Paediatrics Orthopaedics Flashcards
Where are epipheseal growth plates?
Found in bones of children but not adults
Made from hyaline cartilage and divide the epiphysis and the metaphysis (epithysis and metaphysis fuse and growth plates become the epiphyseal lines)
Label this:
What types of bone are in children and adults respectively?
Children = more cancellous bone spongy, highly vascular in centre of bones (more flexible but less strong)
Adults = more cortical bone which is compact, hard bones around the outside
What type of fractures are children more prone to?
Greenstick fractures - one side of bone breaks and other stays intact
Why is bone healing in children better?
Good blood supply (less long term deformity than compared with adults)
Childrens bones are less resistant to compression, what is the result?
Buckle fracture (or torus fracture)
What is bone remodelling?
Process where bone tissue is taken from areas of low tension and deposited in areas of high tension (bone changes to optimum shape for function)
Why is bone remodelling useful in children?
Even if set at incorrect angle - remodels over time to return to correct shape
Label the following fractures:
What classification system is used for growth plate fractures?
Salter-Harris classification
What mnemonic is used for fractures through the growth plate?
SALTR mnemonic
Type 1: Straight across
Type 2: Above
Type 3: BeLow
Type 4: Through
Type 5: CRush
Label the following salter harris fractures?
What is the management of fractures in children?
Safeguarding is important
Firstly achieve mechanical alignment of the fracture:
- Closed reduction via manipulation of the joint
- Open reduction via surgery
Secondly provide relative stability to allow healing
How can bones be fixed in position?
External casts
K wires
Intramedullary wires
Intramedullary nails
Screws
Plates and screws
What is the WHO pain ladder for children?
Step 1: paracetamol or ibuprofen
Step 2: morphine
What pain relief is not used in children and why?
Codeine and tramadol (unpredicatability in their metabolism - effects vary too greatly)
Why is aspirin contraindicated in children?
Risk of Reye’s syndrome(except in certain circumstances e.g.Kawasaki disease)
How may a child present with hip pain?
Limp
Refusal to use affected leg
Refusal to weight bear
Inability to walk
Pain
Swollen or tender joint
What are the differential diagnoses for hip pain in 0-4 year olds?
Septic arthritis
Developmental dysplasia of the hip (DDH)
Transient sinovitis
What are the differential diagnoses of hip pain in 5-10 year olds?
Septic arthritis
Transient sinovitis
Perthes disease
What are some differentials for hip pain in 10-16 year olds?
Septic arthritis
Slipped upper femoral epiphysis (SUFE)
Juvenile idiopathic arthritis
What are some ref flags for hip pain?
Child under 3 years old
Fever
Waking at night with pain
Weight loss
Anorexia
Night sweats
Fatigue
Persistent pain
Stiffness in the morning
Swollen / red joint
When is urgent referral for assessment in a limping child?
Child under 3 years
Older than 9 with a restricted or painful hip
Not able to weight bear
Evidence of neurovascular compromise
Severe pain / agitation
Suspicion of abuse
What investiagtion for hip pain in children?
Blood tests including inflammatory markers (CRP and ESR) for JIA and septic arthritis
Xrays to diagnose fractures, SUFE and other boney pathology
Ultrasound to establish an effusion (fluid) in the joint
Joint aspiration to diagnose or exclude septic arthritis
MRI to diagnose osteomyelitis
What age is septic arthritis most common at?
Children under 4 years (mortality 10%)
Why is septic arthritis an emergency?
Destroys the joint
Causes serious systemic illness
What percent of joint replacement surgery does spetic arthritis occur in?
1% (higher in revision surgery)
How does septic arthritis present?
Hot, red, swollen, painful joint
Refusing to weight bear
Stiffness and reduced range of motion
Systemic symptoms = fever, lethargy and sepsis
What is the most common bacteria causing septic arthritis?
Staphylococcus aureus
Neisseria gonorrhoea (gonococcus)
Group A streptococcus (strep pyogenes)
Haemophilus influenza
Escherichia coli (E. Coli)
What are some differential diagnoses for septic arthritis?
Transient sinovitis
Perthes disease
Slipped upper femoral epiphysis
Juvenile idiopathic arthritis
What is the management of septic arthritis?
Low threshold for treating (caution with immunosuppressed patients)
Admission to hospital under orthopaedic team
Aspirate joint before abx (send for gram staining, crystal microscopy, culture and antibiotic sensitivities)
If severe then may require surgical drainage and washout of the joint
Which antibiotics are used in septic arthritis?
Empirical IV antibiotics given until sensitivities are known (usually continues for 3 to 6 weeks when septic arthritis is confirmed)
What is transient synovitis? When is it seen?
Temporary irritation and inflammation in the synovial membrane of the joint
Most common cause of hip pain in children aged 3-10 years
What is transient synovitis associated with?
Viral upper respiratory tract infection
How does transient synovitis present?
Acute / gradual onset:
- Limp
- Refusal to weight bear
- Groin or hip pain
- Mild low grade temperature
Otherwise well
What is the management of transient synovitis?
Symptomatic - simple analgesia
Must exclude septic arthritis
Aged 3-9 years: managed in primary care if limp present for less than 48 hours and otherwise well - give clear safety net advice to attend A&E immediately if symptoms worsen or develop fever
How long should patients with transient synovitis be followed up for?
48 hours and 1 week to ensure symptoms are improving and then fully resolve
What is the prognosis of transient synovitis?
Significant improvement after 24-48 hours
Symptoms fully resolve within 1-2 weeks without any lasting problems (may recur in 20% of patients)
What happens in Perthes disease?
Disruption of blood flow to the femoral head causing avascular necrosis of the bone
What is the full name of Perthes disease?
Legg-Calvé-Perthes disease
When does Perthes disease most commonly occur?
Boys aged between 5-8 years
What causes Perthes disease?
Idiopathic - no clear cause or trigger for the avascular necrosis (theorised that its due to repeated mechanical stress to the epiphysis)
How does Perthes disease progress?
Revascularisation or neovascularisation and healing of femoral head
What is the main complication of Perthes disease?
Soft and deformed femoral head, leading to early hip osteoarthritis
THR (5% of patients)
How does Perthes disease present?
Pain in hip / groin
Limp
Restricted hip movements
Referred pain to knee
If triggered by minor trauma = slipped upper femoral epiphysis
What is the investigation in Perthes disease?
X-ray (can be normal)
Blood tests (inflammatory markers used to exclude other causes)
Technetium bone scan
MRI scan
What is the management of Perthes disease?
Younger + less severe disease = conservative
Maintain healthy position and alignment to reduce risk of deformity to femoral head:
- Bed rest
- Traction
- Crutches
- Analgesia
Physio to retain range of movement
Regular x-rays to assess healing
Surgery in severe cases, older children or those that are not healing
What is a slipped upper femoral epiphysis (SUFE) also known as?
Slipped capital femoral epiphysis (SCFE)
What is a slipped upper femoral epiphysis?
Head of femur displaces along the growth plate
In which children is SUFE more common?
Boys aged 8-15
More common in obese children
How does SUFE present?
Adolescent, obese male undergoing a growth spurt may be a history of minor trauma that triggers the onset of symptoms
SUFE is pain is disproportionate to the trauma
- Hip, groin, thigh or knee pain
- Restricted ROM
- Limp
Restricted internal rotation
How to diagnose SUFE?
X-ray
Blood tests are normal particularly inflammatory markers (excluding other causes)
Technetium bone scan
CT scan
MRI scan
What is the management in SUFE?
Surgery to return the femoral head to correct position and fix
What is osteomyelitis?
Infection in the bone and bone marrow (typically in the meetaphysis of long bones)
What is the most common bacteria in osteomyelitis?
Staphylococcus aureus
What is the development of osteomyelitis?
May be acute / chronic
How may infection reach the bones?
Open fracture
Travelled through blood (entering through skin/gums)
Who is osteomyelitis most common in?
Boys and children under 10
What are the risk factors for osteomyelitis?
Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
TB
What are the symptoms of osteomyelitis?
Refusing to weight bear
Pain
Swelling
Tenderness
Afebrile (low grade fever - if high fever then may have spread to become septic arthritis)
What are the investigations of osteomyelitis?
X-ray (can be normal)
MRI best imaging for diagnosis
Bone scan (alternative)
Blood tests show raised inflammatory markers (CRP and ESR) and raised white blood cells in response to infection
Blood culture for causative organism
Bone marrow aspiration / bone biopsy with histology and culture
What is the management of osteomyelitis?
Extensive and prolonged antibiotic therapy
Surgery = drainage and debridement of the infected bone
What is osteosarcoma?
Type of bone cancer (normally in 10-20 year olds)
What bones are commonly affected in osteosarcoma?
Femur
Tibia
Humerus
How does osteosarcoma present?
Persistent bone pain (particularly worse at night)
Bone swelling
Palpable mass
Restricted joint movements
How to diagnose osteosarcoma?
X-ray (urgent direct access xray within 48 hours - for unexplained bone pain / swelling)
If possible sarcoma urgent specialist assessment within 48 hours
Blood test may show raised ALP (alkaline phosphatase)
What will an x-ray show for osteosarcoma?
Poorly defined lesion on the bone
“Fluffy” appearance
Periosteal reaction - irritation of the lining of the bone (sun-burst appearance)
What further investigations to better define the lesion?
CT scan
MRI scan
Bone scan
PET scan
Bone biopsy
What is the management of osteosarcoma?
Surgical resection of the lesion (often with limb amputation)
Adjuvant chemo to improve outcomes
Who is involved in the MDT for osteosarcoma?
Paediatric oncologists and surgeons
Specialist nurses
Physio
OT
Psychology
Dietician
Prostetics and orthotics
Social services
What are the main complications of osteosarcoma?
Pathological bone fractures
Metastasis
What is talipes?
Fixed abnormal ankle position which presents at birth
Also known as clubfoot
What is the position of talipes equinovarus?
Ankle in plantar flexion and supination
What is the position of talipes calcaneovalgus?
Ankle in dorsiflexion and pronation
What is talipes treated with?
Ponseti method (good results) - surgery if ponseti method fails
What is the ponseti method?
Foot is manipulated to a normal position and a cast applied - repeated over and over until the foot is in the correct position (started from birth)
Achilles tenotomy is required to release tension in the tendon
After treatment with cast finished then brace is used to hold feet in position when not walking until child is around 4 years old
What is positional talipes?
Resting position of the ankle is in plantar flexion and supination - not fixed and no structural boney issue
Muscles are tight - requires referral to physio (resolves with time)
What is developmental dysplasia of the hip?
Condition where there is structural abnormality in the hip caused by abnormal development of the fetal bones
What is the result of developmental dysplasia of the hip?
Instability - subluxation or dislocation
Can persist into adulthood = recurrent dislocation, abnormal gait, early degenerative changes
When is developmental dysplasia of the hip (DDH) found?
Newborn examination or later with hip asymmetry, reduced ROM in hips / limp
What are some risk factors for developmental dysplasia of the hip?
- First degree FH
- Breech presentation from 36 weeks onwards
- Breech presentation at birth if 28 weeks onwards
- Multiple pregnancy
When is DDH screened for?
Neonatal examination at birth and 6-8 weeks old
What findings may be suggestive of DDH?
Different leg lengths
Restricted hip abduction (on one side)
Bilateral restriction in abduction
Difference in knee level when hips are flexed
Clunking of hips on special tests
What two special tests are used for DDH?
Ortolani test = baby on back, hip and knees flexed. Palms on baby’s knees with thumbs on inner thigh and four fingers on outer thigh. Gently abduct hip apply pressurebehind leg and see if hip dislocates anteriorly
Barlow test = baby on back, hip adducted, knee and hip flexed, downward pressure to see if hip dislocated posteriorly
What is the examination finding on the ‘special tests’ what is the next step?
Clicking due to soft tissue moving over bone (if isolated then doesn’t require further tests)
Clunking indicated DDH and requires an ultrasound
How is the diagnosis of DDH made?
Ultrasound of the hip to establish diagnosis
X-rays are also helpful, particularly in older infants
What is the management of DDH?
Pavlik harness (if presenting less than 6 months of age)
Holds femoral head in correct position to allow acetabulum to develop a normal shape - keeps hip flexed and abducted (can be removed when more stability usually after 6-8 weeks)
Surgery if harness fails or diagnosis made after 6 months - after surgery hip spica cast is used to immobilise the hip
What is rickets?
Condition in older children with defective bone mineralisation causing “soft” and deformed bones - leads to osteomalacia
What are some causes of Rickets?
Vit D / calcium deficiency
Genetic defect resulting in low phosphate (hereditary hypophosphataemic rickets)
Where do vitamin D and calcium come from?
Vitamin D = produced in body in response to sunlight / from food (eggs, oily fish, nutritional supplements)
Calcium = dairy products and green vegetables
What is the mode of inheritance of hereditary hypophosphataemic rickets?
X-linked dominant (has other forms of inheritance)
What is vitamin D?
A hormones (not technically a vitamin) created from cholesterol by the skin in response to UV radiation
Who are more likely to have vitamin D deficiency?
Darker skin (require more vit D)
Malabsorption disorders (e.g. inflammatory bowel disease)
Chronic kidney disease (kidneys are essential in metabolising vitamin D to active form)
What can low vitamin D result in?
Low calcium and phosphate (as vit D is needed to absorb from intestines and kidneys)
Low calcium causes secondary hyperparathyroidism - stimulates increased reabsorption of calcium from bones (causing further problems with bone mineralisation)
What are some potential symptoms of vitamin D deficiency?
Lethary
Bone pain
Swollen wrists
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological / abnormal fractures
What bone deformities can occur in rickets?
Bowing of the legs
Knock knees (knees bow inwards)
Rachitic rosary (ends of ribs expand at the costochondral junctions causing lumps along chest)
Craniotabes (soft skull with delayed closure of the sutures and frontal bossing)
Delayed teeth with under-development of the enamel
What is the diagnostic lab investigation for vit D deficiency?
Serum 25-hydroxyvitamin D (result of less than 25 nmol/L)
What imaging is used to diagnose rickets?
X-ray (may show osteopenia - more radiolucent bones)
What may other investigations reveal in vitamin D deficiency?
Serum calcium is low
Serum phosphate is low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high
What other pathology may explain symptoms of vit D deficiency?
Full blood count and ferritin, for iron deficiency anaemia
ESR and CRP for inflammatory conditions
Kidney function tests, for kidney disease
Liver function tests, for liver pathology
Thyroid function tests, for hypothyroidism
anti-TTG antibodies, for coeliac disease
Autoimmune and rheumatoid tests, for inflammatory autoimmune conditions
What is the management of rickets?
Prevention:
- Breastfed babies are more at risk of vit D deficiency (formula is fortified with vit D) mothers take vit D supplement (10 micrograms per day)
- Children with deficiency take ergocalciferol (vitamin D)
Rickets:
- Referral to paediatrician
- Vit D and calcium supplements
What is achondroplasia?
Most common cause of disproportionate short stature (dwarfism) - type of skeletal dysplasia
Where is the achondroplasia gene?
The fibroblast growth factor receptor 3 (FGFR3) is on chromosome 4
What is the genetic cause of achondroplasia?
Sporadic mutation or inheritance of abnormal copy of gene (inherited in an autosomal dominant pattern)
Homozygous gene mutation is fatal in neonatal period
What is a result of mutation in the FGFR3 gene?
Abnormal function of the epiphyseal plates (growth plates) restricting bone growth in length
What is the average height in achondroplasia?
Which bones are most affected?
4 feet
Femur and humerus (proximal limbs) are affected more than bones of forearm and lower leg
Spine length = less affected
Are intelligence or life expectancy affected by achondroplasia?
No
What are some other features of achondroplasia?
Short digits
Bow legs (genu varum)
Disproportionate skull
Foramen magnum stenosis
Why is there a disproportionate skull in achondroplasia?
Skull base = endochondrial ossification (affected = flattened midface, nasal bridge and foramen magnum stenosis)
Cranial vault = membranous ossification (unaffected = nomal sized vault and frontal bossing - prominent forehead)
Which conditions are associated with achondroplasia?
Recurrent otitis media dueo to cranial abnormalities
Kyphoscoliosis
Spinal stenosis
Obstructive sleep apnoea
Obesity
Foramen magnum stenosis = cervical cord compression and hydrocephalus
Who is in the MDT for achondroplasia?
Pediatricians
Specialist nurses
Physios
OTs
Dieticians
Ortho surgeons
ENT surgeons
Geneticists
What surgery can be used to increase height in achondroplasia?
Leg lengthening surgery - cutting bone (osteotomy) and separating two parts = gap between them (distraction) and bone forms between creating a longre bone = controversial - leads to significant problems including chronic pain and reduced function
What is Osgood-Schlatters disease caused by?
Inflammation at the tibial tuberosity where the patella ligament inserts (common cause of anterior knee pain in adolescents)
Occurs in patients aged 10-15 years
Usually unilateral (can be bilateral)
How does Osgood-Schlatters disease occur?
Patella tendon inserts into tibial tuberosity (at the epiphyseal plate)
Stress from running / movements causes inflammation on the tibial epiphyseal plate causing small avulsion fractures where patella ligament pulls away tiny pieces of the bone leading to growth of the tibial tuberosity causing a visible lump below the knee - initially is tender but as bone heals it becomes hard and non tender
How does osgood-schlatter disease present?
Gradual onset:
- Visible lump at tibial tuberosity
- Pain in the anterior aspect of the knee
- Pain exacerbated by physical activity
What is the management of Osgood-Schlatters disease?
- Reduce physical acitivity
- ICE
- NSAIDs (ibuprofen) for symptomatic relief
Stretching and physio to strengthen the joint and improve function
What is the prognosis of Osgood-Schlatters disease?
Symptoms fully resolve over time (left with boney lumop)
What is a rare complication of Osgood-Schlatters disease?
Avulsion fracture (tibial tuberosity is separated from rest of the tibia) - usually required surgical intervention
What is osteogenesis imperfecta?
Genetic condition which results in brittle bones which are prone to fractures (also known as brittle bone syndrome)
What is osteogenesis imperfecta caused by?
Range of genetic mutations which affect the formation of collagen (essential in maintaining the structure and function of bone - and skin, tendons and other connective tissues)
8 different types (vary in severity)
How does osteogenesis imperfecta present?
Hypermobility
Blue / grey sclera (the “whites” of the eyes)
Triangular face
Short stature
Deafness from early adulthood
Dental problems (particularly with formation of teeth)
Bone deformities e.g. bowed legs and scoliosis
Joint and bone pain
How is osteogenesis imperfecta diagnosed?
Clinical diagnosis
X-ray = diagnose fractures and bone deformites
Genetic testing is possible but not always routine
What is the medical treatment of osteogenesis imperfecta?
Bisphosphates to increase bone density
Vit D supplementation to prevent deficiency
Who is involved in the management of osteogenesis imperfecta?
Physio and OT to maximise strength and function
Paediatricians for medical treatment and follow up
Ortho surgeons to manage fractures
Specialist nurses for advice and support
Social workers for social and financial support
