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Q1: Definition & classification (2 min)
A 12-year-old boy presents with fever, severe pain over the distal femur and a normal early X-ray. Define osteomyelitis. Classify it by pathogenesis (Lew-Waldvogel) and by anatomic stage (Cierny-Mader), and explain why each axis matters for management. Why does the metaphysis get infected preferentially in children? Model answer: Infection of bone and marrow. Lew-Waldvogel: haematogenous (children: long-bone metaphysis; adults: vertebra), contiguous (adjacent wound, ulcer, surgery), chronic (sequestrum + biofilm). The axis matters because haematogenous is single-organism and often medical; contiguous is mixed and needs debridement; chronic always needs surgery. Cierny-Mader: anatomic type I (medullary), II (superficial), III (localised), IV (diffuse) crossed with host A (healthy) / B (compromised) / C (treatment worse than disease) — guides the extent of surgery. Metaphyseal hair-loop capillaries are fenestrated, sluggish, lack a basement membrane — bacteria lodge and multiply; the physis is a barrier (after ~18 months), so the joint is usually spared except where the metaphysis is intracapsular (hip, shoulder, knee).
Q2: Pathophysiology (3 min)
Walk through the cascade from bacterial inoculation to chronic disease. Define sequestrum, involucrum, cloaca and sinus tract. What is the biofilm and why does it change therapy? Why is dead bone inaccessible to antibiotics, and how does this justify surgical debridement to the paprika sign? Where does rifampin fit, and what is the Renz 2021 controversy? Model answer: Inoculation → cytokine release (IL-1, TNF-alpha, IL-6) → neutrophil influx → rising intraosseous pressure in the rigid cortex → venous stasis, thrombosis, ischaemia → cortical necrosis = sequestrum (dead bone). Periosteum reacts → involucrum (new bone). Pus exits via cloaca → sinus tract. Biofilm = sessile bacteria in extracellular polymeric slime, 10 to 1000x more antibiotic-resistant and inaccessible to phagocytes. Sequestrum is avascular → no antibiotic or immune access → surgical debridement to bleeding healthy bone (paprika sign) is the only cure. Rifampin penetrates biofilm and kills adherent staphylococci — added after debridement for staphylococcal implant infection (DAIR). Renz 2021: critical appraisal — evidence has methodological weaknesses but overall guidelines still support its use in staphylococcal implant infection; controversy persists.
Q3: Investigations (2 min)
A normal early X-ray, raised CRP. What bloods and cultures? Which imaging modality is the modality of choice and why — sensitivity and specificity? What is the microbiological gold standard, and why is a sinus tract swab unreliable? In diabetic foot disease, what is the probe-to-bone test and how do you use it? Model answer: Bloods: FBC, CRP (best monitoring marker), ESR (slow baseline), U&E, lactate. Blood cultures before antibiotics (positive ~40% acute haematogenous, 70 to 90% vertebral). Imaging modality of choice = MRI (sens/spec ~90%) — marrow oedema low T1, high T2/STIR; defines extent, abscess, joint involvement; gadolinium for abscess/necrosis. Microbiological gold standard = deep bone biopsy culture (intraoperative or CT-guided) — sinus tract swab is contaminated with skin flora. Diabetic foot: probe-to-bone with sterile blunt metal probe; positive = hard gritty bone felt; high PPV in high-prevalence clinics; combine with MRI and bone biopsy.
Q4: Management & antibiotics (3 min)
Build the empirical antibiotic ladder by scenario (acute haematogenous, MRSA risk, diabetic foot, sickle cell, IVDU, prosthetic). State the durations. When and why do you switch from IV to oral? What is OPAT? Outline the surgical principles of source control (the six steps), and the prosthetic joint infection pathway (DAIR vs one-/two-stage exchange). Model answer: Empirical: cover S. aureus (flucloxacillin 2 g IV 6-hourly or cefazolin); add vancomycin if MRSA risk / prosthetic / severe beta-lactam allergy; add Gram-negative/anaerobic cover (piperacillin-tazobactam) for diabetic foot/contaminated; add Salmonella cover (ceftriaxone/ciprofloxacin) in sickle cell; add Pseudomonas cover (piperacillin-tazobactam/ceftazidime) for IVDU. Duration: 4 to 6 weeks acute, 6 weeks plus chronic, 6 weeks vertebral; add rifampin for staphylococcal biofilm. IV-to-oral switch: afebrile 24 to 48 h, improving, CRP falling, bioavailable oral agent (ciprofloxacin + rifampin, clindamycin, linezolid). OPAT = outpatient parenteral antimicrobial therapy. Surgery: drain abscess; debride all necrotic bone to paprika sign; remove infected hardware; dead-space management (antibiotic PMMA spacer, flap); stabilisation; soft-tissue cover; revascularisation if ischaemic. Prosthetic: acute (<4 wk, mobile implant) → DAIR + rifampin 6 weeks; chronic (>4 wk, loose) → two-stage exchange (remove, antibiotic spacer, 4 to 6 weeks antibiotics, reimplant); not operable → lifelong suppressive.
Q5: Complications, special populations & pearls (2 min)
Name the complications of acute and chronic disease. What is Marjolin ulcer and when do you suspect it? Why must you screen for endocarditis in vertebral disease? In a neonate with osteomyelitis, which organisms and what anatomical feature explains joint involvement? Give the four-word chronic quartet and the single most important principle of management. Model answer: Complications: chronic relapse, septic arthritis, joint destruction, growth arrest/limb-length discrepancy (children), pathological fracture, epidural/paraspinal abscess (vertebral), sepsis, amputation, death. Marjolin ulcer = SCC in a chronic sinus tract (after 10 to 30 years); suspect on any change in a chronic sinus (pain, mass, bleeding) — biopsy. Endocarditis screen in vertebral disease because both share bacteraemic seeding (echo, multiple sets of blood cultures). Neonate: Group B strep, E. coli, S. aureus; transphyseal vessels patent → joint involvement common. Chronic quartet: sequestrum, involucrum, cloaca, sinus tract. Single most important principle: dead bone cannot be cured by antibiotics — surgical source control is the cornerstone.