children's orthopaedics Flashcards

1
Q

What are differences between children’s skeleton and adult skeleton?

A
  • Child’s skeleton has more bones (270) & is in continuous change.
  • Have growth plates (physis) where growth occurs post-natally.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is physis? How many?

A

Most bones have 2 physis (one at proximal end and one at distal end)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do flat bones develop by?

A

Intramembranous ossification (flat bones - cranium, clavicle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do long bones develop by?

A

Endochondral ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the process of intramembranous ossification?

A
  • Condensation of mesenchymal cells that differentiate into osteoblasts (ossification centre forms).
  • They secrete osteoid that traps osteoblasts which become osteocytes.
  • Osteocytes collectively create woven trabecular matrix & immature periosteum.
  • Angiogenesis with blood vessels incorportated between woven bone & trabecular bone form future bone marrow.
  • Immature woven bone remodelled & replaced by mature lamellar bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the process of endochondral ossification pre-natally? Where does bone growth happen prenatally?

A
  • Pre-natally at primary ossification centres (centre of bone).
  • Mesenchymal differentiation, develop cartilage model of future bone, angiogenesis with capillaries penetrating cartilage.
  • Calcification at primary centres forms spongy bone, perichondrium transforms into periosteum.
  • Spongy bone forms up shaft & cartilage and chondrocytes form at ends of bones.
  • Secondary ossification centres develop at ends of bones with own blood supply & begin to calcify the uncalcified matrix into spongy bone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the process of endochondral ossification post-natally? Where does it happen?

A
  • At physis.
  • Physis has different zones with different roles of growth in long bones.
  • At epiphyseal side, hyaline cartilage active & dividing to form hyaline cartilage matrix.
  • At diaphyseal side cartilage calcifies and dies and is replaced by bone.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why are children’s bones more elastic? What does this result in?

A

more elastic due to increased density of haversian canals.

  • Results in plastic deformity so bone can bend more before it breaks giving different fracture patterns.
    1. buckle fracture (it can buckle on itself forming tarus like column.
    2. greenstick fracture - one side snaps and other side buckles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When does physis close? What does this depend on?

A

Growth stops when physis closes.

  • Depends on puberty, menarche, parental height, genetics.
  • In girls closes at 15-16, boys 18-19.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are physeal injuries characterised by and what can they lead to?

A

By salter-harris.

-They can lead to growth arrest, which can lead to deformity if only 1 part of physis injured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the speed and remodelling of bone depend on in a child?

A
  • Depends on location & age of patient. Y
  • ounger child heals more quickly because growing more quickly.
  • Rate at different physis differs (eg upper limb, knee).
  • Ones with more growth have faster healing and remodelling potential.
  • Kids can tolerate large amounts of angulation/deformity because healing very quickly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is developmental dysplasia of the hip? Why does it develop and when? What does normal development of the hip rely on?

A
  • Group of disorders of neonatal hip where head of femur is unstable or incongruous in relation to acetabulum.
  • Happens in utero because of way child sits.
  • Normal development of hip relies on concentric reduction & balanced forces (needs to sit within acetabulum, if sits outside both hip & acetabulum wont develop properly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the different types of developmental dysplasia of the hip and what do they lead to?

A
  1. dysplasia: mild - hip within socket but not centrally placed.
  2. sublaxation - more severe, hip in shallow socket so pops in and out.
  3. dislocation - hip develops outside of socket so acetabulum develops as very shallow cup because of lack of forces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Who is developmental dyspasia of the hip more common in?

A

More common in females, first born, breech position, FH, oligohydramnios (not enough fluid in amniotic sac), more common in native american & laplanders because swaddling of hip once born. Rare in BA/asian.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What examinations should be done for a baby with developmental dyspasia + age ? How is it usually picked up?

A
  • Picked up on baby check screening in UK.
  • Examinations: examine ROM of hip (usually limited hip abduction), leg length (galeazzi).
  • Barlow & ortalani tests (not in 3 months or older because not sensitive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What investigations should be done to a child with developmetnal dysplasia of the hip?

A
  • ultrasound from birth to 4 months, after 4 months x-ray. Before 6-weeks needs to be age-adjusted.
  • Measures acetabular dysplasia & position of hip
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is treatment for developmental dysplasia of the hip? when must be treated & why?

A
  • If reducible hip & under 6 months do pavlik harness.
  • If harness fails or 6-18 month old –> secondary changes (capsule + soft tissue) - do MUA (manipulation under anaesthesia) + closed reduction and Spica.
  • Needs treatment at infant age because progressive (to give normal hip development + avoid injuries)
18
Q

What is congenital talipes equinovarus (club foot) demographics?

A

More males, highest in hawaians, 50% bilateral.

19
Q

What is cause of club foot?

A

Can be genetic, sometimes familial PITX1 gene.

20
Q

What are the deformities in club foot and what are they due to?

A

CAVE deformity due to muscle contracture.

  • Cavus - high arch - tight muscles affect FHL, FDL.
  • Adductus of foot - tight tib posterior and anterior.
  • Varus - tight tendoachilles, tib posterior tib anterior.
  • Equinous - tight tendoachilles
21
Q

Treatment of club foot?

A
  • Ponsetti method - foot placed in series of casts to correct deformity, may require some operative treatment (soft tissue release).
  • After casting may need foot orthosis brace.
  • Mostly sufficient but some need further operation to correct final deformity (soft tissue releases or tendon transfers)
22
Q

What is achondroplasia? What is cause? Pathophysiology?

A
  • Abnormality within physis in proliferation zone.
  • Cause is autosomal dominant - G380 mutation of FGFR23.
  • inhibition of chondrocyte proliferation in proliferative zone results in defect in endochondral bone formation (affects secondary ossification).
23
Q

What does achondroplasia result in? how does it present?

A

-Rhizomelic dwarfism: humerus shorter than forearm, femur shorter than tibia, normal trunk, adult height about 150cm, normal cognitive development, significant spinal issues

24
Q

What is osteogensis imperfecta? What is inheritance? Pathophysiology? How does it present?

A
  • Affects collagen.
  • Autosomal dominant or recessive.
  • Decreased type I collagen either due to decreased secretion or production of abnormal collagen so insufficient osteoid production.
  • Bones brittle so fragility fractures, short stature, spinal manifestations (scoliosis).
  • Other: cardiac abnormalities, blue sclera, dentogenesis imperfecta (brown soft teeth), worwian skull, hypermetabolism PTH pathway
25
Q

What are different patterns of bone fractures and what do they represent?

A
  • Transverse, oblique, spiral, comminuted, avulsion (if bone pulled off ligamentous attachment), tarus or greenstick.
  • Pattern represents energy dissipated through bone.
26
Q

How is the bone divided and what is consideration for children?

A

Proximal, distal, middle (diaphysis).

-In kids proximal and distal thirds have physis so management & considerations differ

27
Q

What is difference between extra-articular & intra-articular fractures?

A

Intra-articular fracture extends into the joint

28
Q

How do fractures heal in children? How do extra-articular fractures heal?

A
  • Can heal by primary bone healing (direct union, no callus formation) - preferred.
  • Or secondary healing - with callus.
  • Extra-articular fractures will heal faster than adults.
  • If affects physis might affect growth
29
Q

What are types of displacement? What is preferred and why?

A
  • Displaced, angulated, shortened, rotated.
  • Preferred for displacement in angle of function.
  • Remodelling not as good in rotated fractures
30
Q

What are the salter-harris classification of phsyseal injury types? Which is most common and how does risk of growth arrest increase?

A
  • Type 1: physeal separation (injury goes through physis)
  • type 2: fracture transverses physis and exits metaphysis (above).
  • Type 3: fracture transverses phsyis and exits epiphysis (lower).
  • Type 4:fracture passes through both physis, epiphysis, metaphysis.
    1. crush injury to physis.

-Type 2 most common, worse risk of growth arrest as types increase

31
Q

What affects growth arrest in physeal injuries? When do you get deformity?

A
  • If closer to physeal closure when injury small amount of potential growth left.
  • Depends on how much physis is affected.
  • If whole physis get limb length discrepancy.
  • If partial angular deformity because unaffected part of physis keeps growing.
  • Depends on potential growth left to be affected
32
Q

What is treatment for deformities in physeal injuries?

A
  • For limb length correction can either shorten long side or lengthen short side.
  • For angular deformity can stop growth on unaffected side or can reform bone on affected side (osteotomy) to surgically balance deformity
33
Q

What are the 4Rs of fracture management?

A

Rescucitate, reduce, restrict, rehabilitate

34
Q

how do you reduce a fracture in a child? why do you reduce it?

A
  • Closed (traction, manipulation) or open (incision, realignment).
  • Correct deformity & displacement and reduce secondary injury to soft tissue/neurovascular structures.
35
Q

How do you restrict a fracture in a child? What is commonly used? When surgery?

A
  • Hold in place to provide stability for healing.
  • Rarely problems with bone not healing but sometimes overgrowth of bone is issue.
  • External (splints & plasters), internal - plates, screws, intramedullary device.
  • Splints/plasters common because fast healing potential.
  • Surgery maybe when fracture affects physis & needs to correct deformity or when beyond potential tolerance of remodelling (plate/screws/intramedullary device)
36
Q

How do you rehabilitate in a child?

A

Faster rehab - play, stiffness not major issue, use/move/strengthen

37
Q

What is septic arthritis? What does it cause? What can it cause and what treatment needed?

A
  • Infection within intra-articular space.
  • Necrotising effect of proteases and due to pressure effect from chondrocytes & cartilage of oedema within space.
  • Can cause irreversible long term problem in joint.
  • Needs surgical lavage of joint to clear infection.
38
Q

How does septic arthritis present?

A

Acute, recent illness (coryzal symptoms), other symptoms.

39
Q

What is kocher’s classification for septic arthritis?

A

Non-weight bearing, ESR>40, WBC >12,000, temp> 38

40
Q

What is transient synovitis? Treatment?

A

Diagnosis once septic arthritis excluded.

  • Inflamed joint in response to systemic illness.
  • Supportive treatment with antibiotics.
41
Q

What is perthes disease? Demographics? What needs to be exlcuded first? How does it present? Treatment? What is seen?

A
  • Idiopathic necrosis of proximal femoral epiphysis.
  • 4-8 year olds, more males.
  • Septic arthritis excluded first.
  • Presentation quite similar to septic arthritis may be more chronic than septic and no temp/inflammatory markers.
  • Diagnose via plain radiograph (epiphysis not symmetrical/well formed as other side).
  • Treatment supportive + refer to specialist
42
Q

What is SUFE (slipped upper femoral epiphysis)? Usual demogrraphic? What is it associated with? What do you exclude? What is treatment?

A
  • Proximal femoral epiphysis slips in relation to metaphysis.
  • Usually obese male 12-13 during rapid growth.
  • Associated with hypothyroidism/hypopituitarism.
  • Family history & underlying endocrine disorder.
  • Exclude septic arthritis
  • Can be acute/chronic/acute-on chronic.
  • Treat with operative fixation with screw to prevent further slip & minimise growth problem.