Children’s Orthopaedics Flashcards

1
Q

Physis

A

Growth plates
Areas from which long bone growth occurs post natally

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2
Q

Difference of children’s skeleton

A

Elasticity
Physis
Speed of healing
Remodelling

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3
Q

Physis of children’s bone

A

Varying growth speed at sites
Growth stops as physis closes (girls 15-16 boys 18-19)
Salter-Harris
Physeal injury - growth arrest - deformities

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4
Q

Speed and remodelling of children’s bone

A

Faster in children
Physis at knee grows more
Physis at extreme of upper limb grows more

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5
Q

Common children’s congenital conditions

A

Development Dysplasia of Hip
Club Foot
Achondroplasia
Osteogenesis Imperfecta

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6
Q

DDH

A

Group of disorder of neonatal hip where head of femur is unstable or incongruous in relation to the acetabulum

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7
Q

DDH Spectrum

A

Dysplasia - Subluxation - Dislocation

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8
Q

DDH stats

A

Dysplasia 2:100
Dislocation 2:1000

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9
Q

DDH Treatment

A

Reducible hip and <6 months
-Pavlik harness 92% effective

Failed Pavlik harness or 6-18 months
- secondary changes - capsule + soft tissue
- MUA + closed reduction and Spica

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10
Q

Clubfoot

A

Neonatal

CAVE deformity
Cavus - high arch: right intrinsic, FHL, FDL
Adductus
Varus
Equinous

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11
Q

Clubfoot treatment

A

Ponseti method
Series of casts to correct deformity
Many require operation
Foot orthosis brace
Some require further surgery

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12
Q

Rhizomelic dwarfism

A

Achondroplasia
Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height at approx 125cm
Normal cognitive development significant spinal issues

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13
Q

Paediatric fractures

A

Pattern
Anatomy
Intra/extra-articular
Displacement

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14
Q

Paediatric fracture pattern

A

Transverse
Oblique
Spiral
Comminuted
Avulsion

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15
Q

Paediatric fracture anatomy

A

Proximal 1/3
Middle 1/3 diaphysis
Distal 1/3

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16
Q

Paediatric fracture intra/extra-articular

A

Primary bone healing
-direct union
-no callus formation
-preferred in intra as minimises risk of post traumatic arthritis

Secondary bone healing
-bone healing by callus

But remember physis

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17
Q

Paediatric fracture displacement

A

Displaced
Angulated
Shortened
Rotated

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18
Q

Classification of physeal injuries

A

Salter-Harris

1-physeal separation
2-fracture transverse physis and exits metaphysis
3-fracture transverse physis and exits epiphysis
4-fracture passes through epiphysis, physis, metaphysis
5-crush injury to physis

Risk of growth are at increased from 1-5

Type 2 injury most common

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19
Q

Growth arrest

A

Caused by injury to physis
Location and timing is key
Whole physis - limb length discrepancy
Partial - angulation as the non affected side keeps growing

20
Q

Growth arrest treatment

A

Limb length correction
-shorten long side
-lengthen short side

Angular deformity
-stop growth of unaffected side
-reform bone (osteotomy)

21
Q

Fracture management

A

Resuscitate
Reduce
Restrict
Rehabilitate

22
Q

Fracture management reduce

A

Correct deformity and displacement
Reduce secondary injury to soft tissue / NV structures

23
Q

Closed reduction

A

Gallows traction
Holding the skin, long bones of lower limb can be reduced
Correct deformities

24
Q

Fracture management restrict

A

Maintain fracture reduction
Provide stability for fracture to heal
Children rarely have issue with bone not healing

Plasters and splints commonly used
Remodelling and huge healing potential mean operative internal fixation often can be avoided

Operative intervention may be required
Consider ongoing growth at physis
Metalwork may need to be removed in the future

25
Fracture management rehabilitate
Children rehabilitate quickly Play is great rehabilitation Stiffness not as major issue as in adults
26
Limping child
Septic arthritis Transient Synovitis Perthes SUFE
27
Septic arthritis
Medical emergency Can cause irreversible long term problem in joint - need surgical washout of joint to clear infection History is key -duration -other recent illness -associated joint pain
28
SUFE
Slipped upper femoral epiphysis Proximal epiphysis slips in relation to metaphysis
29
Intramembranous ossification
Condensation of mesenchymal cells which differentiate into pre-osteoblasts and then osteoblasts - ossification centre forms Secreted osteoid traps osteoblasts which become osteocytes Cells collectively create immature woven trabecular matrix and immature periosteum form Angiogenesis occurs Blood vessels incorporated between woven bone and trabecular bone will form future bone marrow Immature woven bone remodelled and progressively replaced by mature lamellar bone
30
Endochondral ossification sites
Primary - sites of pre-natal bone growth through endochondral ossification from the central part of bone Secondary - occurs post-natally after primary ossification centre and long bones often have several (physis)
31
Endochondral primary ossification
Mesenchymal differentiation at primary centre at centre of bone Cartilage model of future bony skeleton forms Capillaries penetrate cartilage Calcification at primary ossification centre - spongy bone forms Perichondrium transforms into periosteum Cartilage and chondrocytes continue to grow at ends of bone Secondary ossification centres develop
32
Endochondral secondary ossification
Long bone lengthening At physis (physeal plate) Zone of elongation in long bone Contains cartilage Epiphyseal side - hyaline cartilage active and dividing to home hyaline cartilage matrix Diaphyseal side - cartilage calcifies and dies and then replaced by bone
33
Elasticity of children’s bone
Plasticity deformity - bends before break Buckle feature - tarus like the column Greenstick - like the tree, one cortex fractures but does not break the other side Increased density of haversian canals
34
DDH risk factors
Female 6:1 First born Breech Family history Oligohydramnios (not enough fluid in amniotic sac) Native American/Laplanders - swaddling of hip Rare in African American/Asian
35
DDH Examination
Usually picked up on baby check Range of motion of hip -usually limited in hip abduction -leg length In those 3 months or older Barlow and Ortalani are non sensitive
36
DDH investigation
Ultrasound - birth to 4 months X-ray - after 4 months Age adjusted - prior to 6 weeks Measure acetabula dysplasia and position of hip
37
Clubfoot risk factor
1:1000 Highest in Hawaiians M2:F1 50% bilateral 5% likely of siblings Familial in 25%
38
Achondroplasia
Most common skeletal dysplasia Autosomal dominant - G380 mutation of FGFR3 - inhibition of chondrocyte proliferation in proliferation zone of physis - results in defect in Endochondral bone formation
39
Osteogenesis imperfecta
Brittle bone disease Bones -fragility fractures -short stature -scoliosis Non-orthopaedic manifestations -heart -blue sclera -dentinogenesis imperfecta - brown soft teeth -wormian skull -hypermetabolism
40
Osteogenesis imperfecta genetic
Hereditary - autosomal dominant or recessive Decreased type I collagen due to -decreased secretion -production of abnormal collagen Insufficient osteoid production
41
Septic arthritis classification
Kocher’s classification can score probability -non weight bearing -ESR>40 -WBC>12,000 Temperature>38
42
Septic arthritis exclusion
Transient synovitis Inflamed joint in response to systemic illness Supportive treatment with antibiotics is treatment
43
Perthes disease
Idiopathic necrosis of proximal femoral epiphysis Last longer and no fever Diagnostic is radiograph
44
Perthes disease treatment
Supportive
45
Perthes disease risk factor
Usually in those 4-8 years old Male 4:1 Female
46
SUFE risk factor
Usually obese adolescent male -12-13 years old during rapid growth -associated with hypothyroidism/hypopituitrism
47
SUFE treatment
Operative fixation with screw to prevent further slip and minimise long term growth probler