MSK Disorders Flashcards
What is transient synovitis and who does it tend to affect? What is a red flag which should make you reconsider this Dx?
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
How would a child with transient synovitis present and how would you manage them?
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
What criteria can be used to distinguish transient synovitis from septic arthritis?
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
What is septic arthritis and who does it commonly affect?
Infectious arthritis of the synovial joint (75% cases = hip)
- most common in children <2y
- often presents late
What causes septic arthritis? What are some RFs?
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]
How may a child with septic arthritis present?
Sx:
- Single joint affected, usually hip
- Painful/tender, red, warm, reduced ROM (infants will hold limb still - pseudoparalysis and cry)
- Acutely unwell, febrile child
How would you investigate and manage a child with suspected septic arthritis?
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
What is JIA or Still’s disease?
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
How is JIA classified? How may a child present with JIA and Still’s disease?
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
How would you investigate a child with suspected JIA?
Ix:
- Clinical Dx
- Bloods (FBC, CRP/ESR, ANA, RhF, anti-CCP)
- Imaging (classification and prognosis) -> USS +/- MRI
How would you manage a child with JIA?
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
What is reactive arthritis and some common causative organisms?
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)
How would a patient present with reactive arthritis?
Sx:
- > Transient joint swelling (<6w), often the ankles or knees
- > Follows evidence of extra-articular infection
- > Low-grade fever
- > May also have urethritis, conjunctivitis
How would you investigate and manage a child with reactive arthritis?
Ix:
- > Dx of exclusion
- > Normal XR
- > Bloods show normal/mildly elevated CRP
Mx:
- > NSAIDs/Analgesia
- > Self-limiting
What is SUFE and who does it tend to affect?
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
How would SUFE present? (Hx and O/E)?
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
How would you investigate and manage SUFE? What is a key sign on Ix?
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
What is DDH and how do we typically screen for it?
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
What are some risk factors for DDH?
Affects 1-3% of births
RFs:
- > Female (5x more>males)
- > Breech presentation
- > FHx
- > others: restricted intrauterine space = oligohydramnios, first born, multiple pregnancy, high BW
How would DDH present?
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
How would you Ix for DDH?
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
How would you manage DDH?
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)
What is Perthe’s disease? Who does it affect?
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
How does Perthe’s disease present?
Sx:
- insidious presentation
- hip/knee pain, limp
- limb shortening !!
How would you investigate suspected Perthe’s disease?
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
How would you manage a child with Perthe’s disease?
Mx:
- Analgesia for pain
- if <6 years : observe+mobilisation w monitoring, non-surgical containment with splints
- if >6 years : surgery
What is osteochondritis dissecans?
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
What is chondromalacia patellae? How is it managed?
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
What is OSD? How and in who does it present?
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
How would you Ix and Mx OSD?
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
What is Osteomyelitis? Who does it commonly affect and what is the most common organism?
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
How may a child with osteomyelitis present?
Sx:
- Fever
- Acute onset limb pain
- Immobile, swollen skin, tender and erythematous
How would you investigate a child with suspected osteomyelitis?
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
How would you manage a child with osteomyelitis? (acute + chronic)
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
