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Local revision copy · not clinical advice

Infection

Topic 18 · slides 539–546 · 8 slides · 43 questions
8 slides
▸ Slide 539 · InfectionInfection · 2 questions expand
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slide 539
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Q1-Q22 questions — tap to reveal all answerslist
  1. What are the key orthopaedic infections in children?
  2. How would you assess and manage a child with a suspected bone or joint infection?
Answers · Q & A
Q1.What are the key orthopaedic infections in children?
  • Not covered in the speaker notes
Q2.How would you assess and manage a child with a suspected bone or joint infection?
  • Not covered in the speaker notes
▸ Slide 540 · Septic arthritisInfection · 8 questions 1 check expand
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slide 540
Question list
Q1-Q88 questions — tap to reveal all answerslist
  1. What is the differential diagnosis of unilateral hip pain in a child?
  2. What are the causes and risk factors for septic arthritis of the hip in a child?
  3. Describe the pathoanatomy of septic arthritis.
  4. Describe the Gachter classification of septic arthritis.
  5. Why is knee septic arthritis uncommon?
  6. What are the Kocher criteria and the probability of septic arthritis for each score?
  7. How is septic arthritis of the hip managed?
  8. How are the sequelae of septic arthritis of the hip classified and treated (Hunka classification)?
Answers · Q & A
Q1.What is the differential diagnosis of unilateral hip pain in a child?
  • Transient synovitis / osteomyelitis
  • Septic arthritis
  • Perthes disease
  • SCFE
  • Fracture (consider NAI)
  • JRA
Q2.What are the causes and risk factors for septic arthritis of the hip in a child?
  • Routes: haematological spread, direct inoculation, spread from osteomyelitis
  • Neonate with patent transphyseal artery, or the 4 intracapsular physes: proximal humerus, hip, radial head, distal fibula
  • Risk factors: prematurity, C-section (C section), history of invasive trauma
  • Recent infection (URTI, UTI); vaccine (especially H influenzae)
Q3.Describe the pathoanatomy of septic arthritis.
  • Metaphyseal collection from transphyseal vessel: low flow sharp-turn capillary ruptures and spreads to the joint
  • Synovial oedema and hypertrophy with fluid production
  • Frank pus destroys cartilage within 8hr (marginal and central portions) with joint space narrowing
  • Superficial marginal and central bony erosion, then bony ankylosis (chronic)
Q4.Describe the Gachter classification of septic arthritis.
  • 1. Synovitis
  • 2. Pus
  • 3. Cartilage
  • 4. Bone erosion
Q5.Why is knee septic arthritis uncommon?
  • The metaphyseal collection from the transphyseal vessel spreads to the joint only in intra-articular metaphyseal joints
  • The knee is not an intra-articular metaphyseal joint, so knee septic arthritis is uncommon
Q6.What are the Kocher criteria and the probability of septic arthritis for each score?
  • Unable to bear weight; fever >38.5; WBC >12; ESR >40
  • 1 criterion: 3%; 2: 40%; 3: 93%; 4: 99.6%
  • Caird modification (2006 JBJS): CRP >20
Q7.How is septic arthritis of the hip managed?
  • History of trauma, onset and duration of pain, constitutional symptoms; check skin for sinus and whether the child can weight bear
  • X-ray to rule out SCFE, Perthes, fracture; blood WBC, CRP, ESR; USG for effusion and aspiration
  • Drainage: open anterior hip approach, capsulectomy 1cm2, drill holes at metaphysis, thorough irrigation
  • Post-op hip spica for 4-6 weeks
  • Peltola NEJM 2014: a few days IV (3-5) then a short course of oral antibiotics (3 weeks)
Q8.How are the sequelae of septic arthritis of the hip classified and treated (Hunka classification)?
  • I minimal collapse/deformity
  • II head deformity (A intact physis, B physeal arrest) -> femoral osteotomy
  • III pseudoarthrosis -> head viable: BG + valgus osteotomy; head nonviable: resection of head and neck + GT arthroplasty
  • IV complete epiphysis destruction (A neck in acetabulum: adductor tenotomy, B neck not in acetabulum: GT arthroplasty)
  • V complete head and neck loss -> conservative
Fact check

Peltola NEJM 2014 showed that only a few days of IV (3-5) then a short course of oral antibiotics (3 weeks) is sufficient for uncomplicated joint sepsis — misattributed and imprecise — The NEJM 2014 Peltola paper is a review of acute osteomyelitis; the septic arthritis RCT (Clin Infect Dis 2009) showed 10 days total therapy (2-4 days IV then oral) was as effective as 30 days — source

▸ Slide 541 · Pathophysiology of acute osteomyelitisInfection · 10 questions expand
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slide 541
Question list
Q1-Q1010 questions — tap to reveal all answerslist
  1. Describe the pathophysiology of acute osteomyelitis.
  2. Why do bacteria proliferate in the metaphyseal region?
  3. What is a sequestrum?
  4. What is an involucrum?
  5. What is a cloaca?
  6. Which patients with acute osteomyelitis develop septic arthritis?
  7. What are the common pathogens of acute osteomyelitis by age group?
  8. What is the presentation and investigation of acute osteomyelitis?
  9. What are the indications for surgery in acute osteomyelitis?
  10. What are the complications of acute osteomyelitis?
Answers · Q & A
Q1.Describe the pathophysiology of acute osteomyelitis.
  • Haematological spread; bacteria adhere and proliferate in the metaphyseal region
  • Pus formation, drains along Haversian and Volkmann canals, then breaks out as a subperiosteal abscess
  • High intraosseous pressure + poor blood supply due to elevated periosteum -> bone ischaemia (vessel thrombosis) -> sequestrum
  • Subperiosteal new bone -> involucrum; pus breaks through involucrum -> cloaca
Q2.Why do bacteria proliferate in the metaphyseal region?
  • Hairpin turn with sluggish flow
  • Low oxygen tension
  • Acidic environment
Q3.What is a sequestrum?
  • Devitalised bone resulting from high intraosseous pressure and poor blood supply due to the elevated periosteum
  • Caused by bone ischaemia (blood vessel thrombosis)
Q4.What is an involucrum?
  • Subperiosteal new bone formation
Q5.What is a cloaca?
  • Pus breaking through the involucrum
Q6.Which patients with acute osteomyelitis develop septic arthritis?
  • Neonate <1.5 years old with a patent transphyseal artery
  • Infection in the 4 intra-articular epiphyses: proximal humerus, hip, radial head, distal fibula
Q7.What are the common pathogens of acute osteomyelitis by age group?
  • Most common in all ages: Staph aureus
  • Neonates: Group B strep, Haemophilus influenzae
  • 1-16 years: Strep pyogenes, Haemophilus influenzae
  • Infants: also gram-negative rods; consider MRSA
Q8.What is the presentation and investigation of acute osteomyelitis?
  • PMHx, recent injury, failure to thrive, refusal to walk, other source of infection
  • Bloods: WBC, CRP, ESR and cultures
  • X-ray: periosteal reaction at 1 week, lytic lesion at 2 weeks (metaphyseal rarefaction)
  • MRI: early diagnosis and drainable abscess; bone scan: Indium/Technetium + gallium
  • +/- image-guided aspiration
Q9.What are the indications for surgery in acute osteomyelitis?
  • No systemic response to antibiotics for 48hrs (fever not settling, CRP not dropping)
  • Drainable abscess
Q10.What are the complications of acute osteomyelitis?
  • Chronic osteomyelitis (5%)
  • LLD: over- or under-growth, arthritis, pathological fracture
  • 30% have concomitant septic arthritis (shoulder, elbow, hip, ankle can all spread via transphyseal vessels)
▸ Slide 542 · 14 y.o boy from china, chronic leg pain after trivial injuryInfection · 6 questions expand
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slide 542
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Q1-Q66 questions — tap to reveal all answerslist
  1. Describe the X-ray findings in this case of subacute osteomyelitis.
  2. What is the differential diagnosis of this diaphyseal lytic lesion?
  3. What is a Brodie's abscess and how does it arise?
  4. What are the clinical and investigation findings in subacute osteomyelitis?
  5. What is the management principle for subacute/chronic osteomyelitis?
  6. List the stages of acute osteomyelitis.
Answers · Q & A
Q1.Describe the X-ray findings in this case of subacute osteomyelitis.
  • Small lytic lesion at the proximal diaphysis of the leg
  • Concentric and intramedullary
  • Sclerotic rim with a narrow transitional zone
  • Significant periosteal reaction
Q2.What is the differential diagnosis of this diaphyseal lytic lesion?
  • Tumour: Ewing sarcoma in the diaphysis, osteosarcoma in the metaphysis, chondroblastoma in the epiphysis
  • Infection: Brodie's abscess
Q3.What is a Brodie's abscess and how does it arise?
  • Chronic abscess surrounded by sclerotic bone and fibrous tissue
  • Results from partially treated acute osteomyelitis or decreased virulence of bacteria
Q4.What are the clinical and investigation findings in subacute osteomyelitis?
  • PE: discharging sinus, skin erythema, lymph nodes
  • Bloods: raised ESR (50% positive), WBC, CRP
  • Imaging: MRI, CT; Cierny staging (anatomical + physiological A/B/C)
  • May need biopsy to confirm diagnosis before OT
Q5.What is the management principle for subacute/chronic osteomyelitis?
  • Eradicate infection, reconstruct bone and soft tissue defects, minimise complications and hospital stay
  • Debridement: saucerization and sequestrectomy until healthy bleeding (paprika sign)
  • Dead space management: antibiotic-loaded cement spacer, gentamicin beads, VAC dressing
  • Local and systemic antibiotics
  • +/- skeletal stabilisation depending on Cierny staging
Q6.List the stages of acute osteomyelitis.
  • 1. Inflammation
  • 2. Suppuration
  • 3. Necrosis
  • 4. New bone formation
  • 5. Resolution
▸ Slide 543 · Chronic:Infection · 6 questions expand
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slide 543
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Q1-Q66 questions — tap to reveal all answerslist
  1. What are the aims of managing chronic osteomyelitis and how is it assessed?
  2. Describe the X-ray and clinical findings in chronic osteomyelitis.
  3. Describe the Cierny classification and its management.
  4. How is a bone defect after debridement managed?
  5. Describe the Papineau technique.
  6. What are the uses of VAC and what is needed for final soft tissue coverage?
Answers · Q & A
Q1.What are the aims of managing chronic osteomyelitis and how is it assessed?
  • Aims: control infection, look for complications, skeletal stabilisation if pathological fracture
  • PE: skin and soft tissue condition
  • Blood: WBC, CRP, ESR; CT to look for collection
  • Common bacteria: S aureus, polybacteria
Q2.Describe the X-ray and clinical findings in chronic osteomyelitis.
  • Bone destruction at the proximal shaft involving half of the diameter on both AP and lateral
  • Clinically a discharging sinus over the arm
  • History of previous acute osteomyelitis
Q3.Describe the Cierny classification and its management.
  • I intramedullary -> deroof bone for IM debridement
  • II superficial (bone surface) -> debride cortex till paprika sign, may need soft tissue coverage
  • III localized (cortex + medullary) -> saucerization, debridement, antibiotic bead +/- ex fix and flap
  • IV diffuse -> ex fix, debridement, flap
  • Host A/B/C = host immunity
Q4.How is a bone defect after debridement managed?
  • Initially: ex fix + antibiotic-loaded beads, repeated debridement till clean
  • Small <4cm: Papineau or bypass graft (cross union of tibia/fibula)
  • Large >6cm: Masquelet technique, vascularized bone graft, bone transport / distraction osteogenesis
  • Bi/trifocal (2 osteotomy sites) bone transport to reduce time to distraction and consolidation, but bone maturation time is longer
Q5.Describe the Papineau technique.
  • Bed free of infection with healthy granulation tissue (blood supply)
  • Lay morselized bone graft on the defect, not thicker than 2cm
  • As it is taken up and forms granulation tissue, add another layer of bone graft
  • Continue till dead space obliterated, then VAC +/- split thickness skin graft
Q6.What are the uses of VAC and what is needed for final soft tissue coverage?
  • Removes chronic oedema, enhances blood flow, promotes granulation tissue at the floor
  • Final coverage by the soft tissue reconstruction ladder
  • May need a local or distant muscle flap
  • Adequate vascularised soft tissue coverage helps resolution of osteomyelitis
▸ Slide 544Infection · 2 questions expand
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slide 544
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Q1-Q22 questions — tap to reveal all answerslist
  1. What infection-related topic does this slide cover?
  2. What are the key learning points for this infection slide?
Answers · Q & A
Q1.What infection-related topic does this slide cover?
  • Not covered in the speaker notes
Q2.What are the key learning points for this infection slide?
  • Not covered in the speaker notes
▸ Slide 545 · `Infection · 2 questions expand
slide 545
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Q1-Q22 questions — tap to reveal all answerslist
  1. What is the topic of this slide?
  2. Outline the classification and management of the condition shown on this slide.
Answers · Q & A
Q1.What is the topic of this slide?
  • Not covered in the speaker notes
Q2.Outline the classification and management of the condition shown on this slide.
  • Not covered in the speaker notes
▸ Slide 546 · JRAInfection · 7 questions expand
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slide 546
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Q1-Q77 questions — tap to reveal all answerslist
  1. What is the differential diagnosis of recurrent knee effusion in a child?
  2. What is juvenile rheumatoid arthritis (JRA) / juvenile idiopathic arthritis?
  3. What is the genetic association and what are the types of JRA?
  4. What are the diagnostic criteria for JRA?
  5. What are the clinical features of JRA?
  6. What is Still disease and what is the prognosis of JRA?
  7. What investigations and treatments are used in JRA?
Answers · Q & A
Q1.What is the differential diagnosis of recurrent knee effusion in a child?
  • Infection
  • Trauma (NAI)
  • Inflammatory (JRA)
Q2.What is juvenile rheumatoid arthritis (JRA) / juvenile idiopathic arthritis?
  • A persistent autoimmune inflammatory arthritis lasting >6 weeks
  • In a patient younger than 16 years of age
  • Female > male
Q3.What is the genetic association and what are the types of JRA?
  • HLA-DR4 (polyarthritis); HLA-DR8, 5, 2.1; HLA-B27 (pauciarthritis)
  • Polyarthritis >5 joints (similar to RA) - 30%
  • Oligoarthritis <5 joints (similar to seronegative, commonly eye problems) - 50%
  • Systemic (Still disease) - 20%
Q4.What are the diagnostic criteria for JRA?
  • Diagnosis by exclusion plus one of the following:
  • Rash, presence of RF, iridocyclitis, C-spine involvement
  • Pericarditis, tenosynovitis, intermittent fever, morning stiffness
Q5.What are the clinical features of JRA?
  • General: intermittent fever, rash, pericarditis, iridocyclitis (inflammation of iris and ciliary body)
  • Ortho: C-spine involvement (kyphosis, facet ankylosis, atlantoaxial subluxation), tenosynovitis, morning stiffness
  • Osteoporosis with easy fracture; growth retardation (corticosteroid suppression, Shapiro III/V)
  • Ankylosis of joints in systemic type
  • Deformity: external torsion of tibia, distal ulna dysplasia, underdeveloped mandible (micrognathia), short neck and scoliosis
Q6.What is Still disease and what is the prognosis of JRA?
  • Still disease: acute presentation with multiple joint involvement, fever, salmon coloured rash, splenomegaly, usually <3 years old
  • Prognosis: 50% spontaneous resolve, 25% slight limitation, 25% severe disability
  • Best prognosis pauciarticular > polyarticular > systemic
Q7.What investigations and treatments are used in JRA?
  • X-ray: juxta-articular, late osteopenia and joint destruction; C-spine X-ray for atlantoaxial instability
  • Blood: RF (worse prognosis if +ve), ANA (+ve is diagnostic), HLA typing
  • Physiotherapy to maintain range and power
  • DMARD (azathioprine, etanercept) and biological agents (rituximab)
  • Surgery: synovectomy, a la carte