Paediatric orthopaedics Flashcards

1
Q

What is the growth plate ?

A
  • Part of the bone between the metaphysis and epiphysis found in the bones of children.
  • Made of hyaline cartilage and allow bones to grow in length before fusing
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2
Q

What are the 8 types of paediatric fracture?

A
  • Buckle (torus)
  • Transverse
  • Oblique
  • Spiral
  • Segmental
  • Salter-Harris (growth plate fracture)
  • Comminuted (brreaks into a no. of different pieces)
  • Greenstick (one side of the bone breaks, the other remains in tact).
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3
Q

Explain the Salter-Harris classification of growth plate fractures.

A
  • I : Physis only
  • II : Physis and metaphysis
  • III : Physis and epiphysis to include the joint
  • IV : Physis, metaphysis and epiphysis
  • V : Crush injury
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4
Q

What are the 2 principles of managing a fracture ?

A
  • Mechanical alignment with either : closed or open reduction
  • Provide relative stability
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5
Q

What are the two steps to pain management in children.

A
  1. Paracetamol or ibuprofen
  2. Morphine
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6
Q

what pain killers are avoided in children ?

A

-> Codeine and tramadol due to unpredictability of metabolism.
-> Aspirin : risk of reye’s syndrome

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7
Q

Explain the causes of hip pain in children related to age

A

~ 0-4 : septic arthritis, DDH, transient synvotitis

~ 5-10 : septic arthritis, transient synovitis, perthes disease

~ 10-16 : septic arthritis, SUFE and JIA

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8
Q

What are the 7 criteria for urgent referral for assessment in a limping child ?

A
  • Child under 3 years
  • Child older than 9 with a restricted or painful hip
  • Not able to weight bear
  • Evidence of neurovascular compromise
  • Severe pain or agitation
  • Red flags for serious pathology
  • Suspicion of abuse
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9
Q

Give 10 red flags for hip pain

A
  • Child under 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 and when is it most common in children ?

A
  • Infection in a joint
  • <4 years
  • M>F
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11
Q

How does septic arthritis present ?

A

Usually knee or hip :

  • Hot, red, swollen and painful joint
  • Refusing to weight bear
  • Stiffness and reduced range of motion
  • Systemic symptoms such as fever, lethargy and sepsis
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12
Q

What is the most common causative agent of septic arthritis ?

A

Staph aureus

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13
Q

How is the most likely cause of septic arthritis in sexually active teenagers

A

Neisseria gonorrhoea

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14
Q

How is septic arthritis managed ?

A
  • Give empirical IV Abx until microbial sensitivities are known
  • Joint aspirate and send for : gram staining, crystal microscopy, culture and antibiotic sensitivities.
  • Abx continued for 3-6 wks.
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15
Q

what is the Kocher criteria for diagnosing septic arthritis ?

A
  • Fever >38.5 degrees C
  • Non-weight bearing
  • Raised ESR (> 40)
  • Raised WCC (> 12)
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16
Q

What is transient synovitis ?

A
  • Temporary irritation and inflammation in synovial membrane of the hip associated with a viral URTI
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17
Q

In what age group is transient synovitis most common ?

A

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

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18
Q

How does transient synovitis present ?

A
  • Limp/refusal to weight bear
  • Groin or hip pain
  • Low-grade fever : high fever is more suggestive of septic arthritis
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19
Q

How is transient synvotitis managed ?

A
  • Simple analgesia in primary care, if :

~ Limp is present for <48 hrs and are otherwise well

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20
Q

What is DDH

A
  • Structural abnormality of the hip increasing the risk of subluxation and dislocation
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21
Q

Give 7 RF for DDH

A
  • F>M
  • Breech presentation
  • First degree FHx
  • Birth weight >5kg
  • Oligohydramnios
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22
Q

When are babies screened for DDH

A

All babies are screened in the newborn check and 6 week baby check using Barlow and Ortolani test

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23
Q

Which infants will require a routine USS for DDH

A
  • First-degree family history of hip problems in early life
  • Breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery
  • Multiple pregnancy
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24
Q

What is done on clinical examination when looking for DDH

A

~ Barlow test: attempts to dislocate an articulated femoral head
~ Ortolani test: attempts to relocate a dislocated femoral head
~ Other : Symmetry of leg length, level of knees when hips and knees are bilaterally flexed, restricted abduction of the hip in flexion

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25
Q

What imaging is used to confirm the diagnosis of DDH

A
  • USS
  • However if >4.5 mnths old, X-ray is used 1st line.
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26
Q

How is DDH managed ?

A
  • <6mnths : Pavlik harness (6-8 wks)
  • > 6mnths : surgery with hip spica cast afterwards
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27
Q

What is Perthe’s disease

A
  • Degenerative conditon where there is disruption to the flow of blood leading to avascular necrosis of the femoral head (particularly the femoral epiphysis).
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28
Q

Who does perthe’s disease typically affect?

A

Boys aged 5-10

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29
Q

How does Perthe’s disease present ?

A

Slow onset of :

  • Pain in the hip or groin
  • Limp
  • Restricted hip movements
  • There may be referred pain to the knee

No Hx of trauma !

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30
Q

What other Ix are helpful in Perthe’s ?

A
  • Technetium bone scan
  • MRI scan
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30
Q

How is Perthe’s diagnosed ?

A

X-ray : early changes include widening of joint space, later changes include decreased femoral head size/flattening

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31
Q

How is perthe’s managed ?

A

AIM : maintain a healthy position and alignment of the joint.

  • Younger : bed rest, traction, crutches, analgesia
  • Older : surgery
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32
Q

What is the catterall staging of Perthe’s disease ?

A
  • Stage 1 : Clinical and histological features only
  • Stage 2 : Sclerosis with or without cystic changes and preservation of the articular surface
  • Stage 3 : Loss of structural integrity of the femoral head
  • Stage 4 : Loss of acetabular integrity
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33
Q

What are 2 complications of Perthe’s?

A
  • OA
  • Premature fusion of the growth plates
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34
Q

What is SUFE and who does it typically affecr ?

A
  • Slipped upper femoral epiphysis
  • The head of femur is displaced (posteriorly) along the growth plate.
  • Obese boys aged between 10 and 15.
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35
Q

How does SUFE present ?

A
  • Adolescent obese male going through a growth spurt.
  • Minor trauma disproportionate with the pain.
  • Hip, groin, thigh or knee pain
    Restricted range of hip movement
    Painful limp
    Restricted movement in the hip
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36
Q

What movement of the hip is restricted in SUFE ?

A
  • Internal rotation
37
Q

What is the investigation of choice in SUFE ?

A
  • AP and lateral X-ray
38
Q

How is SUFE managed ?

A

Internal fixation

39
Q

Give 4 complications of SUFE

A
  • OA
  • Avascular necrosis of the femoral head
  • Chondrolysis
  • Leg length discrepancy
40
Q

What is an osteosarcoma, who does it usually effect and what bone is most commonly involved ?

A
  • Bone cancer
  • Aged 10-20 yrs
  • Femur is most commonly affected BUT also affects the tibia and humerus
41
Q

How does an osteosarcoma present?

A
  • Persistent bone pain
  • Pain is worse at night and typically disturbs or wakes them from sleep .
42
Q

What do NICE recommend for a child presenting with unexplained bone pain or swelling ?

A

Urgent direct access xray within 48 hours

43
Q

What is seen on X-ray in an osteosarcoma ?

A
  • Poorly defined lesion
  • Destruction of normal bone with a ‘fluffy’ appearance
  • Periosteal reaction described to have a ‘sunburst’ appearance.
44
Q

What might be seen on bloods in someome with an osteosarcoma ?

A

Raised alkaline phosphatase (ALP)

45
Q

What are the main complications of an osteosarcoma ?

A
  • Pathological bone fractures
  • Metastasis
46
Q

What is osteomyelitis and what part of the bone does it usually effect ?

A
  • Infection of the bone and bone marrow
  • Metaphysis of long bones
47
Q

What are the most common causative agents of osteomyelitis ?

A
  • Staph aureus
  • In sickle cell anaemia -> Salmonella
48
Q

What children and more commonly affected by osteomyeltitis

A

Boys <10 yrs

49
Q

What RF predispose a child to osteomyelitis ?

A
  • Open bone fracture
  • Orthopaedic surgery
  • Immunocompromised
  • Sickle cell anaemia
  • HIV
  • TB
50
Q

How does osteomyelitis present ?

A
  • Refusing to use the limb or weight bear
  • Pain
  • Swelling
  • Tenderness
  • Afebrile / low grade fever. A high fever is more suggestive of septic arthritis
51
Q

What is the initial imaging for osteomyelitis and what is the best imaging

A
  • Initial : X-ray
  • Best : MRI
52
Q

How is osteomyelitis managed ?

A
  • flucloxacillin for 6 weeks
  • Clindamycin if penicillin-allergic
53
Q

what is Osgood-Schlatter diease and when does it typically occur?

A
  • Inflammation at the tibial tuberosity causing anterior knee pain
  • Males aged 10-15 and causes anterior knee pain
54
Q

How does Osgood-Schlatter present ?

A
  • Visible or palpable hard and tender lump at the tibial tuberosity
  • Pain in the anterior aspect of the knee
  • Pain is exacerbated by physical activity, kneeling and on extension of the knee
55
Q

How is Osgood-Schlatter’s managed ?

A
  • Reduction in physical activity
  • Ice
  • NSAIDS (ibuprofen) for symptomatic relief
56
Q

What is a rare complication of Osgood-Schlatter’s disease ?

A
  • Avulsion fracture -> the tibial tuberosity separates from the rest of the tibia
57
Q

Give the key features of
Chondromalacia patellae

A
  • Softening of the cartilage of the patella
  • Common in teenage girls
  • Characteristically anterior knee pain on walking up and down stairs and rising from prolonged sitting
  • Usually responds to physiotherapy
58
Q

Give the key features of Osteochondritis dissecans

A
  • Pain after exercise
  • Intermittent swelling and locking
59
Q

Give the key features of patellar subluxation

A
  • Medial knee pain due to
  • Lateral subluxation of the patella
  • Knee may give way
60
Q

Give the key features of patellar tendonitis

A
  • More common in athletic teenage boys
  • Chronic anterior knee pain that worsens after running
  • Tender below the patella on examination
61
Q

Define osteogenesis imperfecta

A

-Genetic condition resulting in brittle bones that are prone to fracture

62
Q

What causes osteogensis imperfecta ?

A
  • Genetic mutations that affect the formation of collagen

- 8 different genetic abnormalities with varying severities

63
Q

How does osteogenesis imperfecta present ?

A
  • Recurrent and inappropriate fractures
  • Hyper-mobility
  • Blue/grey sclera
  • Triangular face
  • Short stature
  • Deafness from early childhood
  • Dental problems
  • Bone deformities : esp bowed legs and scoliosis
  • Joint and bone pain
64
Q

How is osteogenesis imperfecta diagnosed ?

A
  • Usually clinical

- X-ray used in fractures and for bone deformitis

65
Q

How is osteogenesis imperfecta managed ?

A
  • Bisphosphonates to increased bone density (e.g. alendronate)
  • Vit D supplementation to prevent deficiency
  • Physio and occupational therapy
66
Q

Define rickets

A

-Defective bone mineralisation causing ‘soft’ and deformed bones

67
Q

What 2 vitamin deficiencies cause rickets ?

A
  • Vitamin D

- Calcium

68
Q

What are the sources of vitamin D?

A
  • Sunlight

- Eggs, oily fish or forified cereals

69
Q

What are the sources of calcium ?

A
  • Dairy productes

- Green vegetables

70
Q

What is a rare form of rickets?

A
  • Hereditary hypophosphataemic rickets
  • Genetic defect causing low phosphate
  • Most common : X-linked dominant
71
Q

What are the potential symptoms of rickets ?

A
  • Lethargy
  • Bone pain
  • Swollen wrists ! widening of joint space
  • Bone deformity
  • Poor growth
  • Dental problems ! no teeth development
  • Muscle weakness
  • Pathological or abnormal fractures
72
Q

What 5 bone deformities can occur in rickets?

A
  • Bowing of the legs
  • Knock knees
  • Rachitic rosary : ribs expand at the costochondral junctions causing lumps along the chest
  • Craniotabes : soft skull with delayed closure of sutures and frontal bossing
  • Delayed teeth
73
Q

What are the RF for rickets ?

A

Anything that increases the risk of vit d deficiency

  • Darker skin
  • Low exposure to sunlight
  • Live in colder climates
  • Spend majority of their time indoors
74
Q

What are the 5 common blood results in rickets ?

A
  • Serum 25-hydroxyvitamin D of less than 25 nmol/L
  • Calcium : low
  • Phosphate : low
  • Alkaline phosphatase : high
  • Parathyroid hormone : high
75
Q

What investigation is required to diagnose rickets ?

A
  • X ray

- May show joint widening and osteopenia (more radiolucent bones)

76
Q

How is rickets prevented ?

A
  • Breastfeeding women should taken vitamin D supplements (10 micrograms per day)
  • Formula fed babies are at lower risk as it is fortified with vitamin D
77
Q

How is rickets managed ?

A
  • Vitamin D (ergocalciferol) : 6mnths to 12 yrs is 6,000 IU per day for 8-12 wks
  • Calcium supplementation
78
Q

Explain the pathophysiology behind rickets

A
  • Low vitamin D
  • This leads to malabsorption of calcium and phosphate
  • Low calcium and phosphate leads to defective bone mineralisation
  • Low calcium leads to secondary hyperparathyroidism
  • Increased parathyroid hormone leads to increased calcium reabsorption from bone and further issues with bone mineralisation
79
Q

What is Talipes ?

A
  • Clubfoot : fixed abnormal ankle position

- Fixed abnormal ankle position presenting at birth

80
Q

What is talipes equinovarus ?

A

-Ankle in plantar flexion and supination

81
Q

What is talipes calcaneovalgus ?

A

-Ankle in dorsifelxion and pronation

82
Q

How is clubfoot managed ?

A

-Ponseti method

83
Q

What is the ponseti method ?

A
  • Used to treat club foot
  • The foot is manipulated towards a normal position and a cast used to hold it in position. This is repeated until the foot is in the correct position
  • A brace is then used to hold the feet in the correct position when not walking until around 4 yrs of age
84
Q

What is positional talipes ?

A
  • The ankle is in a plantar flexion and supination position but is not fixed
  • The muscles around the ankle are tight but the boney structure is not affected
  • Managed using physio
85
Q

What is achondroplasia ?

A
  • Most common common cause of disproportionate short stature (dwarfism)
  • It is a type of skeletal dysplasia
86
Q

What is the cause of achondroplasia?

A

-Genetic mutations in the FGFR3 gene (fibroblast growth factor receptor 3) on chromosome 4 leading to abnormal function of the epiphyseal plates.

87
Q

What kind of genetic inheritance leads to achondroplasia ?

A
  • Autosommal dominant -> heterozygous

- > Homozygous gene mutations are fatal in the neonatal period

88
Q

What are the main features of achondroplasia ?

A
  • Average height of 4 feet
  • Short digits
  • Bow legs
  • Disproportionate skull
  • Foramen magnum stenosis
  • Frontal bossing
89
Q

Give 6 associations with achondroplasia

A
  • Recurrent otitis media
  • Kyphoscoliosis
  • Spinal stenosis
  • Obstructive sleep apnoea
  • Obesity
  • Cervical cord compression and hydrocephalus as a result of foramen magnum stenosis
90
Q

<3 presenting with acute limp

A

Urgent paediatric assessment

91
Q

Estimated probability of septic arthritis based om kocher’s criteria

A
  • 0 points = very low risk
  • 1 point = a 3% probability of septic arthritis
  • 2 points = a 40% probability of septic arthritis
  • 3 points = a 93% probability of septic arthritis
  • 4 points = a 99% probability of septic arthritis