MSK Disorders Flashcards

1
Q

What is transient synovitis and who does it tend to affect? What is a red flag which should make you reconsider this Dx?

A

Irritable hip, usually affects those 3-10 years old (most common cause of hip pain in children)

-> If aged <3 with an acute limp then URGENT hospital assessment is required

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2
Q

How would a child with transient synovitis present and how would you manage them?

A

Present with:

  • Acute hip pain associated with a viral infection
  • Low grade fever

Ix and Mx:

  • Clinical diagnosis
  • Rule out other Dx if queried (pGALS, ESR/CRP, FBC)
  • Self limiting
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3
Q

What criteria can be used to distinguish transient synovitis from septic arthritis?

A

Kocher Criteria:

  • > more likely to be septic arthritis if:
  • Temperature >38.5 [1]
  • Unable to weight bear on limb [1]
  • ESR >40 [1]
  • WCC >12 [1]

Score of 0 = unlikely SA, 1 = 3% SA risk, 2 = 40%, 3 = 93% and 4 = 100% risk of SA

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4
Q

What is septic arthritis and who does it commonly affect?

A

Infectious arthritis of the synovial joint (75% cases = hip)

  • most common in children <2y
  • often presents late
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5
Q

What causes septic arthritis? What are some RFs?

A

Usually due to haematogenous spread (e.g. puncture around or infected skin lesions)

RFs:

  • Arthritis (RhA, Osteoarthritis, Crystal arthritis)
  • Joint prosthesis
  • Chronic disease, immunosuppression

Organism = usually Staph Aureus [but Salmonella is also associated in those with sickle cell disease]

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6
Q

How may a child with septic arthritis present?

A

Sx:

  • Single joint affected, usually hip
  • Painful/tender, red, warm, reduced ROM (infants will hold limb still - pseudoparalysis and cry)
  • Acutely unwell, febrile child
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7
Q

How would you investigate and manage a child with suspected septic arthritis?

A

Ix:

  • Septic screen
  • Bloods = FBC, CRP/ESR, cultures
  • Joint aspiration and MC&S
  • Imaging - XR (1st line but not evident until >2-3w of symptoms), MRI (2nd line shows soft tissue and effusions)

Mx:
= Antibiotics -> IV (2w) then Oral (4w)
> 1st line = Flucloxacillin
> 2nd line = Clindamycin (in pen-allergy), Vancomycin (if MRSA caused), 3rd gen cephalosporin e.g. Cefotaxime (if Gram-negative)

+ Joint wash out and aspirated to dryness as required (through closed needle aspiration or athroscopically)
- Surgical drainage may be required

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8
Q

What is JIA or Still’s disease?

A

JIA = juvenile idiopathic arthritis where there is persistent joint swelling (6w+) presenting in this aged <16, in the absence of infection/other defined cause

  • > 95% have disease distinct from adult RhA
  • > 1/1000 children affected
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9
Q

How is JIA classified? How may a child present with JIA and Still’s disease?

A

7 clinical subtypes which is based on number of joints affected in first 6 months and presence of HLA B27 and RhF

  • Polyarthritis = >4 joints
  • Oligoarthritis = less than or =4
  • Systemic with fever and rash = Still’s*

Sx:
> Gelling (stiffness following rest periods)
> Morning stiffness and joint pain
> Intermittent limp
> Limited movement
*late signs:
» inflammation +/- bone expansion i.e. knock knees)
» SALMON coloured macular rash (systemic JIA)
» intermittent fever
» Visual impairment - chronic anterior uveitis
» Swan neck deformity and hand problems

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10
Q

How would you investigate a child with suspected JIA?

A

Ix:

  • Clinical Dx
  • Bloods (FBC, CRP/ESR, ANA, RhF, anti-CCP)
  • Imaging (classification and prognosis) -> USS +/- MRI
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11
Q

How would you manage a child with JIA?

A

Mx:

  • > MDT rheumatology approach
  • OT and PT involvement as inactivity leads to disability and decreased bone mass
  • > Analgesia (NSAIDs)
  • > I Intra-articular, oral or IV corticosteroids are useful adjunctive agents (whilst waiting for second-line agents to have an effect) – avoided if possible due to risk of growth suppression and osteoporosis!!
  • > DMARDs e.g. oral/SC methotrexate or 2nd line is sulfasalazine
  • > Biologics e.g. anti-TNF

Prognosis:

  • Most children can expect good disease control and QoL
  • Poor control leads to significant morbidity from joint damage (fractures from osteoporosis) and visual impairment (anterior uveitis)
  • Ensure growth is occurring, no anaemia etc
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12
Q

What is reactive arthritis and some common causative organisms?

A

Reactive arthritis is an inflammatory arthritis occurring after exposure to particular genitourinary or GI infections.

Preceding common causes:

  • > Enteric bacteria (salmonella, shigella, campylobacter, Yersinia)
  • > Viral infections
  • > STIs (in adolescents)
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13
Q

How would a patient present with reactive arthritis?

A

Sx:

  • > Transient joint swelling (<6w), often the ankles or knees
  • > Follows evidence of extra-articular infection
  • > Low-grade fever
  • > May also have urethritis, conjunctivitis
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14
Q

How would you investigate and manage a child with reactive arthritis?

A

Ix:

  • > Dx of exclusion
  • > Normal XR
  • > Bloods show normal/mildly elevated CRP

Mx:

  • > NSAIDs/Analgesia
  • > Self-limiting
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15
Q

What is SUFE and who does it tend to affect?

A

SUFE = slipped upper femoral epiphysis

  • > Displacement of the epiphysis/femoral head posterio-inferiorly
  • > requires prompt treatment to prevent avascular necrosis
  • > Affects those aged 10-15y i.e. during growth spurts
  • > 20% cases are bilateral
  • > RF = OBESITY, male, metabolic/endocrine disease
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16
Q

How would SUFE present? (Hx and O/E)?

A

Sx:

  • Limp/Hip pain (+referred to the knee)
  • insidious or acute onset, i.e. after minor trauma

O/E:

  • LOSS of internal rotation of a flexed hip
  • +ve Trelendenburg test
17
Q

How would you investigate and manage SUFE? What is a key sign on Ix?

A

Ix:

  • Hip XR [of BOTH hips] in AP and frog-lateral view
  • -> Trethowan sign, metaphyseal blanch sign

Mx:

  • > Bed bound
  • > Analgesia
  • > Surgical internal fixation at the growth plate
18
Q

What is DDH and how do we typically screen for it?

A

DDH = developmental dysplasia of the hip
-> spectrum of conditions affecting the joint between the femoral head and acetabulum

Early detection is key to avoid hip dysplasia/complex treatment needs:
-> NIPE exams at birth and 6w aim to screen for this by use of Barlow (adduction/posterior-dislocate) and Ortolani (abduction-relocate) manoeuvres

19
Q

What are some risk factors for DDH?

A

Affects 1-3% of births

RFs:

  • > Female (5x more>males)
  • > Breech presentation
  • > FHx
  • > others: restricted intrauterine space = oligohydramnios, first born, multiple pregnancy, high BW
20
Q

How would DDH present?

A

Sx:

  • Neonatal screening tests +ve
  • Asymmetrical skin folds
  • Limb-length discrepancy (Galeazzi sign - baby on back, legs together and need flexed - observe leg length)
  • LATER: Limp/abnormal gait, delayed crawling
21
Q

How would you Ix for DDH?

A

Ix:
-> <6m = B+O manoeuvres [+ USS if suspicion remains/RFs present**]

-> 6m+ = X-ray

  • *USS is done at 6w regardless for those:
  • > Born breech
  • > Breech at 36w
  • > FHx (1st degree) of DDH
22
Q

How would you manage DDH?

A

Mx:
1st line (newborn/<6m):
-> Pavlik harness worn constantly for several weeks
- most spontaneously resolve by 3-6w
- harness keeps hips flexed and abducted
- progress monitored by repeat USS/XR
- complications = avascular necrosis, temporary demoral nerve palsy

2nd line (>6m)
-> Surgical correction (if conservative measures fail/no progress with harness)
23
Q

What is Perthe’s disease? Who does it affect?

A

Avascular necrosis of the femoral epiphysis from an interruption of blood supply (osteochondritis) –> then followed by revascularisation and resossification over 18-36m
-> Complication = premature fusion of growth plates and osteoarthritis

Affects mainly boys (5x more>girls) aged 4-8y

  • Bilateral in 10-20%
  • Commonly mistaken for transient synovitis
  • RF = short, hyperactivity
24
Q

How does Perthe’s disease present?

A

Sx:

  • insidious presentation
  • hip/knee pain, limp
  • limb shortening !!
25
Q

How would you investigate suspected Perthe’s disease?

A

Ix:

  • Examination = when pt is supine and the affected hip is rolled internally and externally –> guarding or spasm, particularly on internal
  • bilateral hip XR (+/- MRI as early stages may not show on XR)
  • -> increased density of femoral head THEN
  • -> flattened/fragmented and irregular femoral head
26
Q

How would you manage a child with Perthe’s disease?

A

Mx:

  • Analgesia for pain
  • if <6 years : observe+mobilisation w monitoring, non-surgical containment with splints
  • if >6 years : surgery
27
Q

What is osteochondritis dissecans?

A

Reduced blood flow leading to cracks in the articular cartilage and subchondral bone –> avascular necrosis –> fragmentation of bone and cartilage –> pain on activity

Sx:

  • pain after exercise
  • catching/locking/giving way
28
Q

What is chondromalacia patellae? How is it managed?

A

Anterior knee pain from the degradation of the articular cartilage on the posterior patellar surface
- Common in young adults from overuse during physical activity

Sx:

  • Knee pain (anterior)
  • Pain exacerbated by running, climbing stairs, getting up from chairs/squatting
  • Painless passive movements but repeated extension –> GRATING sensation and pain

Mx: Phsyiotherapy

29
Q

What is OSD? How and in who does it present?

A

Osgood-Schlatter Disease:

  • Osteochondritis (inflammation of the cartilage or bone) of the patellar tendon insertion at the knee
  • 4% of 10-15y physically active
  • Bilateral in 25-50%
  • may be caused by many small avulsion fractions from quad contractions as they also insert here

Sx:

  • Gradual knee pain after exercise, relieved by rest
  • Localised tenderness and swelling over tibial tuberosity
  • Hamstring tightness
30
Q

How would you Ix and Mx OSD?

A

Ix:

  • Clinical diagnosis +/- XR (as indicated by the Ottawa knee rules)
  • XR shows fragmentation of the tibial tubercle and overlying soft tissue swelling

Mx:

  • Analgesia (NSAIDs/Paracetamol)
  • Supportive: Ice-packs (less than 3/day for 10-15 mins), Protective knee pads, Stretching
  • Reassure that will resolve over time but may persist until the end of a growth spurt
  • Advise stopping/reducing all sport activity/limit jumping and running due to heavy quads involvement
  • Then when Sx resolve/decrease can gradually increase exercise levels and introduce low-impact quad exercises like cycling/swimming
31
Q

What is Osteomyelitis? Who does it commonly affect and what is the most common organism?

A

Infection of the metaphyses of long bones - most commonly the distal femur and the proximal tibia

  • > Children <5y usually affected
  • > Often due to haematogenous spread; commonly Staph. Aureus

Note: growth plates in children can PREVENT further spread into joints but in infants, before maturation of these plates, there can still be joint destruction

32
Q

How may a child with osteomyelitis present?

A

Sx:

  • Fever
  • Acute onset limb pain
  • Immobile, swollen skin, tender and erythematous
33
Q

How would you investigate a child with suspected osteomyelitis?

A

Ix:

  • Septic screen
  • Bloods - cultures, FBC, CRP/ESR
  • Imaging = XR (but can often be normal early on so also may use MRI)
  • Joint aspiration + MC&S
34
Q

How would you manage a child with osteomyelitis? (acute + chronic)

A

Acute Osteomyelitis Mx:
- High dose IV empirical –> narrow spectrum Abx [2-4w]
1st line –> Flucloxacillin
2nd line –> Clindamycin (pen-allergy), Vancomycin (MRSA)
- Children <5 may receive Cefazolin/Cefuroxime instead
-> Cultures BEFORE starting ABx
-> Transition from IV to oral once CRP is normal, child is afebrile and clinical improvement –> 3-4w of Abx
-> Surgical debridement may be necessary if deadline/biofilm

Chronic Mx:

  • Clinical assessment and disease staging (Cierny-Meder classification
  • IV Abx
  • Surgical debridement
  • Functional rehabilitation