Infectious DiseasesTier 2Disease (DEADMAN)

Osteomyelitis

Description

Infection of bone and marrow -> inflammation, vascular compromise, bone necrosis (sequestrum) and new bone formation (involucrum)
Sequestrum is avascular -> antibiotics do not reach it -> surgical debridement, not longer antibiotics, is what cures chronic disease

Classification - by route

	Features
Haematogenous	Children: metaphysis of long bones (slow sinusoidal flow). Adults: vertebral body
Contiguous spread	Diabetic foot ulcer, pressure injury, dental, sinus, chronic wound
Direct inoculation	Open fracture, surgery, prosthetic joint, penetrating trauma

By chronicity

Acute - days to weeks; systemic features; no sequestrum yet -> antibiotics may cure without surgery
Chronic - sequestrum, involucrum, sinus tract, recurrent flares; surgery is almost always required

Anatomical (Cierny-Mader)

I medullary / II superficial / III localised (full-thickness, stable) / IV diffuse (unstable)
Modified by host: A normal, B compromised (local or systemic), C treatment worse than the disease

Epidemiology

Bimodal: children (haematogenous long bone) and adults >50 (vertebral, diabetic foot, prosthetic)
Vertebral osteomyelitis incidence rising - ageing population, more instrumentation, more IV drug use, more bacteraemia
Diabetic foot osteomyelitis complicates ~20% of moderate and ~60% of severe diabetic foot infections
Staphylococcus aureus causes ~50-70% of all cases across every category
High burden among Aboriginal and Torres Strait Islander people - diabetes, remoteness, delayed presentation
Prosthetic joint infection: ~1-2% of primary arthroplasties

Aetiopathogenesis

Bacterial adherence -> biofilm formation on necrotic bone and hardware
- Biofilm -> metabolically dormant organisms, 1000x antibiotic tolerance, immune evasion
- This is why implant retention often fails and why cure needs debridement or removal
Inflammation -> raised intraosseous pressure -> thrombosis of nutrient vessels -> necrosis
S. aureus invades and survives within osteoblasts and induces RANKL -> osteoclastic bone destruction
Small colony variants -> persistence and relapse years later

Organisms by setting

Setting	Organism
All settings, commonest	Staphylococcus aureus (MSSA and MRSA)
Prosthetic/hardware	Coagulase-negative staphylococci, Cutibacterium acnes (shoulder), S. aureus
Diabetic foot	Polymicrobial - S. aureus, streptococci, Enterobacterales, anaerobes, Pseudomonas
Sickle cell disease	Salmonella (and still S. aureus)
IV drug use	S. aureus, Pseudomonas, Candida; sternoclavicular and vertebral
Vertebral, indolent, endemic exposure	Mycobacterium tuberculosis (Pott disease), Brucella
Puncture through a shoe	Pseudomonas aeruginosa
Human/animal bite	Eikenella, Pasteurella, anaerobes
Neonatal	Group B streptococcus, E. coli, S. aureus

Diagnosis

Clinical

Acute: localised bone pain, fever, tenderness, overlying warmth/swelling, refusal to weight-bear
Vertebral: insidious back pain worse at night and at rest, focal spinal tenderness, often afebrile
- *Any new back pain with raised inflammatory markers, or with S. aureus bacteraemia, is vertebral osteomyelitis until excluded*
- New neurological deficit -> epidural abscess -> urgent MRI and neurosurgical referral
Chronic: sinus tract discharging onto the skin is pathognomonic, non-healing ulcer, deformity
Diabetic foot: neuropathy blunts pain; the ulcer, not the bone, is often the only sign
- Positive probe-to-bone test - a sterile probe passes through the ulcer to gritty bone
  - The most predictive bedside sign of underlying osteomyelitis; high PPV in a high-prevalence setting
- Ulcer >2 cm2, depth >3 mm, duration >1-2 weeks, "sausage toe" all raise probability

Bloods

CRP and ESR - most useful for monitoring response, not for diagnosis (normal values do not exclude, especially in diabetes)
FBE, UEC, glucose/HbA1c
Blood cultures x2 before antibiotics - positive in ~50% of haematogenous and vertebral disease; a positive blood culture may remove the need for bone biopsy

Imaging


Plain X-ray	Normal for the first 10-14 days (needs 30-50% bone loss). Later: periosteal reaction, lucency, sequestrum. Cheap, useful as a baseline and for Charcot
MRI - the imaging test of choice	Sensitivity ~90%, specificity ~80%; marrow oedema, abscess, epidural extension, soft tissue. Positive within days
CT	Best for sequestrum, cortical destruction and surgical planning
Nuclear medicine	Three-phase bone scan sensitive but non-specific; labelled leucocyte SPECT/CT or FDG-PET where MRI is contraindicated or hardware causes artefact

Microbiology - the decisive step

*Obtain bone for culture and histology before starting antibiotics wherever the patient is stable*
- Percutaneous image-guided or open biopsy; ideally off antibiotics for 2 weeks if already started
*Superficial wound and sinus tract swabs do NOT reflect bone pathogens - except S. aureus, which correlates reasonably*
Prosthetic joint infection: >=3-5 periprosthetic tissue samples, sonication of explanted hardware, prolonged incubation (Cutibacterium up to 14 days)
Send for histopathology as well as culture - inflammatory cells plus necrosis confirms osteomyelitis when cultures are negative
Consider mycobacterial and fungal culture in indolent disease or the immunosuppressed

The key differential in the diabetic foot

	Discriminator
Charcot neuroarthropathy	Warm, swollen, deformed midfoot, usually no ulcer; MRI marrow oedema can look identical - distinguish by distribution, joint involvement, and clinical context
Soft tissue infection alone	No bone contact, ulcer <2 cm2, normal X-ray
Gout, fracture, malignancy	History, imaging

Management

Three pillars: microbiological diagnosis, surgical source control, and targeted antibiotics of adequate duration. Vascular supply and glycaemia determine whether any of it works.

1. Get the diagnosis before treating

Delay antibiotics until bone or blood cultures are obtained, unless septic or with rapid neurological deterioration
Empirical broad-spectrum therapy in a stable patient with chronic osteomyelitis destroys the only chance of a targeted regimen

2. Surgery

Debridement to healthy bleeding bone; excise sequestrum, sinus tracts and necrotic tissue
Dead space management: antibiotic-loaded cement/beads, local flap, bone graft
Stabilisation; remove infected hardware once the fracture has united
Prosthetic joint infection: DAIR (debridement, antibiotics, implant retention) only if early (<3-4 weeks), stable implant, susceptible organism; otherwise one- or two-stage revision
Vertebral osteomyelitis is usually managed non-operatively; operate for epidural abscess with neurological deficit, instability, deformity, or failure of medical therapy
Diabetic foot: assess and revascularise before deciding on amputation; conservative surgery (resection of the infected bone) is often preferable to major amputation

3. Antibiotics

Targeted to culture; high dose; bone-penetrating

Organism	Agent
MSSA	Flucloxacillin 2 g IV 4-6 hourly (or cefazolin)
MRSA	Vancomycin (AUC-guided) or daptomycin; oral step-down: clindamycin, doxycycline, trimethoprim-sulfamethoxazole, linezolid
Streptococci	Benzylpenicillin/ceftriaxone
Enterobacterales	Ceftriaxone or ciprofloxacin (excellent bone penetration)
Pseudomonas	Ceftazidime/piperacillin-tazobactam, then ciprofloxacin
Prosthetic/staphylococcal biofilm	Add rifampicin (never as monotherapy - rapid resistance; check interactions)

Duration
- Native bone osteomyelitis: ~6 weeks from the last debridement (or from the start of effective therapy)
- Vertebral osteomyelitis: 6 weeks (12 weeks if undrained abscess, extensive disease or slow response)
- Diabetic foot osteomyelitis: 6 weeks if bone is NOT resected; ~3 weeks if residual infected bone only after minor amputation; ~2-5 days if all infected bone is removed
Oral step-down is evidence-based - OVIVA showed oral therapy non-inferior to IV at 6 weeks, with fewer line complications and lower cost
- Switch at ~1-2 weeks once clinically improving, source controlled, organism known and a highly bioavailable oral agent is available
- Australian practice uses OPAT or oral step-down rather than prolonged inpatient IV therapy

4. Host optimisation - decides the outcome more than the antibiotic

Revascularisation where there is peripheral arterial disease
Glycaemic control, nutrition (albumin, protein, vitamin D), smoking cessation
Offloading - total contact cast or removable device for the diabetic foot
Pressure area care; treat oedema; MDT high-risk foot service

5. Monitoring

Clinical response + CRP trend (CRP falling by ~50% in the first 1-2 weeks predicts response)
Do not repeat MRI early - imaging lags clinical recovery by months
Drug safety monitoring (FBE, UEC, LFT; vancomycin levels; linezolid - cytopenias, neuropathy, serotonin toxicity)

Associations

Diabetes mellitus with peripheral neuropathy and peripheral arterial disease - the dominant Australian context
Staphylococcus aureus bacteraemia - always ask where the metastatic focus is
Injecting drug use, haemodialysis, indwelling vascular catheters
Orthopaedic hardware, prosthetic joints, open fractures, spinal instrumentation
Sickle cell disease (Salmonella), immunosuppression, HIV, malignancy
Pressure injuries, spinal cord injury, peripheral vascular disease
Endocarditis (consider a TTE/TOE in vertebral osteomyelitis with staphylococcal or streptococcal bacteraemia)
Charcot neuroarthropathy - the diagnostic confounder
Tuberculosis (Pott disease), brucellosis, melioidosis (northern Australia), fungal infection
Chronic recurrent multifocal osteomyelitis (CRMO) - sterile, autoinflammatory, paediatric

Natural history & complications

Acute haematogenous osteomyelitis in children: >90% cure with prompt antibiotics alone
Adult chronic osteomyelitis: relapse in 20-30%, sometimes years later (small colony variants, biofilm, residual sequestrum)
- Cure requires adequate debridement - antibiotic duration cannot compensate for retained dead bone
Diabetic foot osteomyelitis
- Remission ~60-80% with combined medical and surgical management and revascularisation
- Major amputation in 10-20%; 5-year mortality after a major amputation exceeds that of many cancers
- Recurrent ulceration in ~40% within a year - lifelong podiatry and footwear
Vertebral osteomyelitis: most recover; residual back pain in ~30%; neurological deficit is usually permanent if established before treatment
Prosthetic joint infection: success ~70-90% for two-stage revision, lower for DAIR
Complications: epidural abscess and cord compression, pathological fracture, sepsis, growth arrest (paediatric physeal involvement), chronic sinus, amputation, secondary amyloidosis, Marjolin ulcer (SCC in a chronic sinus tract)

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