Musculoskeletal Infections — Algorithm

Musculoskeletal (MSK) infections encompass a broad spectrum of conditions including acute haematogenous osteomyelitis, septic arthritis, discitis, psoas abscess, infected prosthetic joints, necrotising fasciitis, and diabetic foot infections. A systematic algorithmic approach to diagnosis and management is essential because delays in treatment lead to irreversible joint destruction, avascular necrosis, chronic osteomyelitis, and life-threatening sepsis. The fundamental principle is: suspect infection early, investigate promptly, and treat aggressively.

• Classification by site: osteomyelitis (bone); septic arthritis (joint); spondylodiscitis (vertebral body + disc); periprosthetic joint infection (PJI); soft tissue infections (cellulitis, necrotising fasciitis, myositis, pyomyositis)
• Classification by duration: acute (<2 weeks); subacute (2 weeks–3 months — often less florid, may present as a Brodie abscess); chronic (>3 months — dead bone, sequestrum, involucrum, sinuses)
• Classification by pathogenesis: haematogenous (blood-borne seeding — the most common route in children; adults more commonly haematogenous in vertebral osteomyelitis); direct inoculation (trauma, surgery, penetrating wound); contiguous spread (from adjacent soft tissue infection — diabetic foot, pressure sore); each pathway has implications for the causative organism and the likely anatomical site of infection

• Step 1 — Clinical suspicion: the classic triad of infection is pain + swelling + fever; however, in immunocompromised patients (HIV, diabetics, those on steroids or DMARDs), the clinical features may be markedly attenuated; a high index of suspicion is required; any child with a painful limb and fever, any patient with a hot swollen joint, or any post-operative patient with wound pain and fever must be evaluated for MSK infection; do NOT wait for all classic features to be present before investigating
• Step 2 — Inflammatory markers: CRP (most useful — rises within 6 hours of infection, peaks at 48 hours, normalises within days of successful treatment; the best marker for monitoring response); ESR (rises more slowly, peaks at 3–5 days, remains elevated for weeks — less useful for acute monitoring but useful for baseline); WBC (often normal in subacute/chronic infection — unreliable as a sole marker); PCT (procalcitonin — the most specific marker for bacterial infection; rapidly rises in bacterial sepsis; useful for distinguishing bacterial from non-bacterial causes)
• Step 3 — Blood cultures: BEFORE antibiotics; at least 2 sets from different sites; yield is approximately 50–60% in acute haematogenous osteomyelitis and septic arthritis; lower in subacute and chronic infection; the causative organism isolated from blood cultures allows targeted antibiotic therapy; starting antibiotics before cultures are taken reduces the diagnostic yield and forces empirical broad-spectrum treatment which increases resistance risk
• Step 4 — Imaging: plain X-rays (first line — may be normal in the first 7–14 days of osteomyelitis; look for periosteal reaction, lytic lesion, joint space changes, soft tissue swelling); MRI (gold standard for osteomyelitis, spondylodiscitis, soft tissue infection — shows bone marrow oedema on STIR/T2 within 3–5 days of infection; best delineates the extent of infection and guides drainage/debridement planning); CT (best for cortical sequestrum, cortical erosion, and CT-guided aspiration/biopsy); USS (for joint effusion aspiration and soft tissue collections — can guide needle aspiration)
• Step 5 — Aspiration/biopsy: BEFORE antibiotics where possible; joint aspiration for all suspected septic arthritis — send fluid for cell count (WBC >50,000/mm³ with >90% neutrophils = septic arthritis until proven otherwise; >100,000/mm³ is highly specific), Gram stain, culture and sensitivity, crystal analysis (to exclude gout and pseudogout); bone biopsy for suspected osteomyelitis where blood cultures are negative — CT-guided core biopsy of the affected bone; the yield of bone biopsy is approximately 60–80% for bacterial organisms
• Step 6 — Source identification and risk stratification: identify the source of haematogenous seeding (dental infection, skin infection, UTI, endocarditis — echocardiography is indicated in all cases of confirmed haematogenous Staphylococcus aureus bacteraemia); assess host factors (diabetes, immunosuppression, renal failure, HIV — all modify treatment intensity and duration)

• Septic arthritis is an orthopaedic emergency: articular cartilage is destroyed within 6–8 hours by bacterial proteases and inflammatory cytokines; delay in joint washout is directly proportional to the degree of permanent joint damage; all suspected septic arthritis must be aspirated within hours of presentation; if the aspirate shows WBC >50,000/mm³ with >90% PMNs, proceed to urgent surgical washout
• Causative organisms: Staphylococcus aureus (the most common cause at all ages — approximately 50–60% of cases); Streptococcus pyogenes; Neisseria gonorrhoeae (the most common cause of septic arthritis in sexually active young adults — consider in any young adult with polyarthralgia, skin rash, and tenosynovitis); coagulase-negative staphylococci (post-operative/PJI); Gram-negatives (neonates, elderly, IV drug users, immunocompromised — E. coli, Pseudomonas); Kingella kingae (children under 4 years — requires specific culture conditions)
• Surgical washout: arthroscopic washout (preferred for knee, shoulder, elbow, and ankle — allows thorough debridement with lower morbidity than open arthrotomy); open arthrotomy (hip — mandatory due to the inaccessibility of the joint for arthroscopy in most centres; also for joints not accessible arthroscopically or for failed arthroscopic washout); repeated washouts may be required if the infection does not settle
• Empirical antibiotic therapy for septic arthritis: IV flucloxacillin 1–2g four times daily (covers Staphylococcus aureus and Streptococcus); add IV gentamicin or ceftriaxone if Gram-negative organisms are suspected (neonate, elderly, immunocompromised, IV drug user); switch to vancomycin if MRSA is suspected or confirmed; duration — IV antibiotics for 2–4 weeks then oral for a further 2–4 weeks (total 4–6 weeks); guided by CRP response and microbiological sensitivities

• Necrotising fasciitis: a surgical emergency; rapidly progressive infection of the deep fascia and subcutaneous tissue with secondary skin necrosis; Type 1 (polymicrobial — most common; affects diabetics, immunocompromised; Gram-positive, Gram-negative, and anaerobes acting synergistically); Type 2 (Group A Streptococcus — the `flesh-eating bacteria`; rapidly progressive; young healthy adults); mortality approximately 25–35% even with treatment; higher with delayed diagnosis
• Clinical features: severe pain disproportionate to skin findings; `wooden` board-like induration of the skin; skin discolouration (dusky blue-grey); blistering; crepitus (gas in tissues — Type 1); rapidly progressing wound margins; paradoxical reduction in pain as the nerves are destroyed (late sign = poor prognosis); the skin may appear relatively normal in early deep fasciitis while the patient is systemically shocked (disproportionate systemic toxicity vs mild skin findings should alarm the clinician)
• LRINEC score: the Laboratory Risk Indicator for Necrotising Fasciitis uses CRP, WBC, haemoglobin, sodium, creatinine, and glucose to stratify risk; score ≥6 = intermediate risk; ≥8 = high risk; sensitivity approximately 89%, specificity 97% for distinguishing NF from severe cellulitis; a high LRINEC score in a patient with a spreading infection mandates urgent surgical exploration
• Management: immediate surgical debridement — the `finger test` (blunt dissection through a skin incision into the fascia; if the finger passes easily along the fascial plane without resistance and the tissue is necrotic = positive test = necrotising fasciitis confirmed = proceed to radical wide debridement); all necrotic tissue is excised to bleeding viable margins; repeated debridements every 24–48 hours until no further progression; broad-spectrum IV antibiotics (piperacillin-tazobactam + clindamycin ± carbapenem for Type 1; benzylpenicillin + clindamycin for Group A Streptococcus Type 2); IV immunoglobulin (IVIG) for streptococcal toxic shock; ICU management; delayed reconstruction with skin grafting/flap after infection is controlled

• The Cierny-Mader classification for chronic osteomyelitis: the anatomical type (Type 1 — medullary; Type 2 — superficial; Type 3 — localised; Type 4 — diffuse) combined with the host category (A — normal host; B — compromised host; C — treatment worse than disease) guides surgical planning; Type 4B or 4C disease (diffuse osteomyelitis in a compromised host) may be best treated with long-term suppressive antibiotics rather than aggressive surgery if the risk of surgical complications exceeds the benefit
• The Masquelet technique (induced membrane technique) for chronic osteomyelitis with bone defects: Stage 1 — radical debridement of all infected bone; the dead space is filled with an antibiotic-impregnated cement spacer (tobramycin + vancomycin); the cement spacer induces formation of a biological membrane around it (the induced membrane) rich in growth factors (BMP-2, VEGF); Stage 2 (6–8 weeks later, after infection is controlled) — the cement spacer is removed while preserving the induced membrane; the membrane is filled with autologous cancellous bone graft (usually from the iliac crest); the induced membrane serves as a biological chamber for the graft, promoting bone formation; this technique is highly effective for defects of 4–25 cm
• Sinus tract culture — a diagnostic pitfall: wound swabs and sinus tract cultures in chronic osteomyelitis grow superficial colonising organisms (typically Pseudomonas, coagulase-negative Staphylococcus, and environmental organisms) that do NOT represent the true causative deep organism; sinus swab cultures should never guide antibiotic therapy in chronic osteomyelitis; bone biopsy from the infected focus (at the time of surgical debridement) is the only reliable way to identify the causative organism

• MSK infection algorithm: clinical suspicion → inflammatory markers (CRP best) → blood cultures BEFORE antibiotics → imaging (MRI gold standard) → aspiration/biopsy BEFORE antibiotics → targeted antibiotics
• Septic arthritis: orthopaedic emergency; cartilage destruction within 6–8 hours; WBC >50,000/mm³ + >90% PMNs on joint aspirate = septic until proven otherwise; urgent washout
• Gonococcal arthritis: most common cause in sexually active young adults; triad of migratory polyarthralgia + skin rash + tenosynovitis; responds rapidly to antibiotics (no surgical washout usually needed)
• Kingella kingae: children under 4 years; requires specific culture media; growing recognition as an important cause of septic arthritis and osteomyelitis in this age group
• Necrotising fasciitis: pain out of proportion + wooden skin induration + systemic shock = NF until proven otherwise; LRINEC score ≥8 = high risk; finger test; immediate radical debridement — delay = death
• Brodie abscess: subacute osteomyelitis; metaphyseal radiolucent lesion + sclerotic rim on X-ray; CT-guided curettage + antibiotics; mimics osteoid osteoma (distinguish — osteoid osteoma has a nidus + night pain relieved by NSAIDs)
• Chronic osteomyelitis: sequestrum (dead bone) + involucrum (reactive new bone); Cierny-Mader staging; debridement to paprika sign (healthy bleeding bone); Masquelet technique for large defects; NEVER rely on sinus swab for antibiotic guidance — bone biopsy only
• CRP: best acute-phase marker; rises within 6 hours; normalises within days of successful treatment; use to monitor treatment response
• MRI: gold standard for all MSK infections; bone marrow oedema on STIR/T2 within 3–5 days (before X-ray changes); delineates extent for surgical planning
• Spondylodiscitis: back pain + fever + elevated CRP/ESR; urgent MRI if neurological deficit (epidural abscess); blood cultures + CT-guided biopsy if negative; surgery for epidural abscess, neurological deficit, instability, or failed medical treatment