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MUSCULOSKELETAL AND RHEUMATOLOGY 2 > CHILDREN'S ORTHOPEDICS > Flashcards

CHILDREN'S ORTHOPEDICS Flashcards

(58 cards)

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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?

25
How is clubfoot diagnosed?
Baby check
26
What is the gold standard treatment for clubfoot?
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
What is achondroplasia and its pathology?
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
What features make up Rhizomelic dwarfism?
Humerus shorter than forearm Femur shorter than tibia Normal trunk
29
Describe the genetics of achondroplasia
Autosomal dominant | - G380 mutation of FGFR3
30
What is osteogenesis imperfecta and pathology?
AKA brittle bone disease Decreased type I collagen due to decreased secretion and production of abnormal collagen. Causes insufficient osteoid production
31
How does osteogenesis imperfecta present?
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
What is the genetics of osteogenesis imperfecta?
Autosomal dominant/recessive
33
What 5 details should be given when describing paediatric fractures?
``` Pattern Anatomy Intra/extra-articular Displacement Salter-Harris (if fracture affects physis) ```
34
What are the different patterns of fractures that can occur in paediatrics?
``` Transverse Oblique Spiral (rotational torque) Comminuted (high energy trauma) Avulsion (bone pulled off by ligamentous attachment) ``` Plastic deformities: - Buckle - Greenstick
35
How are long bone fractures described anatomically?
Affecting physis: - Proximal 1/3 - Distal 1/3 Affected diaphysis: - Middle 1-3
36
What is the preferred healing pathway in intra-articular fractures?
Primary bone healing as minimises risk of post traumatic arthritis
37
Which type of bone healing uses a callus?
Secondary bone healing
38
What is remodelling potential in children dependent on?
Type of displacement and amount
39
What are the different types of displacement?
- Displaced - Angulated - Shortened - Rotated (remodelling not well tolerated and doesn't occur)
40
What is Salter-Harris?
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
How can growth arrest occur?
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
What are the 2 types of growth arrest and what deformities do they cause?
Whole physis - entire limb length discrepancy | Partial physis - angulation as non affected side keeps growing
43
What is the treatment for growth arrest?
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
What are the 4 Rs of fracture management?
Resuscitate Reduce Restrict Rehabilitate
45
What are the aims in reduction?
Correct deformity and displacement | Reduce secondary injury to soft tissue/NV structures
46
What two types of reduction can you do?
Open - incision, realignment of fracture under direct visualisation Closed - no incision e.g. traction and manipulation
47
What are the aims of restriction?
Maintain fracture reduction | Provide stability for fracture to heal
48
What are the 2 types of restriction and why are they done?
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
What does the limping child clinical sign indicate?
SEPTIC ARTHRITIS Transient synovitis Perthes SUFE
50
What is Kocher's classification?
Score for probability of septic arthritis - Non-weight bearing - ESR > 40 - WBC > 12,000 - Temperature > 38
51
When can transient synovitis, perthes and SUFE be diagnosed?
Once septic arthritis has been excluded
52
What is transient synovitis and its treatment?
Inflamed joint in response to a systemic illness | Supportive treatment with antibiotics
53
What is Perthes disease and who does it usually affect?
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
What is the treatment for Perthes disease?
Usually supportive in first instance
55
How is Perthes disease diagnosed?
Plain film radiograph
56
What is SUFE?
Slipped upper femoral epiphysis | - Proximal epiphysis slips in relation to the metaphysis
57
Who does SUFE usually affect?
Obese adolescent male - 12-13 years old during rapid growth - associated with hypothryoidism/pituitrism - family history
58
What is treatment for SUFE?
Operative fixation with screw to prevent further slip and minimise long term growth problem

MUSCULOSKELETAL AND RHEUMATOLOGY 2 (5 decks)

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