MSK 3

Question 1

What is reactive arthritis?

Answer 1

most common form of arthritis in childhood
it is characterised by transient joint swelling (<6 weeks) often of the ankles or knees
it usually follows evidence of extra-articular infection
enteric bacteria are often the cause in children, but viral infections, STIs in adolescents, Mycoplasma & Borrelia burgdoferi (Lyme disease) are other causes
• Enteric bacteria- Salmonella, Shigella, Campylobacter & Yersinia

Question 2

How is reactive arthritis classified?

Answer 2

o Post-streptococcal- rarely seen in developed countries, requires antibiotic treatment
o Classical reactive- inflammation in the absence of bacteria in the joint space
o Post-infective- includes most other

Question 3

How does reactive arthritis present clinically and on investigation?

Answer 3

• Fever is low grade- with inflammation of joints, skin, mucous membranes, urinary and GI tract, the eyes are also commonly affected
• CRP is normal or mildly elevated- X-rays are normal- no treatment or only NSAIDs are required and complete recovery can be anticipated
• HLA-B27 is positive in 65-96% of patients

Question 4

What is the management for reactive arthritis?

Answer 4

• Chronic cases may require steroids and methotrexate if there is no active infection
patient should rest and avoid using the affected joint, as the symptoms improve there should be a graded programme of exercise that is designed to strengthen affected muscle groups and improve the range of movement.

Question 5

What is Perthe’s disease?

Answer 5

avascular necrosis of the capital femoral epiphysis of the femoral head due to interruption of the blood supply- followed by revascularisation and reossification over 18-36 months
Affects boys (5:1) of 5-10yrs
• Prognosis is dependent on early diagnosis- if identified early and less than half the femoral head is affected, only bed rest and traction may be required
Prognosis better in those below 6

Question 6

How does Perthe’s disease present?

Answer 6

presentation is insidious, with the onset of a limp, hip, knee pain- the condition may be mistaken for transient synovitis
it is bilateral in 10-20%
X-ray: increased density in the femoral head, which subsequently becomes fragmented and irregular

Question 7

What is the management for Perthe’s disease?

Answer 7

femoral head needs to be covered by the acetabulum to act as a mould for the re-ossifying epiphysis and is achieved by maintaining the hip in abduction with plaster or calipers, or by performing femoral or pelvic osteotomy
potential for subsequent degenerative arthritis in adult life

Question 8

What is slipped upper femoral ephiphysis SUFE?

Answer 8

Results in displacement of the epiphysis of the femoral head postero-inferiorly requiring prompt treatment in order to prevent avascular necrosis
• It is most common at 10-15yrs of age during the adolescent growth spurt- particularly in obese boys (x2.4) and is bilateral in 20%
Associated with metabolic endocrine abnormalities- hypothyroidism and hypogonadism

Question 9

How does SUFE present?

Answer 9

Limp or hip pain, may be referred to the knee- onset may be acute, following minor trauma or insidious
Restricted abduction and internal rotation of the hip
• Diagnosis is confirmed on x-ray- a frog lateral view should also be requested

Question 10

What is the management for SUFE?

Answer 10

Surgical, usually with pin fixation in situ
based on whether the condition is acute or chronic (>3 weeks) and whether the joint can bear weight or not- following surgery a patient is given crutches for 6-8 weeks to reduce weight bearing, along with a course of physiotherapy
• Analgesia including NSAIDs should also be provided

Question 11

What is transient synovitis?

Answer 11

Most common cause of acute hip pain in children- it occurs in children aged 2-12 years old
it often follows or is accompanied by a viral infection
Managed with bed rest, rarely skin traction- improves within a few days

Question 12

How does transient synovitis present?

Answer 12

sudden onset of pain in the hip or a limp, there is no pain at rest, but there is decreased range of movement, particularly internal rotation, the pain may be referred to the knee
the child is afebrile or has a mild fever and does not appear ill
• In a small proportion of children, transient synovitis precedes the development of Perthes disease

Question 13

What is the pathophysiology of Rickets?

Answer 13

• Vitamin D deficiency usually results from deficient intake or defective metabolism of vitamin D- causing a low serum calcium
• This triggers the secretion of parathyroid hormone and normalises the serum calcium but demineralises the bone
• Parathyroid hormone causes renal losses of phosphate and consequently low serum phosphate levels 
further reducing the potential for bone calcification.

Question 14

What is the aetiology of Ricket’s?

Answer 14

Nutritional
breast-fed in late infancy
extremely preterm infants from dietary deficiency of phosphorus, together with low stores of calcium & phosphorus
• Children with malabsorptive conditions, such as CF, coeliac disease and pancreatic insufficiency
• Drugs, especially anti-convulsants (phenobarbital & phenytoin) interfere with the metabolism of vitamin D and may also cause rickets
• Rickets may also result from impaired metabolic conversion or activation of vitamin D- hepatic and renal disease

Question 15

What are the risk factors for nutritional (primary) Ricket’s?

Answer 15

o Living in northern latitudes
o Dark skin
o Decreased exposure to sunlight  e.g. in some Asian children living in the UK
o Maternal vitamin D deficiency
o Diets low in calcium, phosphorus and vitamin D  e.g. exclusive breast- feeding into late infancy or, rarely,
toddlers on unsupervised ‘dairy-free’
diets
o Macrobiotic  strict vegan diets
o Prolonged parenteral nutrition in infancy with an inadequate supply of parenteral calcium and phosphate
• Intestinal malabsorption
o Small bowel enteropathy  e.g. coeliac disease
o Pancreatic insufficiency  e.g. cystic fibrosis
o Cholestatic liver disease
o High phytic acids in diet  e.g. chapattis
• Defective production of 25(OH)D2
o Chronic liver disease
• Increased metabolism of 25(OH)D3
o Enzyme induction by anticonvulsants
 e.g. phenobarbital
• Defective production of 1,25(OH)2D3
o Hereditary type I vitamin D-resistant (or dependent) rickets  mutation which abolishes activity of renal hydroxylase
o Familial (X-linked) hypophosphataemic rickets  renal tubular defect in phosphate transport
o Chronic renal disease
o Fanconi syndrome  renal loss of phosphate
• Target organ resistance to 1,25(OH)2D3
o Hereditary vitamin D-
dependent rickets type II  due to mutations in vitamin D receptor gene

Question 16

What is the clinical presentation of Ricket’s?

Answer 16

ping-pong ball sensation of the skull (craniotabes) elicited by pressing firmly over the occipital or posterior parietal bones
o	Misery
o	Failure to thrive/short stature
o	Frontal bossing of skull
o	Craniotabes
o	Delayed closure of anterior fontanelle
o	Delayed dentition
o	Rickety rosary
 o	Harrison sulcus
o	Expansion of metaphysis (especially wrist)
o	Bowing of weight-bearing bones (legs)
o	Hypotonia
o	Seizures (late)

Question 17

How is Ricket’s diagnosed?

Answer 17

• Dietary history for vitamin & calcium intake
• Blood tests
o Serum calcium- low or normal
o Phosphorus- low
o Plasma alkaline phosphatase activity- greatly increased
o 25-hydroxyvitamin D- may be low
o PTH- elevated
• X-ray of the wrist joint- shows cupping and fraying of the metaphyses and a widened epiphyseal plate

Question 18

What is the management for Ricket’s?

Answer 18

• Nutritional rickets is managed by advice about a balanced diet, correction of predisposing risk factors and by the daily administration of vitamin D3 (cholecalciferol)
• If compliance is an issue -a single oral high dose of vitamin D3 can be given, followed by the daily
maintenance dose
• Healing occurs in 2-4 weeks and can be monitored from the lowering of alkaline phosphatase, increasing vitamin D levels and healing on x-rays- but complete reversal of bony deformities may take year