children's orthopaedics Flashcards
1
Q
how many bones do children have?
A
More than adults
270
2
Q
what is the physis?
A
growth plates
areas which long bone growth happens post-natally
3
Q
how many physis are there?
A
2 per long bone
4
Q
how does bone development occur?
A
intramembranous or endochondral
5
Q
what does intramembranous development form?
A
mesenchymal cells to bone
flat bones (cranial & clavicle)
6
Q
what does endochondral bone development form?
A
mesenchymal cells -> cartilage -> bone
long bones
7
Q
what is the difference between intramembranous and endochondral ossification
A
intramembranous produces flat bones straight from mesenchymal cells
endochondral produces long bones from mesenchymal cels via cartilage first
8
Q
what is intramembranous ossification responsible for?
A
Formation cranial bones and clavicle
9
Q
how does intramembranous ossification occur?
A
- Condensation of mesenchymal cells which differentiate into preosteoblasts -> osteoblasts
- Ossification centre forms
- These cells synthesise and secrete osteoid
- Secreted osteoid traps osteoblasts which become osteocytes
- These cells collectively create the immature woven trabecular matrix and immature periosteum
- Angiogenesis occurs and blood vessels incorporated between the woven bone trabeculae will form the future bone marrow
- Immature woven Bone is remodelled and replaced by mature lamellae bone
10
Q
what is endochondral ossification responsible for?
A
all other long bone formation (tissue that will become bone formed from cartilage)
11
Q
where does endochondral ossification take place?
A
primary and secondary ossification centres
12
Q
what are primary ossification centres?
A
sites of pre-natal bone growth through endochondral ossification from the central part of the bone (diaphysis)
13
Q
what are secondary ossification centers?
A
occurs post natally after the primary ossification centre
long bones have several 2nd ossification centres (the physis)
14
Q
how does primary ossification develop?
A
- Mesenchymal differentiation at the primary centres
- Develop a cartilage model of the future bony skeleton
- Capillaries penetrate cartilage
- Calcification at the primary ossification centres- spongy bone forms from diaphysis
- Perichondrium transforms into pericardium
- Cartilage and chondrocytes continue to grow at ends of the bone
- Secondary ossification centres develop (at proximal and distal ends) with own blood vessels and calcification at the proximal and distal end- calcification of the matrix
- Cartilage remains at the epiphyseal (growth) plate and at joint surface as articular cartilage
15
Q
where does secondary ossification happen?
A
the physis (physeal plate)
16
Q
how does secondary ossification occur?
A
- Post bone growth through secondary ossification centres (the physis)
- By time fetal skeleton is fully formed and in the children’s skeleton, cartilage remains at the joint surface as articular cartilage and between diaphysis and epiphysis as the epiphysial plate (physis)
- these physis are responsible for the further growth of bones ‘secondary ossification sites;
- Again happens through proliferation of chondrocytes and the subsequent calcification of ECM into immature bone that is subsequently remodelled
- The physis is responsible for the skeletal growth of a child
17
Q
what are the zones of the epiphyseal plate?
A
reserve zone
proliferative zone
mutation and hypertrophy
calcified matrix
zone of ossification
18
Q
what is the difference between child and adult skeleton?
A
- More elastic
- Presence of physis
- Increased speed on healing due to continued growth
- Increased remodelling potential (amount of deformity that can be corrected)
19
Q
what are the elastic properties of child bone?
A
can bend more- more elastic than adult
due to increased density in Haversian canals
plastic deformity- bends before it breaks
20
Q
what are the effects of Haversian canals?
A
canals that circulate blood supply
increased as bone more metabolically active
allow greater elasticity
21
Q
what fractures can occur due to elasticity of bone in children?
A
buckle fracture- bends in on itself causing Taurus like column
green stick fracture- one cortex fracture but does not break the other side
22
Q
why does growth stop in bone?
A
growth occurs at varying rates at various sites
growth stops when the physis closes
23
Q
what are the causes of physis closure?
A
gradual physical closure
puberty, menarche
parental height
24
Q
what is the completion age of physis closure?
A
girls- 15-16
boys 18-19
25
how are physeal injuries categorized?
by Salter-Harris
26
what are the effects of pyseal injuries?
growth arrest= deformity (one part bone continue to grow while another stopped)
27
what are speed and remodelling dependant on?
location and age of patient
younger child heals more quickly
children can handle more angulation and deformity than an adult and return to normal quicker
28
where does physis greater growth occur?
extremes of upper limb and centra of knee
29
what are common children's congenital conditions?
developmental dysplasia of the hip
club foot
achondroplasia
osteogenesis imperfecta
30
what is developmental dysplasia of the hip?
group of disorders of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
packaging disorder- occurs in utero due to way child sits
normal development relies on he concentric reduction and balanced forces through the hip
31
what is the spectrum for developmental dysplasia of the hip?
dysplasia (hip in socket but not centrally placed)
subluxation (hip in socket but comes in and out)
dislocation (hip develops outside socket, acetabulum has shallow cup as not used to joint)
32
what are the risk factors for developmental dysplasia of the hip?
* female
* first born
* breech
* family history
* oligohydramnios (not enough fluid)
* native American/ Laplanders (swaddling of hip)
* rare in african American and Asian population
33
when is developmental dysplasia of the hip usually picked up?
back check- screening in UK
RoM of hip- usually limitation in hip abduction, leg length (Galeazzi)
in those greater than 3 months barlow and artalani are non-sensitive
34
how is developmental dysplasia of the hip monitored?
ultrasound-birth to 4 months (after 4 month XR)- if prior to 6 weeks needs to be age adjusted
measure acetabular dysfunction and hip position
35
what is the treatment for dysfunctional dysplasia of the hip?
* reducible hi and \<6 months
* Pavlik harness 92% effective
* failed Pavlik harness or 6-18 months
* secondary changes in capsule and soft tissue as progressive condition
* MUA and closed reduction and spica
36
what is clubfoot?
congenital talipes equinovirus
congenital deformity of the foot
occurs in utero
deformity usually bilateral (50%)
37
what is the genetic basis of clubfoot?
highest in male and Hawaiins
5% likely of siblings
familial in 24%
PITX1 gene involvement
38
what deformity occurs in cubfoot?
CAVE- due to muscle contraction
**Cavus**- high arch: tight intrinsic, FHL, FDL
**Adductus** of the foot: tight tib post and ant
**Varus**: tight tendoachillies, tib post and ant
**Equinous:** tight tendoachilles
39
when is clubfoot diagnosed?
baby check when baby first born
40
what is the treatment for clubfoot?
gold standard= ponseti method
first series of casts to correct deformity
many require operative treatment- soft tissue release
foot orthosis brace
some will require further operative intervention to correct final deformity- further soft tissue releases, tendon transfers if severe
41
what is achondroplasia?
more common skeletal deformity
autosomal dominant
can cause rhizomelic dwarfism
42
what is the genetic basis of achondroplasia?
autosomal dominant
G380 mutation of GFGR3
inhibition of chondrocyte proliferation in the proliferative zone of the physis
results in defect in endochondral bone formation and affects secondary endochondral ossification
43
what is rhizomelic dwarfism?
humerus shorter than forearm
femur shorter than tibia
normal trunk
adult height approx 125cm
normal cognitive development
significant spinal issues
44
what is oseogenesis inperfecta?
brittle bone disease
hereditary- autosomal dominant or recessive
decreased type 1 collagen
insufficient osteoid production
45
what are the causes of decreased type 1 collagen in osteogenesis imperfecta?
quantitative or qualitative issue
decreased secretion
production of abnormal colagen
46
what are the effects of osteogenesis imperfecta?
* Fragility fractures
* Short stature
* Scoliosis
* Non-orthopedic manifestations
* Heart
* Blue Sclera (eyes)
* Dentinogenesis imperfecta – brown soft teeth
* Wormian skull
* Hypermetabolism
47
what are the principles of fracture description?
* Pattern
* Anatomy
* Intra/extra-articular
* Displacement
* If effects physis used salter-harris classification
48
what are the possible patterns of bone fracture?
* Depends on the way the energy is dissipated
* Transverse
* Oblique
* Spiral- rotation torque
* Comminuted- more than one part due to high energy injuries
* Avulsion- bone pulled off by ligament attachment
49
what are the possible anatomy locations for bone fracture?
* Where in bone fracture is located
* Split long bone into 3rd
* In paediatrics
* Proximal & distal are secondary ossification centres for bone formation (physis)
* Physis may change management compared to an adult
50
what are the ways that bone can heal?
**primary bone healing**- heals by direct union with no callous formation. The preferred healing pathway in intra-articular fracture as minimises risk of post traumatic arthritis
**secondary bone healing-** bone healing by callus formation (see picture)
51
what displacement fractures can occur in child population?
same as adult
1. Displaced
2. Angulated
3. Shortening
4. Rotated
remodelling potential can give allowance for any displacement in child- not in rotation fractures
52
what is salter-harris classificaiton?
classification of physeal injuries
* Mnemonic SALT
1. Physeal **s**eparation
2. Fracture transverses physis and exits metaphysis (**a**bove)
3. Fracture traverses physis and exits epiphysis (**L**ower)
4. Fracture passes **T**hrough epiphysis, physis, metaphysis
5. Crush injury to physis
risk of growth arrest increases from 1-5, type 2 injuries most common
53
what can injuries to physis cause?
growth arrest
location and timing ky
whole physis-limb length discrepancy
partial- angulation as non-affected side keeps growing
54
what is the treatment for growth arrest?
* aim is to correct the deformity
* Minimise angular deformity
* Stop the growth of the unaffected side
* Reform the bone (osteotomy)
* Minimise limb length difference
* Shorten the long sider
* Lengthen the shorter side
55
what are the principles for fracture management?
all patients
Resuscitate
reduce
restrict
rehabilitate
56
what are types of reduction for fracture management?
closed reduction
* Reducing fracture without making incision
* Such as traction and manipulation in A&E
* Normal practice for paediatric patients
open reduction
* Making an incision
* Realignment of the fracture under direct visualisation
57
what is the aim of reduction?
correct deformity and displacement
reduce secondary injury to soft tissue/NV structures
must consider massive remodelling potential- heal quick as child so angular deformities better tolerated
58
what is the aim of restriction in fracture management?
maintain fracture reduction
provide stability for fracture to heal- rarely issue in children
59
what are the types of fracture restriction?
external (common in paeds)- splints and plaster
internal (avoided in paeds as high remodelling/healing potential)
plate and screws, intra-medullary device, metal work may need to be removed in future, often used when affects physis or beyond remodelling tolerance
60
how are children rehabiitated?
quick in children
play is great rehabilitator
stiffness not as major an issue as in adult
use it, move it and strengthen
61
what are the causes of limping in children?
* Septic arthritis (**MUST EXCLUDE FIRST**)
* Transient synovitis
* Perthes
* SUFE
62
what is septic arthritis?
orthopaedic emergency that can cause irreversible long term problems in the joint
is an inflamed joint in response to a systemic illness,
63
how is septic arthritis diagnosed?
Kocher's classification can score probability
* Non-weight bearing on joint
* ESR\>40
* WBC\>12000
* Temperature \>38
history is key (duration, other recent illness, associated joint pain)
64
what is a differential diagnosis of septic arthritis?
transient synovitis- once septic arthritis has been excluded
65
what is the treatment for septic arthritis
surgical washout to clear joint of infection
supportive treatment with antibiotics
66
what is perthes disease?
idiopathic necrosis of the proximal femoral epiphysis
usually 4-8y.o
more common in male than female 4:1
67
what needs to be excluded before diagnosis Perthes disease?
septic arthritis needs to be excluded first
(longer duration and no temp/inflammatory markers)
68
how is Perthes disease diagnosed?
radiograph
69
what is the treatment for Perthes disease?
supportive in first instance
70
what is SUFE?
slipped upper femoral epiphysis
proximal epiphysis sips in relation to the metaphysis
usually obese obsolescent male
71
What population is SUFE prominent?
obese adolescent male
12-13 year old during rapid growth
associated with hypothyroidism/hyperthyroidism
72
what is required for a diagnosis of SUFE?
septic arthritis needs to be excluded first
73
what is the treatment for SUFE?
operative fixation with screw to prevent further slip and minimise long term growth problems
