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MUSCULOSKELETAL AND RHEUMATOLOGY 2 > CHILDREN'S ORTHOPEDICS > Flashcards

CHILDREN'S ORTHOPEDICS Flashcards

1
Q

How many bones does a child have?

A

270 - more than an adults

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2
Q

What are primary ossification centres?

A

Sites of pre-natal bone growth via endochondral ossification

At the diaphysis

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3
Q

What are secondary ossification centres?

A

Sites of post-natal growth after primary ossification centre

At the physis of long bones

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4
Q

How do long bones lengthen?

A

Occurs at physis/physeal plate

Epiphyseal side - hyaline cartilage active and divides to for hyaline cartilage matrix

Diaphyseal side - cartilage calcifies and dies, then replaced by bone

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5
Q

What differences does a children’s skeleton have compared to an adult skeleton?

A

More elastic
Physis - constantly growing
Faster healing
More remodelling potential

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6
Q

What is remodelling potential?

A

Amount of deformity that can be corrected as a result of growth

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7
Q

Why are children’s bones more elastic?

A

Increased density of haversian canals so less dense osteoid bone meaning it can bend more

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8
Q

What does increased elasticity in children’s bone cause in terms of fractures?

A

Plastic deformity - bends before it breaks

Buckle/taurus fracture
Greenstick fracture

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9
Q

What is a greenstick fracture?

A

Bone bends with fracture

Once cortex fractures but does not break other side

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10
Q

When does growth stop?

A

When physis/physeal plates close around puberty

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11
Q

What can physeal injuries cause?

A

Growth arrest and thus deformity

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12
Q

Which bones of children has the fastest healing and greatest remodelling potential?

A

Physis at knee

Physis at extreme of upper limb

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13
Q

Name some common children’s congenital conditions of bone

A

Developmental dysplasia of the hip
Club foot
Achondroplasia
Osteogenesis Imperfecta

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14
Q

What is developmental dysplasia of the hip?

A

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

Normal development of the acetabulum requires concentric reduction and balanced forces through hip which doesn’t occur in this condition

Packaging disorder often due to way the child sits in utero

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15
Q

How does developmental dysplasia of the hip (DDH) present?

A

As a spectrum of:
- Dysplasia (hip in socket but not centrally placed so
socket doesn’t develop into nice cup)
- Subluxation (hip in shallow socket so it pops in and out)
- Dislocation (hip develops out of socket causing
acetabulum to become very shallow since no pressure)

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16
Q

What are some risk factors of DDH?

A 
Female 6:1
First born
Breech position
Family history
Oligohydramnios (not enough fluid in amniotic sac)
Native american/laplanders
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17
Q

How is DDH usually first picked up on?

A

Baby check screening

  • RoM of hip (usually limitation in hip abduction)
  • Barlow and Ortalani non-sensitive in 3 months or older
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18
Q

What investigations can be done for a baby suspected with DDH?

A

Ultrasound - birth to 4 months
X ray - after 4 months

Measure the acetabular dysplasia and the position of the hip

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19
Q

How can DDH be treated?

A

If hip reducible and < 6 months:
- Pavlik harness (holds femoral head in acetabulum so
concentric pressure present)

If Pavlik harness failed/6-18 months:
- MUA + closed reduction and spica

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20
Q

What is clubfoot also known as?

A

Congenital talipes equinovarus

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21
Q

What is a packaging disorder?

A

A deformity which develops in utero

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22
Q

What is clubfoot?

A

Packaging disorder causing CAVE deformity due to muscle contracture.

Primary deformities:

  • Cavus - high arch (tight intrinsic, FHL, FDL)
  • Adductus of foot - tight tib posterior and anterior
  • Varus - tight tendoachilles, tib posterior and anterior
  • Equinous - tight tendoachilles
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23
Q

What demographic is clubfoot most prevalent in?

A

Hawaiians

M:F 2:1

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24
Q

What gene is clubfoot associated with?

A

PITX1 gene

25
Q

How is clubfoot diagnosed?

A

Baby check

26
Q

What is the gold standard treatment for clubfoot?

A

Ponseti method
- Series of casts to correct deformity
- May require operative treatment (soft tissue releases)
- Foot orthosis brace
- Some require further operative intervention to correct
final deformity

27
Q

What is achondroplasia and its pathology?

A

Form of Rhizomelic dwarfism (short limbed dwarfism)

Chondrocyte proliferation in proliferative zone of physis is inhibited causing defect in endochondral bone formation (secondary endochondral ossification)

Significant spinal issues which require operative treatment
Most common skeletal dysplasia

28
Q

What features make up Rhizomelic dwarfism?

A

Humerus shorter than forearm
Femur shorter than tibia
Normal trunk

29
Q

Describe the genetics of achondroplasia

A

Autosomal dominant

- G380 mutation of FGFR3

30
Q

What is osteogenesis imperfecta and pathology?

A

AKA brittle bone disease
Decreased type I collagen due to decreased secretion and production of abnormal collagen. Causes insufficient osteoid production

31
Q

How does osteogenesis imperfecta present?

A

Fragility fractures
Short stature
Scoliosis

Heart problems
Blue sclera
Dentinogenesis imperfecta (brown soft teeth)
Wormian skull (abnormal fusion of cranial sutures)
Hypermetabolism (usually PTH pathway)

32
Q

What is the genetics of osteogenesis imperfecta?

A

Autosomal dominant/recessive

33
Q

What 5 details should be given when describing paediatric fractures?

A 
Pattern
Anatomy
Intra/extra-articular
Displacement
Salter-Harris (if fracture affects physis)
34
Q

What are the different patterns of fractures that can occur in paediatrics?

A 
Transverse
Oblique
Spiral (rotational torque)
Comminuted (high energy trauma)
Avulsion (bone pulled off by ligamentous attachment)

Plastic deformities:

  • Buckle
  • Greenstick
35
Q

How are long bone fractures described anatomically?

A

Affecting physis:

  • Proximal 1/3
  • Distal 1/3

Affected diaphysis:
- Middle 1-3

36
Q

What is the preferred healing pathway in intra-articular fractures?

A

Primary bone healing as minimises risk of post traumatic arthritis

37
Q

Which type of bone healing uses a callus?

A

Secondary bone healing

38
Q

What is remodelling potential in children dependent on?

A

Type of displacement and amount

39
Q

What are the different types of displacement?

A
  • Displaced
  • Angulated
  • Shortened
  • Rotated (remodelling not well tolerated and doesn’t
    occur)
40
Q

What is Salter-Harris?

A

Classification of physeal injuries (SALT):

  1. Physeal (S)eparation
  2. Fracture traverses physis and exits metaphysis (A)bove
  3. Fracture traverses physis and exits epiphysis (L)ower
  4. Fracture passes (T)hrough epiphysis, physis and
    metaphysis
  5. Crush injury to physis

Risk of growth arrest increases through 1-5
Type 2 injuries most common

41
Q

How can growth arrest occur?

A

Injuries to physis

Location and timing is key e.g. if injury closer in time to physeal closure then only small amount of potential growth left so deformity not as bad

42
Q

What are the 2 types of growth arrest and what deformities do they cause?

A

Whole physis - entire limb length discrepancy

Partial physis - angulation as non affected side keeps growing

43
Q

What is the treatment for growth arrest?

A

Correct deformity

If entire limb length:
- Shorten long side (premature fusion of physis using
crossed screws)
- Lengthen short side

If angular deformity:

  • Stop growth of unaffected side
  • Osteotomy (reform bone surgically)
44
Q

What are the 4 Rs of fracture management?

A

Resuscitate
Reduce
Restrict
Rehabilitate

45
Q

What are the aims in reduction?

A

Correct deformity and displacement

Reduce secondary injury to soft tissue/NV structures

46
Q

What two types of reduction can you do?

A

Open - incision, realignment of fracture under direct visualisation

Closed - no incision e.g. traction and manipulation

47
Q

What are the aims of restriction?

A

Maintain fracture reduction

Provide stability for fracture to heal

48
Q

What are the 2 types of restriction and why are they done?

A

External - splints, plaster (more common in paediatrics)

Internal - plate and screws, intra-medullary devise
(Can be avoided due to remodelling and huge healing potential. If fracture affects physis or beyond potential tolerance of remodelling)

49
Q

What does the limping child clinical sign indicate?

A

SEPTIC ARTHRITIS
Transient synovitis
Perthes
SUFE

50
Q

What is Kocher’s classification?

A

Score for probability of septic arthritis

  • Non-weight bearing
  • ESR > 40
  • WBC > 12,000
  • Temperature > 38
51
Q

When can transient synovitis, perthes and SUFE be diagnosed?

A

Once septic arthritis has been excluded

52
Q

What is transient synovitis and its treatment?

A

Inflamed joint in response to a systemic illness

Supportive treatment with antibiotics

53
Q

What is Perthes disease and who does it usually affect?

A

Idiopathic necrosis of proximal femoral epiphysis
Usually 4-8 years old
Male:female 4:1

No temp./inflammatory markers and usually longer than septic arthritis

54
Q

What is the treatment for Perthes disease?

A

Usually supportive in first instance

55
Q

How is Perthes disease diagnosed?

A

Plain film radiograph

56
Q

What is SUFE?

A

Slipped upper femoral epiphysis

- Proximal epiphysis slips in relation to the metaphysis

57
Q

Who does SUFE usually affect?

A

Obese adolescent male

  • 12-13 years old during rapid growth
  • associated with hypothryoidism/pituitrism
  • family history
58
Q

What is treatment for SUFE?

A

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

MUSCULOSKELETAL AND RHEUMATOLOGY 2 (5 decks)

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