Orthopaedics 6 - Orthopaedic Paediatrics
Anil Chopra
1. Describe the anatomy and physiology of the paediatric skeleton
2. Differentiate between paediatric and adult bone and joint pathology
3. Outline the implications of these differences using common paediatric orthopaedic
conditions as examples.
Normal human growth can be divided up into 7 main stages:
 Gamete
 Gametogenesis, meiotic division halves the number of chromosomes
 Early embryo – weeks 1-2
 2 week period from fertilisation to implantation
 Week 1 zygote repeatedly divides and the blastocyst implants on uterine
wall
 Week 2 amniotic cavity forms and the trilaminar embryonic disc is formed
 Early embryo usually aborted if serious genetic defect is present
 Embryo – weeks 3-8
 Organ systems begin to develop, usually consists of 3-8 weeks of
embryology.
 The trilaminar disc begins to develop:
 Different organ buds begin to become recognisable by week 4:
 dermatome becomes skin
 myotome becomes muscle
 sclerotome becomes cartilage and bone
 Hand plates begin to form by week 5
 Individual digits appear by week 6
 Upper and lower limbs apparent by week 7
 By week 8 the fingers are completely separated and the embryo takes
human shape.
 Foetus – weeks 9-birth
 Rapid growth occurs
 Upper limbs become more proportionate in weeks 9-12
 Ossification occurs by Intramembranous ossification (the clavicle mainly)
 Lower limbs become more proportionate in weeks 13-20 and most bones
ossify
 From week 20-birth, the body becomes proportionate
Formation of the Bony Skeleton
The bony skeleton formation occurs in a number of stages:
- condensation of the mesenchymal cells which will eventually become the
future skeleton
- mesenchymal cells differentiate into chondrocytes
- Central portion of cartilaginous anlage (the primordium, the initial clustering
of embryonic cells) undergoes chondrocyte hypertrophy and matrix
calcification
- Cartilage converted to bone by 2 distinct processes
o INTRAMEMBRANOUS OSSIFICATION
o ENDOCHONDRAL OSSIFICATION
Intramembranous Ossification
 Bone forms directly in collagenous matrix (does not require cartilage)
 Osteoblasts form a calcified osteoid within a collagenous framework
 Begins around week 7 in periphery of anlage forming a periosteal sleeve of bone
 Parts of scapula, clavicle and skull
Endochondral Ossification
 During foetal period primary ossification centres form in diaphyses of long bones
 Cartilaginous cells hypertrophy and degenerate
 Vascular ingrowth occurs
 Brings mesenchymal cells that form osteoblasts and osteoclasts
 Core of cartilage model is ossified to form primary ossification centre.
Ossification continues at the bone-cartilage interface, ossification of long bones
occurs before birth, and in infancy for the smaller bones.
Secondary ossification centres form in early childhood and occur at the ends of long
bones. They result in the formation of a growth plate. The primary and secondary
ossification centres fuse in adolescence.
Growth Plate Cartilage
- has a unique blood supply
- is zonal in structure
- has a complex biochemistry
- matrix mineralisation
The role of the growth plate is to produce longitudinal growth by appositional growth
of cells within growth plate, including chondrocytes and osteocytes. They result in the
production and mineralisation of matrix. The zonal structure of the growth plates
represents morphological, metabolic and functional differences:
- Reserve zone: relatively inactive
- Proliferative zone: centre of cartilage cell replication and growth, has a good
blood supply.
- Hypertrophic zone: size of cartilage cells increases, and their matrix is prepared
for calcification, (3 subzones)
o Maturation
o Degenerative
o Provisional calcification
- Metaphysis: vascularisation, bone formation and remodelling occurs here. The
bone is converted to lamellar bone.
The growth plate is often a site of infection, neoplasms, fractures and endocrine and
bone disorders.
Disorders of Growth Plates
Reserve zone
Diastrophic dwarfism
pseudoachondroplasia
Proliferative zone
Achondroplasia
Gigantism
Type 11 collagen defect
Proteoglycan
processing defect
Defect in cell
proliferation
Excessive cell
proliferation
Maturation
mucopolysaccharidosis
Lysosomal enzyme
deficiencies
Degenerative
mucopolysaccharidosis
Lysosomal enzyme
deficiencies
Provisional
calcification
rickets
Calcium or vitamin D
deficiency
Primary spongiosa
Osteomyelitis
Deposition of bacteria
Hypertrophic cells
extend into metaphysis
Metaphyseal dysplasia
Secondary spongiosa Osteogenesis imperfecta
Osteopetrosis
Increase
Deformity
Hitch
Decrease
Deformity


Plastic deformation – bone bent
Incomplete fractures:
Greestick:
Reduction
compleded
Torus:

Growth plate (physis) - Salter Harris type I and
II  good prognosos  germinal layer not
affected (except for femoral head – damage to
blood supply)
Salter- Harris Classification of growth
plate injuries
Epiphysis
I
Germinal
Layer
II
Physis
III
IV
V
Metaphysis
Salter-Harris type III, IV, and V
injuries  Damage to germinal area  Growth plate arrest  Progressive deformity


Treatment of Salter-Harris type III and IV injury – anatomical reduction.
Secondary ossific centres
Apophysis – traction injury (traction apophysis), adolescent growth spurt
Fracture healing and remodelling
 Highest potential in younger children, and metaphyseal fractures
 Up to 40˚ angulation, and 10-20˚ rotatory  deformity corrected
1–
asymmetrical
physial
growth
2 – Bone drift
Implications of these differences
NAI – non accidental injury/child abuse
 Fractures at various stages
 Rib fractures
 Skull fractures
 Foot fractures
 Osteogenesis imperfecta
Developmental dysplasia of the hip (DDH)
Normal



Subluxation
Examination – lower limb deformities, spinal deformities, syndromic child
associated lower limb deformities: forefoot adducts, club foot, congenital vertical
talus, thigh crease asymmetry, torticollis, spina bifida,
Clinical findings – limited abduction in flexion (all ages), positive
Barlow/Ortolani (less than 3 months), limb shortening and limping (at walking
ages)
Ortolani
Elevate the Femur
First, Next Abduct the
Hip

Dislocation
Barlow
Adduct the Hip First,
Next Push the Femur
Posteriorly
Treatment – bracing in flexion and abduction (<6 months), preoperative traction,
EUA + arthrogram, closed reduction and open tendon release + frog plaster (6-24
months), open reduction +/- Corrective Osteotomy & Hip Spica (>2 yrs)
Painful hip in paediatrics – benign in most cases, occasionally sinister
Painful knee  hip pathology
Common conditions:
 Transient synovitis/irritable hip –
o commonest cause of hip pain
o pathology: synovial effusion, raised intra-articular pressure
o presentation: limp, pain, unable to weight bear, generally well
o Examination: hip kept in flexion and external rotation, irritable in internal
rotaion, decreased range of movement, sepsis absent
o Investigations – X-ray, US
o Treatment – reassurance, rest, better within 24-48hrs
 Osteoarticular infections
o Septic arthritis, acute osteomyelitis, neonatal infections, TB
o Septic arthritis and osteomyelitis often coexist
o Staph aureus < 2yrs
o Streptococcus >2 yrs
o Septic arthritis: pain, unwell, unable to weight bear, teat with IV antibiotics
and arthrotomy and washout
o Acute osteomyelitis – unwell, severe pain, unable to weight bear, treat with IV
antibiotics, and surgery for suppuration and late cases.
 Perthes’ disease
o Avascular necrosis of femoral head
o Unknown aetiology
o Necrosis  fragmentation  healing  remodelling
o 75% of untreated Perthes’ disease  good outcome, 25%  poor outcome,
area fragments, head deforms, tissue not very strong  saddle shaped head
o Treatment – surgery (>50% head involvement, >7yrs, significant stiffness)
 Slipped under femoral epiphysis (SUFE)
o Commonest cause of hip pain in adolescents
o 40% present with hip pain
o predisposing factors: obesity, racial, hormonal
(hypogonadism, hypothyroidism, hypopituitarism)
o symptoms: pain, limp, unable to weight bear,
shortening, external rotation
o trethowan’s sign (see picture)
o radiology: 2 views mandatory for detection
o treatment: surgical stabilization (single screw, urgent surgery – unstable
injuries, prophylactic stabilisation – symptoms, hormonal abnormality)
Rotational and angular deformities
 Symptoms
 Symmetry
 Stiffness
 Syndromes
 Systemic
disorders
Equinus
valgus
calcaneous
varus
normal

Normal variants:
o Intoe gait – persistent femoral anteversion, internal tibial rotation, forefoot
adducts
o Bowed legs / knocked knees – Rickets, Blount’s disease, Marfan’s syndrome
o Flat feet – reduced longitudinal arch  rigid (rare) and flexible (common) flat
foot

Talipus equilovarus / club foot
o Hindfoot: varus (below) equines (right)
o forefoot: adductus and cavus
o associated abnormalities:
reduced muscle bulk, reduced
muscle exertion, shorter leg,
smaller foot
o Conservative treatment:
stretching, strapping, serial
casting
o Surgical treatment – failure of
conservative treatment, soft
tissue release, bony correction.
Neuromuscular disorders
o Myopathy
o Duchenne muscular dystrophy
o Neuropathy
o Central – spina bifida
o Peripheral – hereditary sensory motor neuropathy
o Progressive
o Duchenne muscular dystrophy
o Hereditary neuropathies
o Static
o Cerebral palsy – non progressive disorder of immature brain, resulting in
abnormal motor function and posture, caused by: birth asphyxia,
prematurity, low birth weight.
Orthopaedic management: avoid joint contractures (physiotherapy,
orthosis, serial casting, Botulinim A toxin, surgical release), correct hip
dislocation/sublaxation and scoliosis
o Polio
Leg length discrepancy
o Abnormal leg may be long or short
o Less than 2cm difference is common and asymptomatic
o Long term consequences: limping, inefficient gait, back pain, scoliosis
o Congenital (e.g. DDH, congenital short femur, tibia/fibula dysplasia…) or
acquired (e.g. fracture malunion, growth plate injury, neurological damage to
limb)
o Treatment
o Shortening of long leg:
1. Epiphysiodesis for skeletally immature – open growth plate,
gradual correction
2. acute shortening for adults
 Infant: birth – 2 years
 Most rapid growth after birth
 Upper limbs grow faster than lower limbs
 Foot grows disproportionately in lower limbs
 Half adult height around 2 years
 High amounts of subcutaneous fat
 Gross motor development
 Gait immature
 Wide based, unstable and irregular
 High centre of gravity
 Low muscle to body weight ratio
 Immature nervous system and posture control mechanisms
 Child: 2-adolescence
 Growth and development at slower rate than infancy
 Many developemental variations occur
 Physiological variations in growth patterns
 Genu valgum (a condition where the knees angle in and touch one another
when the legs are straightened_
 Genu varum (a deformity marked by medial angulation of the leg in relation to the
thigh, an outward bowing of the legs, giving the appearance of a bow)
 Flat feet
 In toe gait
 Adolescent
 Beginning of puberty – skeletal maturity
 Certain conditions occur in adolescence
 Scoliosis
 Slipped upper femoral epiphysis
 Psychological factors play greater role
 Obesity
Fractures
 Childs bone is more “porous”
 Childs bone more flexible
 Cortical thickness increases in childhood
 Mature bone has lower collagen content
 Mature bone has a higher calcium content
ADULT BONE = GREATER TENSILE STRENGTH AND LOWER FLEXIBILITY