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Aneesha Flashcards BRS 2 > Children's orthopaedics > Flashcards

Children's orthopaedics Flashcards

1
Q

How many bones are found in a child skeleton?

A

270

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2
Q

Describe the steps of intramembranous ossification

A

Mesenchymal cells condense and differentiate to form osteoblasts- ossification centre forms
Osteoblasts secrete osteoid and then become trapped in the osteoid to become osteocytes
Trabecular matrix and periosteum form
Compact bone forms superficial to cancellous bone
Blood vessels condense to become red bone marrow
Immature woven bone is remodelled and progressively replaced by mature lamellae bone

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3
Q

What bones form through intramembranous ossification?

A

Flat bones of cranium, clavicle

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4
Q

What are the two types of ossification centres formed during endochondral ossification

A

Primary ossification centres: sites of pre-natal long bone growth through endochondral ossification from the central part of bone

Secondary ossification centre: sites of post natal growth of long bones, often long bones have several (physes)

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5
Q

Describe the steps of primary ossification in endochondral ossification

A

Mesenchymal cells differentiate at the primary ossification centre in the diaphysis (middle shaft of bone) during the prenatal period.
Cartilage model of future bony skeleton forms
Capillaries pierce cartilage, leading to calcification and formation of spongy bone up the shaft.
Perichondrium becomes periosteum
Chondrocytes and cartilage continue to grow at the proximal and distal ends of bone
Secondary ossification develops at the bone ends with their own blood supply and matrix calcifies and forms immature spongy bone
Left with cartilage at distal and proximal ends of bone with epiphyseal growth plate which will be point of secondary endochondral ossification in post natal period

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6
Q

Describe the steps of secondary ossification

A

By the time the child is born, cartilage remains at the front surfaces of long bone as articular cartilage and between the diaphysis and epiphysis as epiphyseal growth plates (physes)
These physes are responsible for post natal long bone elongation
Epiphyseal side: Hyaline cartilage is active and divides to form hyaline cartilage matrix
Diaphyseal side: cartilage matrix calcifies, dies and is replaced by bone

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7
Q

What are the 4 ways in which a child’s skeleton differs from that of an adult skeleton?

A

Elasticity
Physis- growth occurs at varying rates at different physis sites
Speed of healing and remodelling potential
Remodelling: children have higher remodelling potential

((also thick periosteum?))

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8
Q

Why are children’s bones more elastic than those of adults?

A

Children’s bone contain more Haversian canals (tunnels in bone cortices that circulate blood supply) as child’s bones are more metabolically active since they continually grow

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9
Q

What kind of injury can occur to child’s bones as a result of increased elasticity?

A

Plastic deformity- bones bend before they break
Buckle fractures- Torus fracture
Greenstick fractures- one side of the bone snaps while the other buckles but does not break

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10
Q

When does bone growth stop and what influences this to happen?

A

Bone growth stops on physis closure, influenced by:
Gradual physeal closure
Puberty
Menarche
Parental height

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11
Q

What age does physis closure occur in girls and in boys?

A

Girls- 15-16 years
Boys- 18-19 years

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12
Q

What complication can happen if physeal injury occurs?

A

Growth arrest leading to deformity

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13
Q

What classification system is used to categorise physeal injuries?

A

Salter Harris classification

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14
Q

What are the categories of physeal injury in the Salter Harris classification?

A

type 1- physeal Seperation

type 2- fracture transverses physis and exits metaphysis (Above)

type 3- fracture transverses physis and exits epiphysis (Lower)

type 4- fracture passes Through epiphysis, physis and metaphysis

type 5- crush injury to physis

SALT algorithm (acronym for first four)

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15
Q

What is the most common type of Salter Harris physeal injury and how does risk change across categories?

A

Type 2

risk increases 1-5

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16
Q

What 2 major factors does speed of healing and remodelling potential depend on?

A

Age of patient- younger children heal faster

Location of fracture-
Physis at knee grows more (distal femur, proximal tibia)
Physis at extremes of upper limb grows more (shoulder and wrist)
If bone breaks and reforms along same angle, more likely to heal better

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17
Q

What are the components of the PAID method of describing fractures

A

Pattern
Anatomy
Intraarticular/ Extraarticular
Displacement

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18
Q

What is the pattern of bone fracture reflective of?

A

The way energy is dissipated

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19
Q

Give examples for different patterns of bone fracture

A

Transverse
Oblique
Spiral: rotational torque pattern
Comminuted: high energy fracture with >1 part
Avulsion: Bone fragment is pulled off by its ligament

Can have plastic deformity, buckle fractures, greenstick fractures in children

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20
Q

What does the term anatomy describe in relation to bone fracture?

A

Location of fracture (proximal 1/3, middle 1/3, distal 1/3)

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21
Q

What important consideration is there for children with fractures in proximal and distal 1/3 of bone?

A

Physeal injury may cause growth arrest and deformity, therefore manage differently to adult fractures

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22
Q

What are the 2 ways bone healing occurs?

A

Primary healing- heals through direct union, no callus forms

Secondary healing- callus forms

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23
Q

What is the preferred mode of bone healing in intraarticular fractures and why?

A

Primary healing- minimises risk of post traumatic arthritis

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24
Q

Is secondary healing more common in intraarticular fractures or extraarticular fractures?

A

Extraarticular fractures

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25
Q

When can remodelling allow for displacement and when can it not?

A

Remodelling occurs best in angle of function- translation, angulation, shortened fractures
Remodelling doesn’t occur in rotated fractures

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26
Q

What factors affect the nature of growth arrest caused by physeal injury?

A

Location of injury
Timing of injury

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27
Q

What is difference in the resultant deformities in whole physis injury vs partial physis injury

A

If the whole physis is injured limb length discrepancy occurs
If partial physeal injury occurs there is angulation as uninjured side continues growing

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28
Q

How does timing of physeal injury change outcome?

A
  • If you’re closer to physeal closure when injury happens there’s only a small amount of growth potential left
  • If you get injury to physis when you’re younger, it’s a larger part of the limb’s growth so potential for growth arrest is much greater
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29
Q

What are the aims of growth arrest treatment

A

Minimise limb length discrepancy: either by shortening uninjured side (crossed screws for premature growth arrest) or lengthening injured side (plate and screws)

Minimise angular deformity: cause growth arrest on uninjured side, reform bone on injured side (osteotomy)

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30
Q

What are the 4 Rs of fracture management?

A

Resuscitate: paediatric advanced trauma life support pathway

Reduce: correct displacement and deformity

Restrict: Maintain fracture reduction to provide stability for fracture reduction

Rehabilitate

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31
Q

What is an important consideration in fracture reduction in children?

A

Reduce secondary injury to soft tissue and neuromuscular structures, especially since children have plastic deformity potential and increased elasticity

32
Q

Is closed or open reduction more common in children and why?

A

Closed
Kids have higher remodelling potential and can tolerate even more significant angular deformities than adults

33
Q

What is Gallow’s traction?

A

Long bones of the lower limbs can be reduced through holding the skin

34
Q

In what situations are operations used to treat fracture injuries to children?

A

If fracture affects physis and we need to correct deformity to prevent growth problems in the future
If the injury is beyond the potential remodelling potential of children

35
Q

What factors do we need to consider when treating fracture injuries in children through operation?

A

Prevent further trauma to physis as this can lead to growth arrest
May need to remove metalwork in the future as this can interfere with growth

36
Q

How does rehabilitation after fracture injury work for children?

A

Play is a great rehabilitator

Children generally rehabilitate very quickly and do not have major issues with stiffness as in adults

Based on the principles of use, move, strengthen , weight bear.

37
Q

What are the 4 key differentials for a limping child?

A

Septic arthritis (!!!!always consider first!!!!)
Transient synovitis
Perthes disease
SUFE

38
Q

What is septic arthritis?

A

Orthopaedic emergency where infection is present within the intraarticular space

39
Q

What major complication can arise from septic arthritis?

A

Irreversible long term joint problems due to the necrosing effects of proteases produced by organisms within the joint space and also the effects of pressure caused by oedema in the closed joint space on chondrocytes and cartilage

40
Q

How is septic arthritis treated?

A

Surgical washout of the joint along with IV antibiotic treatment

41
Q

What classification system can be used to classify probability of septic arthritis?

A

Kocher’s classification
Non-weight bearing
ESR>40mm/hr
WBC>12000 per micro litre
Fever>38 degrees centigrade

42
Q

What components of patient history are key in diagnosing septic arthritis?

A

Duration

Other recent illnesses and coryza symptoms (cold like symptoms like cough, sore throat, malaise, rhinorrhoea)

Associated joint pain, rashes, vomiting, diarrhoea

43
Q

What is transient synovitis?

A

Inflamed joint in response to systemic illness

44
Q

How is transient synovitis treated?

A

Supportive treatment with antibiotics

45
Q

What is Perthes’ disease

A

Idiopathic necrosis of proximal femoral epiphysis, usually in children aged 4-8
M:F ratio is 4:1

46
Q

How does presentation of Perthes’ diseases differ from that of septic arthritis or transient synovitis

A

Generally more chronic presentation
Wouldn’t expect to see inflammatory markers and temperature as in other two

47
Q

What diagnostic test is used to diagnose Perthes’ disease?

A

Usually a plain film radiograph- affected side will be less symmetrical and well formed as other side

48
Q

How is Perthes’ disease treated?

A

Initial treatment is usually supportive
Once diagnosed, specialist referral for continued observation and management

49
Q

What is SUFE?

A

Slipped upper femoral epiphysis- proximal epiphysis slips in relation to metaphysics

50
Q

In what groups does SUFE usually occur?

A

Usually in obese adolescent males, around 12-13 during rapid growth

Also associated with hypothyroidism or hypopitiutarism

51
Q

How does SUFE presentation differ from that of septic arthritis?

A

Not as acute as septic arthritis
Wouldn’t expect to see inflammatory markers/ temperature

52
Q

How can SUFE presentation be classified

A

Acute
Chronic
Acute on chronic (episodes of suddenly worsening pain and limping)

There’s another classification system to differentiate whether a child can weight bear or not

53
Q

How is SUFE treated?

A

Operative treatment- screw to prevent further slippage and minimise long term growth problems

54
Q

Name four common congenital orthopaedic conditions in children

A

Developmental dysplasia of the hip (DDH)
Congenital talipes equinovarus
Achodroplasia
Osteogenesis imperfecta

55
Q

What is developmental dysplasia of the hip?

A

Group of disorders of the neonatal hip in which the head of the femur is unstable/ incongruous in relation to the the acetabulum
Packaging disorder

56
Q

What does normal development of hip within acetabulum rely on?

A

concentric reduction
balanced forces through hip

57
Q

Describe the spectrum of developmental dysplasia of the hip

A

Dysplasia (mild): hip lies within the socket but not centrally placed so socket doesn’t develop into a cup

Subluxation:hip may be within socket but socket is shallow so hip pops in and out of socket

Dislocation (severe): hip develops outside the socket and socket develops as a very shallow cup

58
Q

How common is
a) dysplasia in developmental dysplasia of the hip
b) dislocation in developmental dysplasia of the hip

A

a)2:100
b)2:1000

59
Q

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

A

Family history
Female
First born
Breech
Oligohydramnios (not enough fluid in amniotic sac)
Native American/ Laplander (due to hip swaddling when child is born)

(Lower risk if Asian/ African American)

60
Q

How is developmental dysplasia of the hip examined?

A
  • Usually picked up on baby check- screening in UK
  • Range of motion of hip checked
    • Usually limitation in hip abduction
  • Leg length (Galeazzi)
  • Special tests done- Barlow and Ortalani → in those 3 months or older it becomes non-sensitive
61
Q

How is developmental dysplasia of the hip investigated?

A

US from birth- 4 months
If prior to 6 weeks you need to age adjust the test since you can find abnormal results in premature children

Xray after four months since US isn’t sensitive after 4 months(secondary ossification centres only ossify after 4 months)

62
Q

How is developmental dysplasia of the hip treated?

A

Pavlik’s harness if hip is reducible and <6 months
If 6-18 months/ if Pavlik’s harness fails: Surgery (MUA + closed reduction and spica)

63
Q

What is the aim of treatment in developmental dysplasia of the hip?

A

It’s not about preventing morbidity but to give child normal development of hip because DDH is progressive so when adolescent the patient has no issues

64
Q

What is congenital talipes equinovarus?

A

congenital deformity of the foot (club foot)
Most common in Hawaiians
M:F is 2:1
Bilateral in 50%

65
Q

What is the gene implicated in congenital talipes equinovarus?

A

PITX1

66
Q

What deformities are present in congenital talipes equinovarus?

A

CAVE deformity (due to muscle contracture)
Cavus: high arch-tight intrinsic, flexor halluces longus, flexor digitorum longus
Adductus of foot: tight tibia anteriorly and posteriorly
Varus: tight tendoachilles, tight anterior and posterior tibia
Equinous: tight tendoachilles

67
Q

What is the gold standard for treating congenital talipes equinovarus?

A

Ponseti method

Series of casts to gradually correct deformity
May need operative treatment e.g. soft tissue releases
Foot orthosis brace
Some require operative treatment to correct final deformity

68
Q

What is the most common skeletal dysplasia?

A

Achondroplasia

69
Q

What causes achondroplasia

A

G380 mutation of FGFR3
Inhibits chondrocyte proliferation proliferative zone of epiphysis and consequently defects in endochondral bone formation

70
Q

What is the pattern of inheritance of achondroplasia?

A

Autosomal dominant

71
Q

How does achondroplasia present?

A

Rhizomelic dwarfism
Forearm longer than humerus
Tibia longer than femur
Normal trunk
Normal cognitive abilities
Adult height roughly 125cm
Significant spinal issues

72
Q

What is the pattern of inheritance of osteogenesis imperfecta?

A

Autosomal dominant or recessive

73
Q

What is deficient in osteogenesis imperfecta?

A

Type I collagen
Either due to decrease in secretion (quantity)
or due to synthesis of abnormal type I collagen (quality)

74
Q

How does osteogenesis imperfecta manifest in bones?

A

Fragility fractures
Short stature
Scoliosis

75
Q

What are the non-orthopaedic manifestations of osteogenesis imperfecta?

A

Cardiovascular problems
Blue sclera
Brown soft teeth (dentinogenesis imperfecta)
Wormian skull due to abnormal fusion of cranial sutures
Hypermetabolism- typically affects parathyroid pathway

Aneesha Flashcards BRS 2 (47 decks)

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