11. Locomotor + 12. Nutrition Flashcards

1
Q

What age does septic arthritis typically occur?

A

-Young children - half of cases present in first 2 years
-Twice as common in males

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2
Q

What causes septic arthritis?

A

-Osteomyelitis (neonates) - spreads via transphyseal vessels
-Haematogenous spread of infection / direct inoculation
-Infected skin wounds eg staph aureus, GBS, GAS
-Underlying joint disease (mostly lower limb)

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3
Q

How does septic arthritis present differently in different age groups?

A

-Hot, warm, swollen joint
-Inability to weight bear
INFANTS
-Typically do not appear systemically ill
OLDER CHILDREN
-Systemic symptoms - fever
-Acute onset
-Decreased range of movement + pain on passive movement

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4
Q

How should you investigate septic arthritis?

A

JOINT ASPIRATION (most useful)
-Synovial fluid gram stain + culture
Bloods
Imaging
-USS
-XR - widened joint space suggests effusion, may see late signs on subluxation / dislocation / erosive changes
-MRI to exclude osteomyelitis
-Bone scan if multiple sites
LP - only if H influenza is causative organism (risk of meningitis)

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5
Q

How should septic arthritis be managed?

A

-IV cefuroxime / vancomycin for 3 weeks followed by oral for a further 4-6 weeks
-Surgery if recurrent / hip involvement
-Physio to avoid joint stiffness
-Usually a good prognosis unless diagnosis is delayed
-10% recurrence so follow up is needed

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6
Q

What happens in developmental dysplasia of the hip compared to a normal hip?

A

-Normally, the femoral head fits firmly into the acetabulum socket
-In DDH, the acetabulum is shallow so does not adequately cover / secure the femoral head
-Can develop from birth, more common in left hip
-20% of cases are bilateral

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7
Q

What risk factors are there for DDH?

A

-Female sex
-Swaddling baby
-Breech position
-FHx
-First born
-Oligohydramnios
-High birth weight

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8
Q

How does DDH present?

A

-Delay in walking
-Waddling gait
-Shortened affected leg
-Hips examined on day 1 and at 6 weeks:
–BARLOW TEST = hips flexed and pressed down with finger over trochanter (would dislocate)
–ORTOLANI TEST = hips flexed and abducted (relocate a dislocated hip)
-Most fix themselves by 3-6 weeks

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9
Q

How would you managed DDH?

A

-Double nappies for 3 weeks
-Brace with Pavlik harness for 3 months if no suxxess
-Older children may require surgery
-Long term risk of OA, lower back pain

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10
Q

What causes irritable hip?

A

-Transient synovitis
-Acute hip pain associated with viral infection
-More common in boys aged 2-10

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11
Q

How does irritable hip present?

A

-Can vary from slight limp / difficulty weight bearing
-No systemic symptoms
-Single joint pain, no pain at rest
-Hx of viral URTI
-Normal Xray, raised CRP, USS may show effusion

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12
Q

How should irritable hip be managed?

A

-NSAIDs and rest - should resolve in 2 weeks
-If significant physical signs or ? infection refer to orthopaedics

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13
Q

What causes reactive arthritis and how does it present?

A

-Most cases follow a viral illness especially dysentry or STI
-May be part of Reiter’s syndrome (uveitis, urethritis, arthritis)
-Treat with NSAIDs

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14
Q

What is juvenile idiopathic arthritis?

A

-Joint inflammation lasting at least 6 weeks in <16s
-Associated with HLA-DR4
-May be:
–Oligoarticular (up to 4 joints)
–Polyarticular (>4 joints)
–Still’s Disease (systemic with fever, rash, uveitis, weight loss)

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15
Q

What biochemical changes would you expect to see on blood results in JIA?

A

-Increased WCC, ESR, CRP
-Negative rheumatoid factor
-Positive antinuclear factor (70% of polyarticular JIA)

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16
Q

How should JIA be managed?

A

-Mild exercise + rest each day, hot baths, NSAIDs
-Physio + splints
-Long term –> methotrexate, corticosteroids
-Resolves spontaneously in 80%

17
Q

What can cause a limp in a child?

A

-Growing pains
–Worse at night, pain in muscle not bone
-Irritable hip
-Septic arthritis
-Osteomyelitis
–Fever, diagnosed by radiography
-Perthes disease
–Necrosis of femoral head leading to fracture, sometimes following irritable hip
-Slipped capital femoral epiphysis
–Typically in overweight teenage boys, gradual onset
-JIA
-Neoplastic disease
-Trauma
-Osgood Schlatters
–Active children

18
Q

What is Perthe’s disease?

A

-Osteochondritis of the femoral head
-Typically occurs in 4-8 year-olds
-Caused by / can develop into avascular necrosis of femoral head

19
Q

How does Perth’s disease present?

A

-Progressive hip pain
-Reduced range of movement
-Leg length discrepancy, limp
-Widened joint space on Xray

20
Q

How should Perth’s disease be managed?

A

-If good appearance on imaging –> non-weight bearing callipers
-If poor appearance + >6 –> surgery

21
Q

How does a slipped upper femoral epiphysis present?

A

-Arthralgia
-Limp
-Restricted ROM
-Externally rotated hip. may be slightly shorter than the other, presents similarly to neck of femur fracture

22
Q

How should a slipped upper femoral epiphysis be managed?

A

-Surgical fixation + closure of epiphysis
-Bed rest + analgesia
-May lead to chondrolysis and AVN

23
Q

What is a normal calorie requirement for a child?

A

0-1yr = 110kcal/kg/day
1+ = 1000 + ageX100kcal/day
150ml of milk = 110kcal

24
Q

What can cause malnutrition?

A

-Diet low in protein, energy, micronutrients
-Diseases causing malabsorption
–Severe GORD
–Immunodeficiency
–Chronic infection
–CF
-Eating disorders

25
Q

How can you assess malnutrition?

A

Measuring:
-BMI
-Recent weight loss (>10% in 3 months = significant)
-Serial height + weight plot (fall of 2 centiles = significant)
-% Weight for height
-Mid-arm circumference divided by head circumference
-Detailed dietary assessment with 5-7 day food diary
-Serum albumin

26
Q

What main types of protein deficiency are there?

A

KWASHIORKOR
-Severe protein / amino acid deficiency
-Growth retardation
-Diarrhoea
-Apathy, anorexia
-Oedema
-Skin / hair depigmentation
-Abdo distension + fatty liver
-Hypoalbuminaemia + normo-microcytic anaemia
MARARSMUS
-Severe calorie deficiency
-Height is preserved
-Wasted appearance
-Muscle atrophy
-Diarhhoea / constipation
-Hypoalbuminaemia

27
Q

How should you manage severe malnutrition?

A

-Correct dehydration + electrolyte imbalance
-Treat underlying infections / parasites / concurrent / causative disease
-Treat specific nutritional deficiencies
-May need parental or central feeding
-Slow oral referring - caution of referring syndrome

28
Q

What is Rickets?

A

-Disorder of growing bone due to inadequate mineralisation (vitamin D, calcium, phosphate) as it is laid down at the epiphyseal growth plates
-Occurs in growing children

29
Q

What are the 3 characteristic stages of Rickets disease progression?

A
  1. Low plasma calcium + normal plasma phosphate
  2. Normal plasma calcium –> restored due to compensatory hyperparathyroidism
  3. Low plasma calcium + phosphate
    –Advanced bone disease, clinical features present
30
Q

How does Rickets present?

A

-Widening of the end of long bones
-Osteomalacia
–Inadequate mineralisation of mature bone
–Bone pain, fractures, muscle tenderness, proximal myopathy
-Growth delay / arrest
-Skeletal deformities
–Swelling of wrists + costochondral junctions
–Bowing of long bones
–Frontal cranial bossing
–Craniotabes (softening of the skull)

31
Q

What risk factors are there for Rickets?

A

-6-18 months
-Inadequate sun exposure
-Calcium / phosphate deficiency
-FHx
-Dark skin complexion

32
Q

What is the difference between vitamin D-dependent rickets type 1 + 2?

A

TYPE 1
-Autosomal recessive
-Enzyme deficiency (vit D remains in inactive form)
-Presents <2yrs
-Requires calcitriol to treat
TYPE 2
-Autosomal recessive
-Due to mutations in vit D receptor gene –> end-organ resistance to vitamin D
-Total alopecia
-Presents from birth / <1yr
-Requires supra physiological doses of calcitriol