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MUSCULOSKELETAL > 1b Children's Orthopaedics > Flashcards

1b Children's Orthopaedics Flashcards

1
Q

What is the area where long bone growth occurs post-natally called?

A

Physis

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2
Q

By what mechanism do bones develop in utero?

A

Flat bones form via intramembranous ossification

Long bones form via endochrondral ossification

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3
Q

How many physes do normal long bones have?

A

2 - one at the distal end and one at the proximal end

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4
Q

Which bones are formed through intramembranous ossification?

A

Flat bones of the skull, clavicle and mandible

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5
Q

Describe how the process of intramembranous ossification occurs?

A

A group of mesenchymal cells in the central ossification centres differentiate first into pre-osteoblasts and then into osteoblasts. - forms an OSSIFICATION CENTER

These cells synthesise and secreteosteoid and the osteoblasts further differentiate into osteocytes

These cells then collectively create the immature woven trabecular matrix and immature periosteum

Angiogenesis occurs and Blood vessels incorporated between the woven bonetrabeculae will form the future bone marrow.

Later, the woven bone is remodelled and is progressively replaced by mature lamellar bone

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6
Q

What is endochondral ossification?

A

Development of long bone by replacing the hyaline cartilage precursor

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7
Q

What is endochondral ossification?

A

Development of long bone by replacing the hyaline cartilage precursor

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8
Q

What is the primary and secondary ossification center?

A

Primary = sites of pre natal bone growth via endochrondral ossification from the central part of the bone

Secondary = occurs post natally, after primary and at the physis’s (long bones often have more than one)

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9
Q

Describe how primary endochrondral ossification occurs?

A

During endochondral ossification, the tissue that will become bone is firstly formed from cartilage. The first site of ossification occurs in the primary centre of ossification, which is in the middle of diaphysis of the bone - prenatal

a) Mesenchymal Differentiation at the primary centre

b) The cartilage model of the future bony skeleton forms

c) Capillaries 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 with its own blood vessel and calcification at the proximal and distal end – calcification of the matrix

f) Cartilage remains at epiphyseal (growth) plate and at joint surface as articular cartilage.

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10
Q

In children, where does secondary ossification occur?

A

physis

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11
Q

What are the four differences between the adult and child skeleton?

A
  1. elasticity
  2. physis
  3. speed of healing
  4. remodelling
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12
Q

By the time the foetal skeleton is fully formed, cartilage remains at the joint surface. What is this cartilage known as?

A

Articular cartilage

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12
Q

By the time the foetal skeleton is fully formed, cartilage remains at the joint surface. What is this cartilage known as?

A

Articular cartilage

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13
Q

By the time the foetal skeleton is fully formed, cartilage remains at the joint surface. What is this cartilage known as?

A

Articular cartilage

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13
Q

During endochondral secondary ossification what happens at the epiphyseal side of the long bone?

A

Hyaline cartilage active and dividing to form hyaline cartilage matrix

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14
Q

During endochondral secondary ossification what happens at the diaphyseal side of the long bone?

A

Cartilage calcifies and dies and then replaced by bone.

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15
Q

Why are children’s bones most elastic than adult bones?

A

due to increased density of the haverisan canals as bones are more metabolicallt active

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15
Q

What are the three types of deformities you can get oin childrens bones due to the fact they are more elastic?

A
  1. Buckle Fracture
  2. Plastic Deformity
  3. Greenstick fractures
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16
Q

Why are children’s bones most elastic than adult bones?

A

due to increased density of the haverisan canals as bones are more metabolicallt active

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17
Q

What is the mechanism for a Buckle fracture?

A

Buckle/Torus fracture - one side of bone bends raising a little buckle without breaking the other side of the bone.

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18
Q

What is a plastic deformity and how does it occur?

A

When childrens bones bend rather than snapping

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19
Q

What is the cause of bone growth stopping?

A

When the physis closes

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20
Q

When does the physis close in girls?

A

aged 15-16

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21
Q

when does the physis close in boys?

A

18-19

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22
Q

What scoring system is used to characterise physeal injuries?

A

Salter-harris

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23
Q

What can physeal injuries lead to?

A

Growth arrest -> deformity, as one side of the bone could keep growing and the other stops for example

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24
Q

What is the speed of healing dependant on in childrens bones?

A

The location and age of the patient

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25
Q

Which location in the body do the physis grow quickly?

A

Knee and extremities of the upper limb

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26
Q

What is the method used to describe paediatric fractures?

A

PAID

Pattern
Anatomy
Intra/extra articular
Displacement

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27
Q

What are some patterns of paediatric fractures?

A

Transverse
Oblique
Spiral
Comminuted
Avulsion
Plastic Deformity
greenstick
Torus Fracture

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28
Q

What causes fractures to occur in different patterns?

A

depends on the way the energy dissipates through the bone

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29
Q

How does displacement of the bone affect the ability to remodel?

A

Remodelling can occur when displacement is in the angle of function, but not when rotated

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30
Q

What is the Salter-Harris Classification of physeal injuries?

A
  1. physeal SEPARATION
  2. fracture ABOVE physis
  3. fracture LOWER than physis
  4. fracture THROUGH the physis = demoltion = arrest of growth

SALT

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31
Q

What occurs as a consequence of an injury affecting the whole physis?

A

Whole limb length discrepancy = different lengths

32
Q

What occurs as a result of an injury affecting a part of the physis?

A

angulation as the non-affected side keeps growing

33
Q

What are the aims when correcting physeal damage?

A
  1. minimise angular deformity
  2. minimise limb length difference4
34
Q

How is limb length differences corrected?

A

Shorten the long side by prematurely fusing the physis
Lengthen the short side

35
Q

How is angular deformity corrected?

A

Stop growth of unaffected side
reform the bone - osteotomy

36
Q

What are the four R’s of paediatric fracture management?

A

Resusitate
Reduce
Restrict
Rehabillitate

37
Q

What are the two forms of reduction?

A

Open and closed reduction

38
Q

What does restriction involve in terms of fracture management?

A

Maintain fracture reduction and provide stability for healing by using forms of fixation so movement of the bones cannot occur

39
Q

What are the fixation options in paediatric fractures?

A
  1. plasters and splits - remodelling and huge healing potential means that operative internal fixation can be avoided
40
Q

What are the differentials for a limping child?

A

Septic Arthritis
Transient Synovitis
Perthes
SUFE - Slipped Upper Femoral Epiphysis

41
Q

Why is diagnosis of septic arthritis important?

A

Is an ortho emergency

42
Q

What is the treatment for septic arthritis?

A

Washing out the joint surgically

43
Q

What are the things on the Kocher’s classification for septic arthritis diagnosis?

A
  1. Non-weight bearing
  2. ESR > 40
  3. WBC > 12000
  4. temperature > 38 (FEVER)
44
Q

What is transient synovitis?

A

Inflammed joint in response to systemic illness

45
Q

When is transient synovitis diagnosed?

A

Diagnosis of exclusion - only once septic arthritis can be excluded

46
Q

What is the treatment for TS?

A

Supportive treatment with antibiotics - will usually go away in 2 weeks

47
Q

What is Perthes Disease?

A

Idiopathic necrosis of the proximal femoral epiphysis

48
Q

What age does Perthes disease usually occur in?

A

4-8 year olds

49
Q

What differentiated Septic Arthritis and Perthes Disease?

A

Unlikely to see biochemical markers and fever in Perthes

50
Q

What is the classic patient who might suffer from SUFE?

A

Obese adolescent male, 12-13 years of age

51
Q

Which endocrine conditions of SUFE associated with?

A

Hypothyroidism and hypopituitarism

52
Q

What is the treatment for SUFE?

A

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

53
Q

What is the investigation of choice for a SUFE?

A

X Ray

54
Q

What is a Slipped Upper Femoral Epiphysis (SUFE)?

A

Proximal epiphysis slips in relation to the metaphysis

55
Q

What is the treatment for Perthes disease?

A

Treatment is usually supportive in the first instance

Osteotomy - bone cut to shorten or lengthen it or change it’s alignment

-

56
Q

What is the key diagnostic tool for Perthes disease?

A

Plain radiograph - X-ray

(Epiphyses on left side isn’t as well formed as on the right side)

57
Q

Does Perthes Disease have a longer or shorter duration upon presentation than septic arthritis?

A

Longer

58
Q

Limping child…what is the key differential?

A

SEPTIC ARTHRITIS

59
Q

What is a great rehabilitator for paediatric fractures in younger children?

A

Playing

60
Q

What are the 2 types of restriction?

A

External and Internal

61
Q

What type of restriction is more often used in paediatric fractures and why?

A

External - great healing potential therefore no need for surgery

62
Q

What is DDH?

A

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

63
Q

What are the risk factors for DDH?

A

Female
First born

64
Q

What is meant by DDH being a packaging disorder?

A

A ‘Packaging Disorder’ - occur during pregnancy when the foetus is squished so abnormal bending of the arms or legs

65
Q

What is the spectrum of DDH?

A

Dysplasia
Subluxation
Dislocation

66
Q

What is Oligohydramnios?

A

Too little amniotic fluid

67
Q

How is DDH usually picked up?

A

Baby check → screening in the UK

Range of motion of hip usually limited in hip abduction; leg length

In those 3 months or older Barlow and Ortalani are non-sensitive

-

68
Q

What investigation is done in infants from in the age range 0 to 4 months to check for DDH?

A

Ultrasound - measures the acetabular dysplasia and position of the hip

69
Q

How id DDH treated if less than 6 months old?

A

Pavlik harness

70
Q

If The Pavlik Harness has failed as a DDH treatment, what is the next treatment option?

A

(Manipulation under Anaesthesia) MUA + closed reduction an Spica

71
Q

What is CTE?

A

Congenital Talipes Equinovarus

72
Q

What deformities occur in CTE? (CAVE)

A

C avus - high arch
A dductus of foot - pointing inwards
V arus
E quinous

Tight tendoachillies

73
Q

What is the gold standard treatment in Club Foot (Congenital Talipes Equinovarus)

A

Ponseti Method

  1. First a series of casts to correct deformity
  2. Many require operative treatment
    Soft tissue releases
  3. Foot orthosis brace
  4. Some will require further operative intervention to correct final deformity.
74
Q

What is the genetic inheritance pattern of Achondroplasia?

A

Autosomal dominant

75
Q

What mutation causes Achondroplasia?

A
  • G380 mutation ofFGFR3
  • inhibition of chondrocyte proliferation in theproliferative zoneof thephysis
  • results in defect in endochondral bone formation
76
Q

What is Rhizomelic dwarfism?

A

Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height of approx. 125cm

77
Q

What is Osteogenesis Imperfecta?

A

Brittle Bone Disease

78
Q

Which ECM protein is reduced in OI?

A

Collgen - type 1, due to decreased secretion and production of abnormal collagen

79
Q

What are the effects of OI on the bones?

A

Fragility fractures
Short stature
Scoliosis

80
Q

What are the non-orthopaedic manifestations of OI?

A

Heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull
Hypermetabolism

MUSCULOSKELETAL (13 decks)

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