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:
v Gamete
n Gametogenesis, meiotic division halves the number of chromosomes
v Early embryo – weeks 1-2
n 2 week period from fertilisation to implantation
n Week 1 zygote repeatedly divides and the blastocyst implants on uterine wall
n Week 2 amniotic cavity forms and the trilaminar embryonic disc is formed
n Early embryo usually aborted if serious genetic defect is present
v Embryo – weeks 3-8
n Organ systems begin to develop, usually consists of 3-8 weeks of embryology.
n The trilaminar disc begins to develop:
n Different organ buds begin to become recognisable by week 4:
Ø dermatome becomes skin
Ø myotome becomes muscle
Ø sclerotome becomes cartilage and bone
n Hand plates begin to form by week 5
n Individual digits appear by week 6
n Upper and lower limbs apparent by week 7
n By week 8 the fingers are completely separated and the embryo takes human shape.
v Foetus – weeks 9-birth
n Rapid growth occurs
n Upper limbs become more proportionate in weeks 9-12
n Ossification occurs by Intramembranous ossification (the clavicle mainly)
n Lower limbs become more proportionate in weeks 13-20 and most bones ossify
n 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
n Bone forms directly in collagenous matrix (does not require cartilage)
n Osteoblasts form a calcified osteoid within a collagenous framework
n Begins around week 7 in periphery of anlage forming a periosteal sleeve of bone
n Parts of scapula, clavicle and skull
Endochondral Ossification
n During foetal period primary ossification centres form in diaphyses of long bones
n Cartilaginous cells hypertrophy and degenerate
n Vascular ingrowth occurs
n Brings mesenchymal cells that form osteoblasts and osteoclasts
n 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 dwarfismpseudoachondroplasia / Type 11 collagen defect
Proteoglycan processing defect
Proliferative zone / Achondroplasia
Gigantism / 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
Metaphyseal dysplasia / Deposition of bacteria
Hypertrophic cells extend into metaphysis
Secondary spongiosa / Osteogenesis imperfecta
Osteopetrosis
· Plastic deformation – bone bent
· Incomplete fractures:
Greestick:
Torus:
· Growth plate (physis) - Salter Harris type I and II à good prognosos à germinal layer not affected (except for femoral head – damage to blood supply)
Salter-Harris type III, IV, and V injuries à Damage to germinal area à Growth plate arrest à 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 à deformity corrected
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)
· 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)
· 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 à 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 à fragmentation à healing à remodelling
o 75% of untreated Perthes’ disease à good outcome, 25% à poor outcome, area fragments, head deforms, tissue not very strong à 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
· 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 à 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
v Infant: birth – 2 years
n Most rapid growth after birth
n Upper limbs grow faster than lower limbs
n Foot grows disproportionately in lower limbs
n Half adult height around 2 years
n High amounts of subcutaneous fat
n Gross motor development
n Gait immature
n Wide based, unstable and irregular
n High centre of gravity
n Low muscle to body weight ratio
n Immature nervous system and posture control mechanisms
v Child: 2-adolescence
n Growth and development at slower rate than infancy
n Many developemental variations occur
n Physiological variations in growth patterns
n Genu valgum (a condition where the knees angle in and touch one another when the legs are straightened_
n 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)
n Flat feet
n In toe gait
v Adolescent
n Beginning of puberty – skeletal maturity
n Certain conditions occur in adolescence
Ø Scoliosis
Ø Slipped upper femoral epiphysis
n Psychological factors play greater role
n Obesity
Fractures
n Childs bone is more “porous”
n Childs bone more flexible
n Cortical thickness increases in childhood
n Mature bone has lower collagen content
n Mature bone has a higher calcium content
ADULT BONE = GREATER TENSILE STRENGTH AND LOWER FLEXIBILITY