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Year 4 - Paediatrics > Orthopaedics > Flashcards

Orthopaedics Flashcards

1
Q

Differences between children and adult bones.

A

Children bones:
- growth plates present
- more cancellous bone*

*therefore children can have plastic deformity / greenstick fractures.

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2
Q

How are fractures through the growth plate classified?

A

Salter-Harris classification

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3
Q

Principles of fracture management in children.

A

Mechanical alignment of the fracture:
- closed reduction (MUA)
- open reduction

Hold the alignment to allow healing:
- external casts
- K wires
- intramedullary wires
- intramedullary nails
- screws
- plates and screws

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4
Q

Pain management in children.

A

Step 1: paracetamol or ibuprofen

Step 2: morphine

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5
Q

Presentation fo hip pain.

A
  • limp
  • refusal to use the affected leg
  • refusal to weight bare
  • inability to walk
  • pain
  • swollen or tender joint
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6
Q

Causes of joint pain in children aged 0-4 years.

A
  • septic arthritis
  • developmental dysplasia of the hip
  • transient synovitis
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7
Q

Causes of joint pain in children aged 5-10 years.

A
  • septic arthritis
  • transient synovitis
  • Perthes disease
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8
Q

Causes of joint pain in children aged 10-16 years.

A
  • septic arthritis
  • slipped upper femoral epiphysis (SUFE)
  • juvenile idiopathic arthritis
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9
Q

Red flags for hip pain.

A
  • child <3 years
  • fever
  • waking at night with pain
  • weight loss
  • anorexia
  • night sweats
  • fatigue
  • persistent pain
  • stiffness in the morning
  • swollen or red joint
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10
Q

What is septic arthritis?

A

Infection inside the joint, causing destruction of the joint and serious systemic illness.

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11
Q

Presentation of septic arthritis.

A
  • hot, red, swollen and painful joint
  • refusing to weight bare
  • stiffness and reduced ROM
  • systemic symptoms (ie. fever, lethargy, sepsis)
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12
Q

Common causative organisms of septic arthritis.

A

Staphylococcus aureus is the most common causative organism.

Other bacteria:
- Neisseria gonorrhoea in sexually active teenagers
- Group A Streptococcus
- Haemophilus influenzae
- E. coli

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13
Q

Differentials for septic arthritis.

A
  • transient synovitis
  • Perthes disease
  • SUFE
  • juvenile idiopathic arthritis
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14
Q

How to differentiate between septic arthritis and transient synovitis.

A

Kocher criteria:
- inability to weight bare
- pyrexia
- elevated WCC
- elevated ESR

Score ≥3 indicates septic arthritis.

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15
Q

Diagnostic workup of septic arthritis.

A

Routine bloods: FBC, CRP, ESR, urate levels. Blood cultures (x2).

Joint aspiration BEFORE antibiotics.

Plain radiograph of the joint.

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16
Q

Management of septic arthritis.

A

Broad spectrum antibiotics as per trust guidelines until microbial sensitivities are known.

Patients may require surgical drainage and irrigation of the affected joint in severe cases.

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17
Q

What is transient synovitis?

A

The transient inflammation of the synovial membrane of the joint.

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18
Q

Presentation of transient synovitis.

A
  • lump
  • refusal to weight bare
  • groin or hip pain

Children with transient synovitis typically do not have a fever; children with joint pain and a fever need urgent management for septic arthritis.

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19
Q

Management of transient synovitis.

A

Analgesia to help ease the discomfort.

Safety net advice to attend A&E immediately if the symptoms worsen or they develop a fever.

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20
Q

Prognosis of transient synovitis.

A

Symptoms typically improve within 48 hours.

Symptoms fully resolve within 1-2 weeks without lasting problems.

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21
Q

What is Pethes disease?

A

Disruption of blood flow to the femoral head, resulting in avascular necrosis of the femoral head.

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22
Q

Prognosis of Perthes disease.

A

Over time, there is revascularisation and neovascularisation and healing of the femoral head.

However, this can lead to early hip arthritis.

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23
Q

Presentation of Perthes disease.

A
  • pain in the hip or groin
  • limp
  • restricted hip movements
  • referred pain to the knee

No history of trauma

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24
Q

Diagnostic workup of Perthes disease.

A
  • xray of affected joint (showing AVN of femur)
  • blood tests (normal)
  • MRI scan
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25
Q

Management of Perthes disease.

A

Conservative management initially:
- bed rest
- traction
- crutches
- analgesia for pain

Physiotherapy is used to retain the range of movement in the muscles and joints.

Regular xrays to assess healing.

Surgery used in severe cases, older children or those that are not healing.

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26
Q

What is slipped upper femoral epiphysis?

A

SUFE is where the head of the femur is displaced across the growth plate.

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27
Q

Risk factors for SUFE.

A
  • obesity
  • age 8-15 years
  • male
  • growth spurt
  • minor trauma
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28
Q

Presentation of SUFE.

A

Minor trauma that triggers the onset of symptoms:
- hip, groin, thigh or knee pain
- restricted range of hip movement
- painful limp
- restricted movement in the hip (particularly internal rotation)

Pain is disproportionate to the severity of trauma.

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29
Q

Diagnostic workup of SUFE.

A

xray of affected joint.

Blood tests are normal.

CT scan or MRI may be considered for surgical planning.

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30
Q

Management of SUFE.

A

Surgery is required to return the femoral head to the correct position and fix it in place to prevent it slipping further.

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31
Q

What is osteomyelitis?

A

Infection in the bone and bone marrow, typically occurring in the metaphysis of the long bones.

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32
Q

Most common causative organism of osteomyeltitis.

A

Staphylococcus aureus.

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33
Q

How can osteomyelitis be introduced?

A
  • open fracture
  • haematogenous
34
Q

Risk factors for osteomyelitis.

A
  • open bone fracture
  • orthopaedic surgery
  • immunocompromised
  • sickle cell anaemia
  • HIV
  • tuberculosis
35
Q

Presentation of osteomyelitis.

A
  • refusing to weight bare
  • pain
  • swelling
  • tenderness
  • fever
36
Q

Diagnostic workup of osteomyelitis.

A
  • xray
  • bone scan
  • CRP and ESR raised
  • WCC
  • blood culture
  • bone marrow aspiration
  • bone biopsy
37
Q

Management of osteomyelitis.

A

Extensive and prolonged antibiotic therapy.

Surgical drainage and debridement of the infected bone.

38
Q

Most common age affected by osteosarcoma.

A

10 - 20 years

39
Q

Common sites of osteosarcoma.

A
  • femur
  • tibia
  • humerus
40
Q

Presentation of osteosacoma.

A

Persistent bone pain:
- worse at night
- wake from sleep

Bone swelling, palpable mass and restricted joint movements may be present.

41
Q

Diagnostic workup for osteosarcoma.

A

Urgent xray (48 hours).

LFTs showing raised ALP.

Further scans can better define the lesion and stage the cancer:
- CT scan
- MRI scan
- bone scan
- PET scan
- bone biopsy

42
Q

Xray appearance of osteosarcoma.

A

Poorly defined lesion in the bone, with destruction of normal bone and a ‘fluffy’ appearance.

There will be periosteal reaction described as a sunburst appearance.

43
Q

Management of osteosarcoma.

A

Surgical resection of the lesion, often with limb amputation.

Adjuvant chemotherapy is used alongside surgery to improve outcomes.

44
Q

MDT involved in managing osteosarcoma.

A
  • paediatric oncologists
  • specialist nurses
  • physiotherapy
  • occupational therapy
  • psychology
  • dietician
  • prosthetics and orthotics
  • social services
45
Q

Complications of osteosarcoma.

A
  • pathological bone fracture
  • metastasis
46
Q

What is talipes?

A

Fixed abnormal ankle position that presents at birth - AKA clubfoot.

47
Q

Examination findings of

a) Talipes equinovarus

b) Talipes calcaneovalgus

A

a) plantar flexion and supination

b) dorsiflexion and pronation

48
Q

Treatment of talipes

A

Ponseti method:

Foot is manipulated toward a normal position and a cast is applied to hold is in position.

Eventually, an achilles tenotomy is used to release tension in the achilles tendon.

49
Q

What is positional talipes?

A

Resting position of the ankle is plantarflexion and supination, however it is not fixed in this position.

It will resolve with time and physiotherapy.

50
Q

What is developmental dysplasia of the hip?

A

Structural abnormality in the hips caused by abnormal development of the fetal bones during pregnancy.

This leads to instability in the hips and a tendency for potential for subluxation or dislocation.

51
Q

Risk factors for developmental dysplasia of the hip.

A
  • first degree family history
  • breech presentation
  • multiple pregnancy
52
Q

Screening for developmental dysplasia of the hip.

A

Often picked up on the NIPE at birth and/or 6-8 weeks old.

53
Q

NIPE findings consistent with developmental dysplasia of the hip.

A
  • different leg lengths
  • restricted hip abduction on one side
  • significant bilateral resistance in abduction
  • difference in knee level when hips flexed
  • clunking of the hips on special tests
54
Q

What are the special tests used to test for developmental dysplasia of the hip?

A

Ortolani test - pressure to abduct the hips and try to dislocate anteriorly.

Barlow test - downward pressure on adducted and flexed knees to see if femoral head dislocated posteriorly.

55
Q

How is developmental dysplasia of the hips diagnosed?

A

Ultrasound of the hips.

56
Q

Management of developmental dysplasia of the hips.

A

Pavlik harness fitted to hold the femoral head in the correct position, allowing the acetabulum to mould around it.

Surgery is required when the harness fails or if the diagnosis is made after 6 months.

57
Q

What is rickets?

A

A deficiency in vitamin D or calcium resulting in defective bone mineralisation. This causes soft and deformed bones.

58
Q

Physiology of vitamin D synthesis.

A

A hormone created from cholesterol by the skin in response to UV radiation.

59
Q

Roles of vitamin D (normal physiology).

A
  • calcium and phosphate absorption from the kidneys and intestines
  • regulating bone turnover and promoting bone reabsorption
60
Q

Pathophysiology of Rickets.

A

Inadequate vitamin D levels leads to a lack of calcium and phosphate in the blood. This results in defective bone mineralisation.

Low calcium results in secondary hyperparathyroidism, stimulating increased reabsorption of calcium from bones. This causes further issues with bone mineralisation.

61
Q

Presentation of Rickets.

A
  • lethargy
  • bone pain
  • swollen wrists
  • bone deformity
  • poor growth
  • dental problems
  • muscle weakness
  • abnormal fractures
62
Q

Bone deformities characteristic of Rickets.

A
  • bowing of the legs
  • knock knees
  • delayed closure of sutures
  • delayed teeth (under-development of enamel)
63
Q

Risk factors for Rickets.

A
  • darker skin
  • lower exposure to sunlight
  • cold climates
  • time spent indoors
64
Q

Diagnostic workup of Rickets.

A
  • vitamin D (deficient)
  • serum calcium (low)
  • serum phosphate (low)
  • serum ALP (high)
  • PTH (high)
65
Q

Management of Rickets.

A

Referral to paediatrician.

Vitamin D supplementation - either via tablets or fortified formula feeding.

66
Q

Genetics of achondroplasia?

A

FGFR3 gene causes abnormal function of the epiphyseal plates, restricting bone growth in length.

Note homozygous gene mutations are fatal; pts with achondroplasia therefore have one normal gene and one abnormal gene.

This leads to short bones and short stature.

Most common cause of dwarfism.

67
Q

Features of achondroplasia.

A
  • short stature
  • short digits
  • bow legs
  • disproportionate skull
  • foramen magnum stenosis
68
Q

Achondroplasia associations.

A
  • recurrent otitis media
  • kyphoscoliosis
  • spinal stenosis
  • obstructive sleep apnoea
  • obesity
  • foramen magnum stenosis (cervical cord compression, hydrocephalus)
69
Q

Management of achondroplasia.

A

MDT:
- paediatricians
- specialist nurses
- physiotherapy
- occupational therapists
- dieticians
- orthopaedic surgeons
- ENT surgeon
- geneticists

There is no cure for the underlying genetic condition.

70
Q

Prognosis of achondroplasia.

A

Normal life expectancy.

Obesity due to small stature.

Psychosocial implications to disproportionate short stature.

71
Q

What is Osgood-Schlatters disease?

A

Inflammation at the tibial tuberosity where the patellar ligament inserts - it is a common cause of anterior knee pain in adolescents.

72
Q

Pathophysiology of Osgood-Schlatter disease.

A

Stress from running, jumping and other movements causes stress on the tibial tuberosity, where the patellar tendon inserts.

As the tibial tuberosity is at the epiphyseal growth plate, this causes inflammation of the growth plate. It also results in multiple avulsion fractures, leading to growth of the tibial tuberosity.

73
Q

Presentation of Osgood-Schlatter disease.

A

Gradual onset of symptoms:
- visible / palpable lump at the tibial tuberosity
- pain in anterior knee
- pain exacerbated by physical activity, kneeling and on extension of knee

74
Q

Management of Osgood-Schlatter disease.

A
  • reduction in physical activity
  • ice
  • NSAIDs for symptomatic relief

Once symptoms settle, stretching and physiotherapy can be used to strengthen the joint and improve function.

75
Q

Prognosis of Osgood-Schlatter disease.

A

Symptoms will fully resolve over time - patient is left with a hard boney lump on their knee.

76
Q

Complications of Osgood-Schlatter disease.

A

Full avulsion fracture of tibial tuberosity, requiring surgical intervention.

77
Q

What is osteogenesis imperfecta?

A

A genetic condition that disrupts the formation of collagen, causing brittle bones that are prone to fracture.

78
Q

Presentation of osteogenesis imperfecta.

A
  • hypermobility
  • blue / grey sclera
  • repeated fractures
  • deafness from early adulthood
  • joint and bone pain
79
Q

Diagnostic workup of osteogenesis imperfecta.

A

Clinical diagnosis - xrays can be helpful and genetic testing is available, but not routinely a part of diagnosis.

80
Q

Management of osteogenesis imperfecta.

A
  • bisphosphonates (increase bone density)
  • vitamin D supplementation

MDT:
- physiotherapy and occupational therapy
- paediatricians
- orthopaedic surgeons for fractures
- specialist nurses
- social workers

Year 4 - Paediatrics (17 decks)

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