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1B Musculoskeletal > children's orthopaedics > Flashcards

children's orthopaedics Flashcards

1
Q

how many bones do children have?

A

More than adults

270

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2
Q

what is the physis?

A

growth plates

areas which long bone growth happens post-natally

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3
Q

how many physis are there?

A

2 per long bone

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4
Q

how does bone development occur?

A

intramembranous or endochondral

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5
Q

what does intramembranous development form?

A

mesenchymal cells to bone

flat bones (cranial & clavicle)

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6
Q

what does endochondral bone development form?

A

mesenchymal cells -> cartilage -> bone

long bones

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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

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8
Q

what is intramembranous ossification responsible for?

A

Formation cranial bones and clavicle

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9
Q

how does intramembranous ossification occur?

A
  1. Condensation of mesenchymal cells which differentiate into preosteoblasts -> osteoblasts
    • Ossification centre forms
  2. These cells synthesise and secrete osteoid
  3. Secreted osteoid traps osteoblasts which become osteocytes
  4. These cells collectively create the immature woven trabecular matrix and immature periosteum
  5. Angiogenesis occurs and blood vessels incorporated between the woven bone trabeculae will form the future bone marrow
  6. Immature woven Bone is remodelled and replaced by mature lamellae bone
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10
Q

what is endochondral ossification responsible for?

A

all other long bone formation (tissue that will become bone formed from cartilage)

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11
Q

where does endochondral ossification take place?

A

primary and secondary ossification centres

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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)

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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)

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14
Q

how does primary ossification develop?

A
  1. Mesenchymal differentiation at the primary centres
  2. Develop a cartilage model of the future bony skeleton
  3. Capillaries penetrate cartilage
    1. Calcification at the primary ossification centres- spongy bone forms from diaphysis
    2. Perichondrium transforms into pericardium
  4. Cartilage and chondrocytes continue to grow at ends of the bone
  5. 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
  6. Cartilage remains at the epiphyseal (growth) plate and at joint surface as articular cartilage
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15
Q

where does secondary ossification happen?

A

the physis (physeal plate)

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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
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17
Q

what are the zones of the epiphyseal plate?

A

reserve zone

proliferative zone

mutation and hypertrophy

calcified matrix

zone of ossification

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18
Q

what is the difference between child and adult skeleton?

A
  1. More elastic
  2. Presence of physis
  3. Increased speed on healing due to continued growth
  4. Increased remodelling potential (amount of deformity that can be corrected)
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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

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20
Q

what are the effects of Haversian canals?

A

canals that circulate blood supply

increased as bone more metabolically active

allow greater elasticity

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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

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22
Q

why does growth stop in bone?

A

growth occurs at varying rates at various sites

growth stops when the physis closes

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23
Q

what are the causes of physis closure?

A

gradual physical closure

puberty, menarche

parental height

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24
Q

what is the completion age of physis closure?

A

girls- 15-16

boys 18-19

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25
Q

how are physeal injuries categorized?

A

by Salter-Harris

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26
Q

what are the effects of pyseal injuries?

A

growth arrest= deformity (one part bone continue to grow while another stopped)

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27
Q

what are speed and remodelling dependant on?

A

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

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28
Q

where does physis greater growth occur?

A

extremes of upper limb and centra of knee

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29
Q

what are common children’s congenital conditions?

A

developmental dysplasia of the hip

club foot

achondroplasia

osteogenesis imperfecta

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30
Q

what is developmental dysplasia of the hip?

A

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
Q

what is the spectrum for developmental dysplasia of the hip?

A

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
Q

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

A
  • female
  • first born
  • breech
  • family history
  • oligohydramnios (not enough fluid)
  • native American/ Laplanders (swaddling of hip)
  • rare in african American and Asian population
33
Q

when is developmental dysplasia of the hip usually picked up?

A

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
Q

how is developmental dysplasia of the hip monitored?

A

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
Q

what is the treatment for dysfunctional dysplasia of the hip?

A
  • 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
Q

what is clubfoot?

A

congenital talipes equinovirus

congenital deformity of the foot

occurs in utero

deformity usually bilateral (50%)

37
Q

what is the genetic basis of clubfoot?

A

highest in male and Hawaiins

5% likely of siblings

familial in 24%

PITX1 gene involvement

38
Q

what deformity occurs in cubfoot?

A

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
Q

when is clubfoot diagnosed?

A

baby check when baby first born

40
Q

what is the treatment for clubfoot?

A

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
Q

what is achondroplasia?

A

more common skeletal deformity

autosomal dominant

can cause rhizomelic dwarfism

42
Q

what is the genetic basis of achondroplasia?

A

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
Q

what is rhizomelic dwarfism?

A

humerus shorter than forearm

femur shorter than tibia

normal trunk

adult height approx 125cm

normal cognitive development

significant spinal issues

44
Q

what is oseogenesis inperfecta?

A

brittle bone disease

hereditary- autosomal dominant or recessive

decreased type 1 collagen

insufficient osteoid production

45
Q

what are the causes of decreased type 1 collagen in osteogenesis imperfecta?

A

quantitative or qualitative issue

decreased secretion

production of abnormal colagen

46
Q

what are the effects of osteogenesis imperfecta?

A
  • Fragility fractures
  • Short stature
  • Scoliosis
  • Non-orthopedic manifestations
    • Heart
    • Blue Sclera (eyes)
    • Dentinogenesis imperfecta – brown soft teeth
    • Wormian skull
    • Hypermetabolism
47
Q

what are the principles of fracture description?

A
  • Pattern
  • Anatomy
  • Intra/extra-articular
  • Displacement
  • If effects physis used salter-harris classification
48
Q

what are the possible patterns of bone fracture?

A
  • 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
Q

what are the possible anatomy locations for bone fracture?

A
  • 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
Q

what are the ways that bone can heal?

A

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
Q

what displacement fractures can occur in child population?

A

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
Q

what is salter-harris classificaiton?

A

classification of physeal injuries

  • Mnemonic SALT
  1. Physeal separation
  2. Fracture transverses 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, type 2 injuries most common

53
Q

what can injuries to physis cause?

A

growth arrest

location and timing ky

whole physis-limb length discrepancy

partial- angulation as non-affected side keeps growing

54
Q

what is the treatment for growth arrest?

A
  • ­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
Q

what are the principles for fracture management?

A

all patients

Resuscitate

reduce

restrict

rehabilitate

56
Q

what are types of reduction for fracture management?

A

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
Q

what is the aim of reduction?

A

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
Q

what is the aim of restriction in fracture management?

A

maintain fracture reduction

provide stability for fracture to heal- rarely issue in children

59
Q

what are the types of fracture restriction?

A

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
Q

how are children rehabiitated?

A

quick in children

play is great rehabilitator

stiffness not as major an issue as in adult

use it, move it and strengthen

61
Q

what are the causes of limping in children?

A
  • Septic arthritis (MUST EXCLUDE FIRST)
  • Transient synovitis
  • Perthes
  • SUFE
62
Q

what is septic arthritis?

A

orthopaedic emergency that can cause irreversible long term problems in the joint

is an inflamed joint in response to a systemic illness,

63
Q

how is septic arthritis diagnosed?

A

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
Q

what is a differential diagnosis of septic arthritis?

A

transient synovitis- once septic arthritis has been excluded

65
Q

what is the treatment for septic arthritis

A

surgical washout to clear joint of infection

supportive treatment with antibiotics

66
Q

what is perthes disease?

A

idiopathic necrosis of the proximal femoral epiphysis

usually 4-8y.o

more common in male than female 4:1

67
Q

what needs to be excluded before diagnosis Perthes disease?

A

septic arthritis needs to be excluded first

(longer duration and no temp/inflammatory markers)

68
Q

how is Perthes disease diagnosed?

A

radiograph

69
Q

what is the treatment for Perthes disease?

A

supportive in first instance

70
Q

what is SUFE?

A

slipped upper femoral epiphysis

proximal epiphysis sips in relation to the metaphysis

usually obese obsolescent male

71
Q

What population is SUFE prominent?

A

obese adolescent male

12-13 year old during rapid growth

associated with hypothyroidism/hyperthyroidism

72
Q

what is required for a diagnosis of SUFE?

A

septic arthritis needs to be excluded first

73
Q

what is the treatment for SUFE?

A

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

1B Musculoskeletal (7 decks)

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