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Paediatrics > Paediatrics Orthopaedics > Flashcards

Paediatrics Orthopaedics Flashcards

1
Q

Where are epipheseal growth plates?

A

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)

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2
Q

Label this:

A
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3
Q

What types of bone are in children and adults respectively?

A

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

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4
Q

What type of fractures are children more prone to?

A

Greenstick fractures - one side of bone breaks and other stays intact

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5
Q

Why is bone healing in children better?

A

Good blood supply (less long term deformity than compared with adults)

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6
Q

Childrens bones are less resistant to compression, what is the result?

A

Buckle fracture (or torus fracture)

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7
Q

What is bone remodelling?

A

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)

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8
Q

Why is bone remodelling useful in children?

A

Even if set at incorrect angle - remodels over time to return to correct shape

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9
Q

Label the following fractures:

A
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10
Q

What classification system is used for growth plate fractures?

A

Salter-Harris classification

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11
Q

What mnemonic is used for fractures through the growth plate?

A

SALTR mnemonic

Type 1: Straight across

Type 2: Above

Type 3: BeLow

Type 4: Through

Type 5: CRush

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12
Q

Label the following salter harris fractures?

A
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13
Q

What is the management of fractures in children?

A

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

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14
Q

How can bones be fixed in position?

A

External casts

K wires

Intramedullary wires

Intramedullary nails

Screws

Plates and screws

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15
Q

What is the WHO pain ladder for children?

A

Step 1: paracetamol or ibuprofen

Step 2: morphine

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16
Q

What pain relief is not used in children and why?

A

Codeine and tramadol (unpredicatability in their metabolism - effects vary too greatly)

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17
Q

Why is aspirin contraindicated in children?

A

Risk of Reye’s syndrome(except in certain circumstances e.g.Kawasaki disease)

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18
Q

How may a child present with hip pain?

A

Limp

Refusal to use affected leg

Refusal to weight bear

Inability to walk

Pain

Swollen or tender joint

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19
Q

What are the differential diagnoses for hip pain in 0-4 year olds?

A

Septic arthritis

Developmental dysplasia of the hip (DDH)

Transient sinovitis

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20
Q

What are the differential diagnoses of hip pain in 5-10 year olds?

A

Septic arthritis

Transient sinovitis

Perthes disease

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21
Q

What are some differentials for hip pain in 10-16 year olds?

A

Septic arthritis

Slipped upper femoral epiphysis (SUFE)

Juvenile idiopathic arthritis

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22
Q

What are some ref flags for hip pain?

A

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

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23
Q

When is urgent referral for assessment in a limping child?

A

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

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24
Q

What investiagtion for hip pain in children?

A

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

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25
Q

What age is septic arthritis most common at?

A

Children under 4 years (mortality 10%)

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26
Q

Why is septic arthritis an emergency?

A

Destroys the joint

Causes serious systemic illness

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27
Q

What percent of joint replacement surgery does spetic arthritis occur in?

A

1% (higher in revision surgery)

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28
Q

How does septic arthritis present?

A

Hot, red, swollen, painful joint

Refusing to weight bear

Stiffness and reduced range of motion

Systemic symptoms = fever, lethargy and sepsis

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29
Q

What is the most common bacteria causing septic arthritis?

A

Staphylococcus aureus

Neisseria gonorrhoea (gonococcus)

Group A streptococcus (strep pyogenes)

Haemophilus influenza

Escherichia coli (E. Coli)

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30
Q

What are some differential diagnoses for septic arthritis?

A

Transient sinovitis

Perthes disease

Slipped upper femoral epiphysis

Juvenile idiopathic arthritis

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31
Q

What is the management of septic arthritis?

A

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

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32
Q

Which antibiotics are used in septic arthritis?

A

Empirical IV antibiotics given until sensitivities are known (usually continues for 3 to 6 weeks when septic arthritis is confirmed)

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33
Q

What is transient synovitis? When is it seen?

A

Temporary irritation and inflammation in the synovial membrane of the joint

Most common cause of hip pain in children aged 3-10 years

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34
Q

What is transient synovitis associated with?

A

Viral upper respiratory tract infection

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35
Q

How does transient synovitis present?

A

Acute / gradual onset:

  • Limp
  • Refusal to weight bear
  • Groin or hip pain
  • Mild low grade temperature

Otherwise well

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36
Q

What is the management of transient synovitis?

A

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

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37
Q

How long should patients with transient synovitis be followed up for?

A

48 hours and 1 week to ensure symptoms are improving and then fully resolve

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38
Q

What is the prognosis of transient synovitis?

A

Significant improvement after 24-48 hours

Symptoms fully resolve within 1-2 weeks without any lasting problems (may recur in 20% of patients)

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39
Q

What happens in Perthes disease?

A

Disruption of blood flow to the femoral head causing avascular necrosis of the bone

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40
Q

What is the full name of Perthes disease?

A

Legg-Calvé-Perthes disease

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41
Q

When does Perthes disease most commonly occur?

A

Boys aged between 5-8 years

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42
Q

What causes Perthes disease?

A

Idiopathic - no clear cause or trigger for the avascular necrosis (theorised that its due to repeated mechanical stress to the epiphysis)

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43
Q

How does Perthes disease progress?

A

Revascularisation or neovascularisation and healing of femoral head

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44
Q

What is the main complication of Perthes disease?

A

Soft and deformed femoral head, leading to early hip osteoarthritis

THR (5% of patients)

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45
Q

How does Perthes disease present?

A

Pain in hip / groin

Limp

Restricted hip movements

Referred pain to knee

If triggered by minor trauma = slipped upper femoral epiphysis

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46
Q

What is the investigation in Perthes disease?

A

X-ray (can be normal)

Blood tests (inflammatory markers used to exclude other causes)

Technetium bone scan

MRI scan

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47
Q

What is the management of Perthes disease?

A

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

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48
Q

What is a slipped upper femoral epiphysis (SUFE) also known as?

A

Slipped capital femoral epiphysis (SCFE)

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49
Q

What is a slipped upper femoral epiphysis?

A

Head of femur displaces along the growth plate

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50
Q

In which children is SUFE more common?

A

Boys aged 8-15

More common in obese children

51
Q

How does SUFE present?

A

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

52
Q

How to diagnose SUFE?

A

X-ray

Blood tests are normal particularly inflammatory markers (excluding other causes)

Technetium bone scan

CT scan

MRI scan

53
Q

What is the management in SUFE?

A

Surgery to return the femoral head to correct position and fix

54
Q

What is osteomyelitis?

A

Infection in the bone and bone marrow (typically in the meetaphysis of long bones)

55
Q

What is the most common bacteria in osteomyelitis?

A

Staphylococcus aureus

56
Q

What is the development of osteomyelitis?

A

May be acute / chronic

57
Q

How may infection reach the bones?

A

Open fracture

Travelled through blood (entering through skin/gums)

58
Q

Who is osteomyelitis most common in?

A

Boys and children under 10

59
Q

What are the risk factors for osteomyelitis?

A

Open bone fracture

Orthopaedic surgery

Immunocompromised

Sickle cell anaemia

HIV

TB

60
Q

What are the symptoms of osteomyelitis?

A

Refusing to weight bear

Pain

Swelling

Tenderness

Afebrile (low grade fever - if high fever then may have spread to become septic arthritis)

61
Q

What are the investigations of osteomyelitis?

A

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

62
Q

What is the management of osteomyelitis?

A

Extensive and prolonged antibiotic therapy

Surgery = drainage and debridement of the infected bone

63
Q

What is osteosarcoma?

A

Type of bone cancer (normally in 10-20 year olds)

64
Q

What bones are commonly affected in osteosarcoma?

A

Femur

Tibia

Humerus

65
Q

How does osteosarcoma present?

A

Persistent bone pain (particularly worse at night)

Bone swelling

Palpable mass

Restricted joint movements

66
Q

How to diagnose osteosarcoma?

A

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)

67
Q

What will an x-ray show for osteosarcoma?

A

Poorly defined lesion on the bone

“Fluffy” appearance

Periosteal reaction - irritation of the lining of the bone (sun-burst appearance)

68
Q

What further investigations to better define the lesion?

A

CT scan

MRI scan

Bone scan

PET scan

Bone biopsy

69
Q

What is the management of osteosarcoma?

A

Surgical resection of the lesion (often with limb amputation)

Adjuvant chemo to improve outcomes

70
Q

Who is involved in the MDT for osteosarcoma?

A

Paediatric oncologists and surgeons

Specialist nurses

Physio

OT

Psychology

Dietician

Prostetics and orthotics

Social services

71
Q

What are the main complications of osteosarcoma?

A

Pathological bone fractures

Metastasis

72
Q

What is talipes?

A

Fixed abnormal ankle position which presents at birth

Also known as clubfoot

73
Q

What is the position of talipes equinovarus?

A

Ankle in plantar flexion and supination

74
Q

What is the position of talipes calcaneovalgus?

A

Ankle in dorsiflexion and pronation

75
Q

What is talipes treated with?

A

Ponseti method (good results) - surgery if ponseti method fails

76
Q

What is the ponseti method?

A

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

77
Q

What is positional talipes?

A

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)

78
Q

What is developmental dysplasia of the hip?

A

Condition where there is structural abnormality in the hip caused by abnormal development of the fetal bones

79
Q

What is the result of developmental dysplasia of the hip?

A

Instability - subluxation or dislocation

Can persist into adulthood = recurrent dislocation, abnormal gait, early degenerative changes

80
Q

When is developmental dysplasia of the hip (DDH) found?

A

Newborn examination or later with hip asymmetry, reduced ROM in hips / limp

81
Q

What are some risk factors for developmental dysplasia of the hip?

A
  • First degree FH
  • Breech presentation from 36 weeks onwards
  • Breech presentation at birth if 28 weeks onwards
  • Multiple pregnancy
82
Q

When is DDH screened for?

A

Neonatal examination at birth and 6-8 weeks old

83
Q

What findings may be suggestive of DDH?

A

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

84
Q

What two special tests are used for DDH?

A

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

85
Q

What is the examination finding on the ‘special tests’ what is the next step?

A

Clicking due to soft tissue moving over bone (if isolated then doesn’t require further tests)

Clunking indicated DDH and requires an ultrasound

86
Q

How is the diagnosis of DDH made?

A

Ultrasound of the hip to establish diagnosis

X-rays are also helpful, particularly in older infants

87
Q

What is the management of DDH?

A

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

88
Q

What is rickets?

A

Condition in older children with defective bone mineralisation causing “soft” and deformed bones - leads to osteomalacia

89
Q

What are some causes of Rickets?

A

Vit D / calcium deficiency

Genetic defect resulting in low phosphate (hereditary hypophosphataemic rickets)

90
Q

Where do vitamin D and calcium come from?

A

Vitamin D = produced in body in response to sunlight / from food (eggs, oily fish, nutritional supplements)

Calcium = dairy products and green vegetables

91
Q

What is the mode of inheritance of hereditary hypophosphataemic rickets?

A

X-linked dominant (has other forms of inheritance)

92
Q

What is vitamin D?

A

A hormones (not technically a vitamin) created from cholesterol by the skin in response to UV radiation

93
Q

Who are more likely to have vitamin D deficiency?

A

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)

94
Q

What can low vitamin D result in?

A

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)

95
Q

What are some potential symptoms of vitamin D deficiency?

A

Lethary

Bone pain

Swollen wrists

Bone deformity

Poor growth

Dental problems

Muscle weakness

Pathological / abnormal fractures

96
Q

What bone deformities can occur in rickets?

A

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

97
Q

What is the diagnostic lab investigation for vit D deficiency?

A

Serum 25-hydroxyvitamin D (result of less than 25 nmol/L)

98
Q

What imaging is used to diagnose rickets?

A

X-ray (may show osteopenia - more radiolucent bones)

99
Q

What may other investigations reveal in vitamin D deficiency?

A

Serum calcium is low

Serum phosphate is low

Serum alkaline phosphatase may be high

Parathyroid hormone may be high

100
Q

What other pathology may explain symptoms of vit D deficiency?

A

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

101
Q

What is the management of rickets?

A

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
102
Q

What is achondroplasia?

A

Most common cause of disproportionate short stature (dwarfism) - type of skeletal dysplasia

103
Q

Where is the achondroplasia gene?

A

The fibroblast growth factor receptor 3 (FGFR3) is on chromosome 4

104
Q

What is the genetic cause of achondroplasia?

A

Sporadic mutation or inheritance of abnormal copy of gene (inherited in an autosomal dominant pattern)

Homozygous gene mutation is fatal in neonatal period

105
Q

What is a result of mutation in the FGFR3 gene?

A

Abnormal function of the epiphyseal plates (growth plates) restricting bone growth in length

106
Q

What is the average height in achondroplasia?

Which bones are most affected?

A

4 feet

Femur and humerus (proximal limbs) are affected more than bones of forearm and lower leg

Spine length = less affected

107
Q

Are intelligence or life expectancy affected by achondroplasia?

A

No

108
Q

What are some other features of achondroplasia?

A

Short digits

Bow legs (genu varum)

Disproportionate skull

Foramen magnum stenosis

109
Q

Why is there a disproportionate skull in achondroplasia?

A

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)

110
Q

Which conditions are associated with achondroplasia?

A

Recurrent otitis media dueo to cranial abnormalities

Kyphoscoliosis

Spinal stenosis

Obstructive sleep apnoea

Obesity

Foramen magnum stenosis = cervical cord compression and hydrocephalus

111
Q

Who is in the MDT for achondroplasia?

A

Pediatricians

Specialist nurses

Physios

OTs

Dieticians

Ortho surgeons

ENT surgeons

Geneticists

112
Q

What surgery can be used to increase height in achondroplasia?

A

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

113
Q

What is Osgood-Schlatters disease caused by?

A

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)

114
Q

How does Osgood-Schlatters disease occur?

A

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

115
Q

How does osgood-schlatter disease present?

A

Gradual onset:

  • Visible lump at tibial tuberosity
  • Pain in the anterior aspect of the knee
  • Pain exacerbated by physical activity
116
Q

What is the management of Osgood-Schlatters disease?

A
  • Reduce physical acitivity
  • ICE
  • NSAIDs (ibuprofen) for symptomatic relief

Stretching and physio to strengthen the joint and improve function

117
Q

What is the prognosis of Osgood-Schlatters disease?

A

Symptoms fully resolve over time (left with boney lumop)

118
Q

What is a rare complication of Osgood-Schlatters disease?

A

Avulsion fracture (tibial tuberosity is separated from rest of the tibia) - usually required surgical intervention

119
Q

What is osteogenesis imperfecta?

A

Genetic condition which results in brittle bones which are prone to fractures (also known as brittle bone syndrome)

120
Q

What is osteogenesis imperfecta caused by?

A

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)

121
Q

How does osteogenesis imperfecta present?

A

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

122
Q

How is osteogenesis imperfecta diagnosed?

A

Clinical diagnosis

X-ray = diagnose fractures and bone deformites

Genetic testing is possible but not always routine

123
Q

What is the medical treatment of osteogenesis imperfecta?

A

Bisphosphates to increase bone density

Vit D supplementation to prevent deficiency

124
Q

Who is involved in the management of osteogenesis imperfecta?

A

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

Paediatrics (18 decks)

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