysplasia of the hip? And what type of disorder is it?
Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum. A ‘Packaging Disorder’
33
What is a packaging disorder?
occurs in utero, due to the way a child sits
34
What is the normal development of the hip dependent on?
the concentric reduction and balanced forces through the hip
35
What is the spectrum of developmental dysplasia of the hip? (3)
dysplasia or subluxation or dislocation Dysplasia 2: 100 Dislocation 2:1000
36
What are risk factors for developmental dysplasia of the hip? (6)
Female 6:1 First born Breech FHx Oligohydramnios Native American/Laplanders – swaddling of hip
37
How is developmental dysplasia of the hip examined?
Usually picked up on baby check – screening in UK Range of motion of hip - Usually limitation in hip abduction - Leg length (Galeazzi) In those 3 months or older Barlow and Ortalani are non-sensitive
38
What are the investigations for developmental dysplasia of the hip?
Ultrasound – birth to 4 months - After 4 months X-ray - If prior to 6 weeks needs to be age adjusted Measures the acetabular dysplasia and the position of hip
39
What is the treatment for developmental dysplasia of the hip?
Reducible hip and <6 months - Pavlik harness 92% effective Failed Pavlik Harness or 6-18 months - Secondary changes- capsule + soft tissue - MUA (manipulation under anaesthetic) + Closed reduction and Spica
40
What is clubfoot?
Congenital deformity of the foot packaging disorder
41
What is the epidemiology of clubfoot?
1:1000 Highest in Hawaiians M2:1F 50% are bilateral
42
What is the risk factor of clubfoot?
Genetic... Approx. 5% likely of siblings Familial in 25% PITX1 gene CAVE
43
What causes CAVE deformity?
due to muscle contracture
44
What is CAVE deformity?
deformity of Clubfoot Cavus –high arch: tight intrinsic, FHL, FDL Adductus of foot: Tight tib post and ant Varus: Tight tendoachillies, tib post, tib ant Equinous: tight tendoachilles
45
What is the treatment for clubfoot?
Ponseti Method Gold standard 1. First a series of casts to correct deformity 2. Many require operative treatment - Soft tissue releases or tendon transfers (more extreme is tendon) 3. Foot orthosis brace 4. Some will require further operative intervention to correct final deformity.
46
What is achondroplasia?
The most common skeletal dysplasia
47
What is the pathophysiology of achondroplasia?
Autosomal Dominant - G380 mutation of FGFR3 - inhibition of chondrocyte proliferation in the proliferative zone of the physis - results in defect in endochondral bone formation affects secondary ossification
48
What does achondroplasia lead to?
rhizomelic dwarfism
49
What is a part rhizomelic dwarfism?
Humerus shorter than forearm Femur shorter than tibia Normal trunk Adult height of approx.125cm Normal cognitive development Significant spinal issues
50
What is osteogenesis imperfecta?
brittle bone disease decreased type 1 collagen
51
Why is there decreased collagen in osteogenesis imperfecta? And what does that lead to?
Decreased Type I Collagen due to: - Decreased secretion - Production of abnormal collagen leading to insufficient osteoid production
52
How do you get osteogenesis imperfecta?
hereditary- autosomal dominant or recessive
53
What are the manifestations of osteogenesis imperfecta on bones? (3)
Fragility fractures Short stature Scoliosis
54
What are the non-orthopaedic manifestations of osteogenesis imperfecta? (5)
Heart Blue Sclera Dentinogenesis imperfecta – brown soft teeth Wormian skull Hypermetabolism
55
What is wormian skull?
abnormal fusion of cranial sutures
56
What should you consider with paediatric fractures? (5)
Pattern Anatomy Intra/Extra-articular Displacement Salter-Harris
57
What does the pattern of the fracture reflect?
reflects the way the energy is dissipated
58
What are the types of patterns in fracture?
comminuted= high E, more than 1 part fractured
59
What should you consider with anatomy and fractures?
where on the bone the fracture is
60
What are the 2 methods of bone healing?
primary and secondary bone healing
61
Which method of healing is prefered for intra-articular fractures?
primary bone healing is the preferred healing pathway in intra-articular fracture as minimises risk of post traumatic arthritis
62
What is primary bone healing?
heals by direct union no callus formation
63
What is secondary bone healing?
bone healing by callus *but remember... - if the fracture affects the physis it affects growth
64
What are the steps of secondary bone healing?
1. haematoma formation 2. fibrocartilaginous callus formation 3. bony callus formation 4. bone remodelling
65
What are the types of displacements in fractures? (4)
*remodelling potential gives more allowance for displacement for children *rotated is not well tolerated *can be multiple at the same time
66
How are physeal injuries classified?
Salter Harris
67
How does Salter Harris classify physeal injuries?
Classification of physeal injuries (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 Risk of growth arrest increases from 1 -5
68
Which type of physeal injury is most common and least common?
2 most common 5 least common
69
What do injuries to the physis possibly lead to?
growth arrest
70
What is key in growth arrest>
the location and timing how much potential growth is affects diff parts of the skeleton grow at diff rates
71
What are the types of physeal injuries? (2)
Whole physis – limb length discrepancy Partial – angulation as the non affected side keeps growing
72
What are the aims of treatment for growth arrest?
Aim is to correct the deformity Minimise angular deformity Minimise limb length difference
73
How can you treat limb length?
shorten the longer side or lengthen the shorter side
74
How can you treat angular deformity?
stop the growth of the unaffected side or reform the bone (osteotomy)
75
What are the 4 Rs for fracture management?
Resuscitate Reduce Restrict Rehabilitate
76
What does it mean by reduce, for fracture management?
Correct the deformity and displacement Reduce secondary injury to soft tissue / NV structures
77
What are the 2 types of reduction?
closed and open
78
What is a closed reduction?
Reducing a fracture without making an incision Such as traction and manipulation in A&E
79
What is an open reduction?
Making an incision The realignment of the fracture under direct visualisation
80
Give an example of closed reduction.
gallows traction - commonly used for long bone fractures holding the skin, the long bones of the lower limb can be reduced
81
What is restriction for?
Maintain the fracture reduction Provides the stability for the fracture to heal
82
What do children rarely have issues with when it comes to bone fractures? And what can they have issues with?
with bone not healing - however can have issues with too much healing
83
What are the 2 broad categories of restriction?
external and internal
84
What are examples of external and internal restriction? (2 each)
85
What type of restriction is commonly used in paeds? And why?
external plasters and splints Remodeling and huge healing potential means that operative internal fixation often can be avoided
86
What do you do when operative intervention may be required for restriction?
87
Do you have to rehabilitate children?
Children generally rehabilitate very quickly Play is a great rehabilitator Stiffness not as major issue as in adults Use it, Move it and Strengthen!
88
Is operation more or less likely in children?
less as children have quicker healing
89
What are causes of the limping child? (4)
Septic Arthritis Transient Synovitis Perthes SUFE
90
What is septic arthritis? And what is so important about it?
presence of infection in intra-articular space child orthopaedic emergency - can cause irreversible long term problems in the joint (therefore needs surgical washing of the joint to clear the infection)
91
What is the score used to find out the probability of a child having septic arthritis, and what is in it?
Kocher’s classification - Non weight bearing - ESR >40 - WBC >12,000 - Temperature >38
92
What is the diagnosis if septic arthritis has been excluded?
Transient synovitis is a diagnosis once septic arthritis has been excluded Is a inflamed joint in response to a systemic illness Supportive treatment with antibiotics is the treatment
93
What is key in septic arthritis? (3)
the history... - duration - other recent illness - associated joint pain
94
What is Perthes disease?
Idiopathic necrosis of the proximal femoral epiphysis
95
With who is perthes disease most common?
usually in those 4-8 male 4:1
96
What must be done before diagnosis of Perthes and what is the treatment?
Septic arthritis needs to be excluded first Treatment is usually supportive in the first instance - once diagnosed they are referred to a specialist
97
What would you not expect to see in Perthes, that you would see in septic arthritis?
raised temp and inflamm markers
98
What is SUFE?
Slipped upper femoral epiphysis The proximal epiphysis slips in relation to the metaphysis
99
In who is SUFE most common in?
Usually obese adolescent male - 12-13 years old during rapid growth
100
What is the treatment for SUFE?
Treatment is operative fixation to prevent further slip and minimise long term growth problems - Septic arthritis needs to be excluded first

BRS MUSCULOSKELETAL (12 decks)

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