Children's Orthopaedics Flashcards
How does a child’s skeleton differ from an adult’s skeleton?
Paediatric skeleton is NOT a miniaturised version of an adult
Children have more bones - 270 bones that are in continuous change
- Bones contain physis (growth plates) - in long bones (2 physes in each long bone)
- More elastic
- Increased speed of healing
- Greater remodeling potential - i.e. amount of deformity that can be corrected as a result of the growth that the child is going through
What are the two pathways of bone development?
Intramembraneous = development of flat bones i.e. how the cranial bones and clavicle are formed Endochondral = how all the other long bones in the body are formed
How does intramembraneous ossification take place?
Condensation of mesenchymal cells which differentiate into osteoblasts – ossification centre forms
These cells secrete osteoids, which trap further osteoblasts
Osteoblasts become osteocytes –> these create the immature, woven trabecular matrix and periosteum
After this, angiogenesis occurs and the crowded blood vessles incorporated between the woven and trabecular bone condence to form the future red bone marrow
Finally, this immature woven bone is remodelled ad progressively replaced by mature lamellar bone
Compact bone develops superficial to cancellous bone
What is endochondral ossification?
The tissue that will become bone is firstly formed as cartilage
How does endochondral ossification take place?
Occurs in 2 different ways:
- Primary Ossification Centres = sites of pre-natal bone growth through endochondral ossification from the central part of the bone i.e. the diaphysis
- Secondary Ossification Centres = occurs post-natal after the primary ossification centre at the physis, and long bones often have several physis
What is primary endochondral ossification?
Occurs at the primary centres i.e. the middle of the diaphysis / shaft of the bone
Occurs during the prenatal period
- Mesenchymal Differentiation at the primary centre
- Develops into a cartilage model of the future bony skeleton forms
- Via angiogenesis, capillaries penetrate cartilage creating the primary ossification centre
Calcification at the primary ossification centre = spongy bone formation in the middle of the bone sfhaft, spreading to the ends
Perichondrium transforms into periosteum - Cartilage and chondrocytes continue to grow at ends of the bone
- Secondary ossification centres develop with its own blood vessel and the blood supply allows for calcification at the proximal and distal end = calcification of the previously uncalcified matrix into immature spongey bone
- Cartilage remains at epiphyseal (growth) plate and at joint surface as articular cartilage
What is the role of the physis?
It is the secondary ossification centre - responsible for the further growth of bones via secondary endochondral ossification
What happens if the physis are faulty?
Any congenital malfunction to this area or acquired insult – whether it is traumatic/infective or otherwise will therefore have a subsequent impact on growth of the child
What is secondary endochondral ossification?
Responsible for long bone lengthening
Once the child is born, cartilage remains at the joint surface as articular cartilage between the diaphysis and epiphysis as the epiphyseal plate AKA a physis
Physis contain various zones
All zones have a role in the growth of the long bone - occurs via proliferation of the chondrocytes and subsequent calcification of extracellular matrix into immature bone, which is then remodelled
How do the different zones in the physis carry out secondary endochondral ossification?
Zone of elongation in long bone
Contains cartilage
Epiphyseal side – hyaline cartilage active and dividing to form hyaline cartilage matrix
Diaphyseal side – Cartilage calcifies and dies and then replaced by bone
Why are children’s bones more elastic (more bendy) than an adults?
Children’s bones have an increased density of Haversian Canals - these are microscopic tunnels within the cortices of the bones that circulate the blood supply
Why do children have more Haversian Canals?
Children’s bones are more metabolically active as they are continuously growing so they require a greater density of haversian canals
What are the 3 properties of a child’s bone due to the increased elasticity from the Haversian Canals?
- Plastic deformity - when an energy is dissipated though the bone, the bone will bend more before it eventually breaks, therefore differet fracture patters are seen when children sustain injuries
- Buckle fracture - caused from the bone bending more before fracturing, e.g. when a child falls onto an outstretched hand, instead of the bone fractures, it actually buckles in on itself and creates this tarus like structure
- Greenstick injury - bone does not snap in half, bendiness causes one side to break but the other side buckles and bends
Are the growths at all the physis the same?
No, growth rates at different physis vary
Upper limb = extremes i.e. shoulder and wrist
Lower limb = around the knees i.e. distal femur, proximal tibia
When and why does growth stop?
When the physis close (gradual physeal closure) - dependent on puberty, menarche, parental height
When does growth stop in girls and boys?
Girls = 15-16 Boys = 18-19
How are physeal injuries categorised and what are physeal growth deformities?
Physeal injuries are categorised by Salter-Harris
Physeal injuries can lead to growth arrest
Growth arrest can lead to deformity
What does the speed of healing and remodeling depend on?
Age and location
So esp. in children, at the physis where there is the greatest growth, there is the fastest healing due to the largest remodelling potential
Why do children heal more quickly?
As they have significantly greater remodelling potential
What are common children’s congenital conditions?
Development dysplasia of the hip
Club foot
Achondroplasia
Osteogenesis Imperfecta
What is Development dysplasia of the Hip (DDH)?
Group of disorders of the neonatal hip where the head of the femur is unstable or incongruous in relation to the acetabulum
A ‘Packaging Disorder’
When and why does DDH occur?
Occurs in utero and depends on how they sit in the womb - affects the way the hip sits within the acetabulum as the normal development of the hip and acetabulum rely on the concept of concentric reduction and blances forces through the hip
As DDH is a group of disorders, what is it comprised of?
It is a spectrum, from mild to severe:
Dysplasia (mild - hip within the socket but not quite centrally placed so socket does not develop into ‘cup’) –> subluxation (moderate - at times the hip is in the socket, but the shallow nature of the socket means the hip pops in and out) –> dislocation (severe - the hip has never been inside the socket and so develops outside of it so cup is v. v. shallow)
How common is dysplasia and dislocation?
Dysplasia = 2:100 Dislocation = 2:1000
What are the risk factors for developing DDH?
Risk factors = Female 6:1 First born Breech FH (family history) Oligohydramnios - not enough fluid within the amniotic sac) Native American/Laplanders – swaddling of hip once child is born Rare in African American/ Asian
How is DDH picked up / diagnosed?
During baby check - routine part of screening in the UK for all newborns
How is DDH examined?
Examine range of motion of the hip - usually limitation in hip abduction and leg length (Galeazzi), so perform some special tests known as Barlow’s and Otalani’s
In those 3 months or older Barlow and Ortalani are non-sensitive
What investigations are performed for suspected DDH?
Ultrasound – birth to 4 months
After 4 months X-ray - no benefit of doing this before as the secondary ossification centres had not ossified yet
If prior to 6 weeks needs to be age adjusted
Measures the acetabular dysplasia and the position of hip - i.e. measurement of the acetabulum angles and position of the hip
What is important to remember when undertaking investigations in babies?
Sometimes there are abnormal examinations - so examinations need to be age adjusted
What is the treatment for DDH?
Pvlik Harness - hips are flexed and abducted as it aims to hold the femoral head within the acetabulum so concentric pressure travels though the hip joints as the child grows
90% efficacy
If the Pavlik harness fails, or baby is 6-18 months, then it is too late for it to be effective so child may need surgical intevention
What is the aim of DDH treatment?
DDH = progressive condition
So the treatment given is not to prevent morbidity in infancy
But to allow for as normal hip development as possible to avoid problems in later life
What is congential talipes equinovarus?
Congenital deformity of the foot - AKA clubfoot
A packaging disorder - so occurs in utero
1:1000
Highest in Hawaiians
M2:1F (predisposition in males more than females)
50% are bilateral
What is the genetic aspect of clubfoot?
Approx. 5% likely of siblings
Familial in 25%
PITX1 gene
What are the clinical presentations of club foot?
CAVE deformity due to muscle contracture
Cavus – high arch: tight intrinsic muscles, FHL (flexor hallucis longus), FDL (flexor digitorum longus)
Adductus of foot: tight tib post and ant
Varus: tight tendoachillies, tib post, tib ant
Equinous: tight tendoachilles
When is clubfoot diagnosed?
Baby check
What is the gold standard treatment for clubfoot?
Ponseti method:
- First a series of casts to correct deformity - deformities corrected as per the CAVE acronym
- Many require operative treatment - in the form of soft tissue releases
- Foot orthosis brace - looks like child’s feet on a skateboard
Usually this is enough for most children
- Some will require further operative intervention to correct final deformity - e.g. further soft tissue releases or tendon transfer
What is achondroplasia?
The most common skeletal dysplasia
Autosomal Dominant
G380 mutation of FGFR3
Occurs if there is an abnormality in the proliferation zone of the physis - inhibition of chondrocyte proliferation, which results in defect in endochondral bone formation
What are the effects of achondroplasia?
Rhizomelic dwarfism:
- Humerus shorter than forearm
- Femur shorter than tibia
- Normal trunk
- Adult height of approx. 125cm
They also often have significant spinal issues that require operative intervention
But they have normal cognitive development
What is osteogenesis imperfecta (OI)?
Brittle bone disease
Hereditary – autosomal dominant or recessive
Decreased Type I Collagen due to:
Decreased secretion (quantitative issue)
Production of abnormal collagen (qualitative issue)
What are the bone/orthopaedic effects of osteogenesis imperfecta (OI)?
Fragility fractures - due to brittle bones and patient fragility
Short stature
Scoliosis
What are the non-orthopaedic manifestations of OI?
Heart - cardiac abnormalities
Blue Sclera
Dentinogenesis imperfecta – brown soft teeth
Wormian skull - abnormal fusion of cranial sutures
Hypermetabolism
How do we describe paediatric fractures?
PAID(S) acronym
Pattern Anatomy Intra/Extra-articular Displacement Salter-Harris - physeal injury
What is the pattern of fracture representative of?
How the energy was dissipated through the bones
What are the different patterns of bone fracture?
Transverse (-) Oblique (/) Spiral Comminuted (multiple) Avulsion - bone pulled off ligament Tarus or greenstick
How is anatomy of a fracture described?
Where the fracture is
Split long bones into thirds - Proximal, middle and distal thirds
What is meant by intra/extra articular?
Intra - primary bone healing
Extra - secondary bone healing
What is primary bone healing?
Heals by direct union
No callus formation
Preferred healing pathway in inta-articular fracture as it minimises the risk of post traumatic arthritis
What is secondary bone healing?
Bone healing by callus Haematoma formation Finrocartilaginous callus formation Bony callus formation Bone remodelling
What is displacement?
Displaced
Angulated
Shortened
Rotated
Can be one or many of this
How does remodelling potential coincide with displacement?
Remodelling potential can give significant amount of allowances for any level of displacement - except in rotated fractures
How does Salter-Harris classify physeal injuries?
SALT acronym
- Physeal Separation - injury goes through the physis
- Fracture traverses physis and exits via metaphysis (above)
- Fracture traverses physis and exits via epiphysis (lower)
- Fracture passes through epiphysis, physis, metaphysis
- Crush injury to physis
Risk of growth arrest increases from type 1 to type 5
Type 2 injuries most common
What is growth arrest caused by and what is important to consider?
Any injury to the physis can cause growth arrest (stopping growth)
BUT the location and timing (age) is key
How much potential growth is there left?
How much of the physis is affected?
What are the outcomes that depend on how much of the physis is affected?
Whole physis – limb length discrepancy
Partial – angulation as the non affected side keeps growing
What is the treatment of growth arrest?
Treatment dependent on previous factors
Aim is to correct the deformity by:
1. Minimising angular deformity - either shorten the long sid OR lengthen the short side
2. Minimise limb length difference - either stop the growth of the unaffected side OR reform the bone (osteotomy)
What are the four R’s of fracture management?
Resuscitate - paediatric advanced trauma life support
Reduce
Restrict
Rehabilitate
What is the point of reduction and what are the 2 types of reduction?
To correct the deformity and displacement and to reduce secondary injury to soft tissue / surrounding structures
Closed reduction:
Reducing a fracture without making an incision
Such as traction and manipulation in A&E
Open reduction:
Making an incision
The realignment of the fracture under direct visualisation
What is important to remember about paediatric patients when it comes to remodelling?
Their increased remodelling potential - so significant angular deformities can be tolerated as these will remodel out
So it is common practice to manage paediatric fractures using closed reduction methods e.g. plasters, gallows traction
What is Gallows traction?
Skin traction applied to the femur with a weight
Holding the skin, the long bones of the lower limb can be reduced
What is fracture restriction?
Maintaining the fracture reduction
What is the purpose of restricting a fracture?
Provides the stability for the fracture to heal
Children rarely have issues with bone not healing
But they can have issues with too much healing
What are the internal and external holding methods?
Internal: (performed intraoperatively)
Plates
Screws
Intramedullary devices
External:
Plaster
Splints
Which restriction method is used more commonly in children?
External restriction - due to children’s faster healing times and increased remodelling potential
When is operative intervention required for a fracture in a child?
When the fracture affects the physis and potential deformities need to be corrected to prevent growth problems
OR
If fracture is beyond the tolerance of remodelling
What is important to remember during operative intervention?
To not further damage the physis
What are the features to consider with fixation in children?
Operative intervention may be required
Consider the ongoing growth at the physis
Metalwork may need to be removed in the future
What are the main features of paediatric rehabilitation?
Children generally rehabilitate very quickly
Play is a great rehabilitator
Stiffness not as major issue as in adults
Use it, Move it and Strengthen it
What can cause a limp in child? Why is it important?
Septic arthritis - presence of an infection within the intra-articular space
Transient synovitis - inflamed joint to due system illness
Perthes - idiopathic necrosis of the proximal femoral epiphysis
SUFE - slipped upper femoral epiphysis, proximal epiphysis slips in relation to the metaphysis
These differentials can have huge ramifications on the child’s functional outcome
Why is septic arthritis important to always consider in a limping child?
Septic arthritis in a child is a orthopaedic emergency - therefore MUST ALWAYS BE EXCLUDED FIRST int he differentials
Can cause irreversible long term problems in the joint - due to necrosing effect of the proteases and due to pressure effect from the chondrocytes and the cartilages that comes from the oedema within the closed space
Therefore needs surgical washout of the joint to clear the infection
What is Kocher’s classification?
Kocher’s classification can help score probability of septic arthritis
Non weight bearing - not wanting to move their knee / hip
ESR >40
WBC >12,000
Temperature >38 or <36 - fever
What is key in the history when considering septic arthritis?
What symptoms they are having
Duration
Other recent illness
Associated joint pain / rashes / diarrhoea / vomitting
What is transient synovitis?
Diagnosis once septic arthritis has been excluded
Common condition often secondary to a coryzal illness
Is an inflamed joint in response to a systemic illness
Supportive treatment with antibiotics, fluids and obsevation compared to the surgical washout required for septic arthritis
What is Perthes disease and what demographic is it usually seen in?
Less common diagnosis - septic arthritis needs to be ruled out first
Idiopathic necrosis of the proximal femoral epiphysis
Usually in those 4-8 years old
Male 4:1 Female
How can you differentiate Perthes disease and Septic Arthritis / Transient Synovitis?
History - symptoms have been persisting for longer in perthes
No fever / inflammatory markers
What is the key diagnostic test for Perthes disease?
Plain film radiograph - epiphysis looks less symmetrical and less well formed
What is the treatment for Perthes?
Treatment is usually supportive in the first instance - then referred to specialist
What is SUFE and what demographic group is it usually seen in
Slipped upper femoral epiphysis
The proximal epiphysis slips in relation to the metaphysis
Seen in a slightly older age group - 12-13 year olds
Usually obese adolescent males
Associated with hypothyroidism / hypopituitarism
But septic arthritis needs to be excluded first
What is the treatment for SUFE?
Operative fixation with screw to prevent further slip and minimise long term growth problems
