Childrens Prthopaedics Flashcards
(46 cards)
What are the physis
Growth plates
The areas from which long bone growth occurs post natally
Bone development-how are flat and long bones formed
Flat bones
Intramembranous
Mesenchymal cells>bone
Long bones
Endochondral
Mesenchymal>cartilage>bone
Intramembranous ossification
Condensation of mesenchymal cells which differentiate into osteoblasts forming an ossification centre
Secreted osteoid traps osteoblasts which become osteocytes
Trabecular matrix and periosteum form
Compact bone develops superficial to cancellous bone. Crowded blood vessels condense into red bone marrow
Form cranial bones and clavicle
Endochondral ossification
All other long bone formation at both the primary and secondary ossification centre
Primary ossification centre
Sites of pre natal bone growth through endochondral ossification from the central part of the bone
Secondary ossification centers
Occurs post Nataly after the primary ossification centre and long bones often have several (physis)
Where is the first ossification centre
Middle of diaphysis of bone
Prenatal bone growth
Mesenchymal, differentiation at primary centre
The cartilage model of the future bony skeleton forms
Capillaries penetrate the cartilage. Calcification at the primary ossification centre spongy bone forms
Perichondrium transforms into periosteum
Cartilage and chondrocytes continue to grow at the ends of the bone
Secondary ossification centers develop
Secondary ossification centers
Long bone lengthening
Happens at physis (physeal plate)
Zone of elongation in a long bone
Contains cartilage
Epiphyseal side hyaline cartilage active and dividing to form hyaline cartilage matrix
Diaphyseal side cartilage calcified and dies and then replaced by bone
How are children’s and adults skeleton different
Elasticity
Physis
Speed of healing
Remodeling
Elasticity of children’s bone
Children’s bone bends more and is more elastic than an adults
Increased density of haversian canals therefore
plastic deformity (bends before breaks)
Buckle fracture (tarus like column)
Greenstick (like the tree,one cortex fractures but doesn’t break the other side)
Growth rate
Growth stops when physeal plates close
Gradual closure affected by puberty menarche and parenteral height
For girls complete at 15-16
For boys at 18-19
What can physeal injuries cause
Leads to growth arrest
This can lead to deformity
Are categorized by salter Harris
Common children congenital conditions
Developmental dysplasia of the hip
Club foot
Achondroplasia
Osteogenesis imperfecta
Developmental dysplasia of the hip
Group of disorder of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
A packaging disorder
Spectrum with dysplasia-subluxation-dislocation
(Ball not in socket)
Risk factors of developmental dysplasia
Female 6:1
First born
Breech
FH
Oligohydramnios
Native American/laplanders swaddling of hip
Rare in African American or Asian (less amniotic fluid)
Examination if developmental dysplasia of the hip
Picked up on baby check screening
Rom of hip -limitation in hip abduction,leg length (galeazzi)
In those 3 months or older barlow and ortalani are non sensitive
Ivx of developmental dysplasia of hip
US from birth to 4 months
After 4 months do X ray
If prior to 6 weeks needs to be age adjusted
Measures the acetabular dysplasia and the position of the hip
Treatment of developmental dysplasia of hip
Reducible hip and <6months
Palvik harness is 92% effective
Failed palvik harness or 6-18 months
-secondary changes in capsule and soft tissue
MUA and closed reduction and spica
Clubfoot and treatment
Congenital talipes equinovarus
Deformity of the foot
Highest in Hawaiians
50% bilateral
Genetic
5% likely of siblings
Familial in 25%
PITX1 gene
Treatment
Ponseti method is the gold standard
1.series of casts to correct deformity
2.many require operative treatment,soft tissue releases
3.foot orthosis brace
4.slme will require further operative intervention to correct final deformity
CAVE deformity
Cavus-high arch:tight intrinsic,FHL,FDL
Adductus of foot-tight tib post and ant
Varus-tight tendoachilies, tib post,tib ant
Equinous-tight tendoachiles
Achondroplasia
Most common skeletal dysplasia
Autosomal dominant
G380 mutation of FGFR3
Inhibition of chondrocyte proliferation in the proliferative zone of physis
Results in defect in Endochondral bone formation
Normal cognitive development
Significant spinal issues
(Proliferative zone affected via fgfr3)
Rhizomelic dwarfism
Humerus shorter than forearm
Femur shorter than tibia
Normal trunk
Adult height approx 125cm
Normal cognitive development
Significant spinal issues
Osteogenesis imperfecta
Brittle bone disease
Hereditary-autosomal dominant or recessive
Decreased type 1 collagen due to decreased secretion,production of abnormal collagen
Insufficient osteoid production
What does OI affect
Bones
-fragility fractures,short stature,scoliosis
Non orthopedic manifestation
Heart,blue sclera,dentinogenesis imperfecta (brown soft teeth,worminian skull,hypermetabolism
Paediatric fractures
Pattern
Anatomy
Intra/extra articular
Displacement
Salter Harris
