Children's Orthopaedics Flashcards

1
Q

What is intramembranous ossification used for?

A

Flat bone development - clavicle and cranium

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2
Q

Describe process of intramembranous ossification

A
  1. A group of mesenchymal cells in the central ossification centres differentiate first into preosteoblasts and then intoosteoblasts.
  2. Cells then synthesize and secreteosteoidand the trapped osteoblasts further differentiate into osteocytes.
  3. Then collectively create the immature woven trabecular matrix and immature periosteium.
  4. Angiogenesis occurs and blood vessels incorporated between the woven bonetrabeculaewill form the future bone marrow. Later, the woven bone is remodeled and is progressively replaced by mature lamellar bone.
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3
Q

Describe stages of endochondral ossification

A

Used to form all other long bones. Occurs at primary and secondary ossification centres. Primary ossification centres are sites of pre-natal bone growth through endochondral ossification from the central part of the bone. Secondary ossification centres occur post-natally after the primary ossification centre and long bones often have several (the physis).

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4
Q

Describe process of endochondral ossification

A

The first site of ossification occurs in the primary center of ossification, which is in the middle ofdiaphysis 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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5
Q

What happens at secondary ossification centres?

A

In the children’s skeleton, cartilage remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate (physis). Physis is responsible for the futher growth of bones.
The physis has various zones. On epiphyseal side, hyaline cartilage active and dividing to form hyaline cartilage matrix. On diaphyseal side, cartilage calcifies and dies and is then replaced by bone.

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6
Q

How does growth at physis occur and why is it key?

A

By the proliferation of chondrocytes and the subsequent calcification of the extracellular matrix into immature bone that is then subsequently remodelled. Physis is responsible for skeletal growth of child. Any congenital malfunction to this area or acquired insult – weather it is traumatic/infective or otherwise will therefore have a subsequent impact on growth of the child.

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7
Q

Why are children’s skeletons more elastic than adult ones?

A

Increased density of Haversian canals as bone is more metabolically active since continuously growing. Hence more plastic deformity occurs (bending before breaking). Torus fractures (buckle) common in children following FOOH as wrist absorbs impact and compresses on one side but remains intact on other side creating bulge. Greenstick fractures also common where bone doesn’t break all the way through.

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8
Q

What are 2 points about physis?

A
  1. Growth occurs at varying rates at varying sites
  2. Growth stops as the physis closes - gradual physeal closure depends on puberty, menarche and parental height - occurs for girls around 15/16 and boys 18/19.
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9
Q

What is the consequence of physeal injury?

A

Categorised by Slater-Harris and lead to growth arrest. This leads to deformity.

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10
Q

What is the speed and remodelling of bone dependent on?

A

Location and age of patient. Younger child heals more quickly. Distal femur and proximal tibia grow more – injuries in areas where there is more growth heal faster in a child as physis at knee and extremes of upper limb grow more.

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11
Q

What is developmental dysplasia of the hip?

A

Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum. Normal development relies on the concentric reduction and balanced forces through the hip in utero and hence is a packaging disorder.

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12
Q

Describe spectrum of developmental dysplasia of hip

A

Mild cases dysplasia – hip within socket but not centrally placed and therefore socket doesn’t develop into cup shape.
Subluxation more severe – hip in the socket but due to shallow nature of socket, pops in and out.
Dislocation – hip has never been in the socket and develops outside of it so acetabulum is extremely shallow as never had the pressure.

Dysplasia affects 2 in 100
Dislocation affects 2 in 1000

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13
Q

What are risk factors for developmental dysplasia of hip?

A

Female 6:1
First born
Breech position of baby
Family history
Oligohydramnios - when not even amniotic fluid
Native American/Laplanders – swaddling of hip
Rare in African American/Asian

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14
Q

Describe examination and investigations used for developmental dysplasia of hip

A

Usually picked up on baby check screening - range of movement limited in hip abduction and Galaezzi test (leg length). Barlow and Ortalani test insensitive in those 3 months or older.
Ultrasound used to investigate from birth to 4 months as secondary ossification centres not developed and so X-ray cannot be used. If prior to 6 weeks, must be age adjusted.

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15
Q

What is the treatment for developmental dysplasia of hip?

A

If reducible hip and less than 6 months old, Pavlik harness is 92% effective. Pavlik harness holds the femoral head within the acetabulum so as child grows, get the concentric pressures through the hip joint which supports further normal development. If Pavlik harness fails or abnormalities picked up too late, surgical intervention may be needed. Manipulation under anaesthetic with closed reduction and spica may be needed.

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16
Q

Describe epidemiology of congenital talipes equinovarus

A
  1. Congenital deformity of the foot
  2. Affects 1 in 1000, especially those in Hawaii
  3. Twice as many males as females
  4. 50% bilateral
  5. Genetic - PITX1 gene. 5% chance of affecting siblings and familial in 25% of cases.
17
Q

What is a CAVE deformity?

A

Occurs due to muscle contracture.
Cavus - high arch. Tight intrinsic flexor hallucis longus and flexor digitorum longus.
Adductus of foot - due to tight tibialis posterior
Varus - tight tendoachilles, tibialis posterior, tibialis anterior
Equinus - tight tendoachilles

18
Q

What is the Ponsetti method of treatment?

A
  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.

Treating congenital talipes equinovarus (clubfoot)

19
Q

What is achondroplasia and what is it caused by?

A

Most common skeletal dysplasia. Is autosomal dominant - G380 mutation ofFGFR3. Involves inhibition of chondrocyte proliferation in theproliferative zoneof thephysis which results in defect in endochondral bone formation.

20
Q

What is rhizomelic dwarfism?

A

Humerus shorter than forearm. Femur shorter than tibia. Normal trunk. Adult height of approx. 125cm. Normal cognitive development. Significant spinal issues.

21
Q

What is osteogenesis imperfecta?

A

Hereditary – autosomal dominant or recessive. Results in decreased Type I Collagen due to:
Decreased secretion
Production of abnormal collagen
Insufficient osteoid production

22
Q

What are the effects of osteogenesis imperfecta?

A

Bones:
Fragility fractures
Short stature
Scoliosis

Non-orthopaedic manifestations:
Effects on heart
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull
Hypermetabolism
23
Q

What are patterns of paediatric fractures?

A

Transverse, Oblique, Spiral, Comminuted and Avulsion. T/O if rotational torque type of injury. S also possible if rotatory force applied. High energy can cause C type. If bone pulled off by ligament in attachment, can get avulsion.

24
Q

Describe the anatomy of paediatric fractures?

A

Long bone usually divided into a proximal, medial (diaphysis) and distal 1/3. Transverse, oblique, spiral and comminuted usually occur in disaphysis.

25
Q

How does healing of intra and extrarcticular fractures differ?

A

Primary healing occurs via direct union of bones - no callus formation - the preferred healing pathway in intra-articular fracture as minimises risk of post traumatic arthritis. Secondary healing occurs via callus formation and faster than in adults.

26
Q

What is the Salter-Harris SALT classification of physeal injuries?

A
  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. Type 2 most common.

27
Q

What is growth arrest?

A

Injuries to physis cause growth arrest. Location and timing are key. If whole physis affected, limb length discrepancy occurs. If one side affected, angulation occurs as unaffected side grows normally.

28
Q

What are the 4 R’s of fracture management?

A

Resuscitate, Reduce, Restrict, Rehabilitate

29
Q

What is the aim of reduction and how is it carried out?

A

Aim is to correct deformity + displacement and reduce injury to soft tissue + neurovascular structures.
Closed reduction involves reducing a fracture without making an incision such as traction and manipulation in A&E.
Open reduction involves making an incision and the realignment of the fracture under direct visualisation.

30
Q

What is a type of closed reduction?

A

Gallows traction - Holding the skin, the long bones of the lower limb can be reduced.

31
Q

What is the aim of restriction?

A

To maintain the fracture reduction and provide stability for the fracture to heal. Children rarely have issues with bone not healing. External methods of restriction include splints and plaster. Internal methods of restriction include plate and screws/intra-medullary devices.

32
Q

Why is external fixation preferred in the case of paediatric cases?

A

Plasters and splints commonly used in paediatric fracture. Remodeling and huge healing potential means that operative internal fixation often can be avoided. However, operative intervention may be needed but due to continual growth at the physis, metalwork may need to be removed in the future.

33
Q

What are 4 causes of a limping child?

A

Septic arthritis, transient synovitis, perthes and SUFE (slipped upper femoral epiphysis)

34
Q

Describe septic arthritis in children

A

Orthopaedic emergency. Can cause irreversible long term problems in joint so requires surgical washout to clear infection. Probability of septic arthritis scored based on Kocher classification.

35
Q

What is the Kocher classification?

A
Non weight bearing
ESR >40
WBC >12,000
Temperature >38
Each scored 1 or 0 and indicates probability of septic arthritis.
36
Q

What is transient synovitis?

A

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.

37
Q

What is Perthes disease?

A

Idiopathic necrosis of the proximal femoral epiphysis. Septic arthritis needs to be excluded first. Affects those 4-8 years old in a 4:1 ration of M:F. At first instance, simply supportive treatment.

38
Q

What is SUFE?

A

Slipped upper femoral epiphysis. The proximal epiphysis slips in relation to the metaphysis. Usually obese adolescent male - 12-13 years old during rapid growth. Associated with hypothyroidism/hypopituitrism. Septic arthritis must be excluded first. Treatment is operative fixation with screw to prevent further slip and minimise long term growth problems.