Bacterial Bone Infection | Biofilm Formation | Chronic Sequestration
CIERNY-MADER CLASSIFICATION
Critical Must-Knows
- Staphylococcus aureus causes 80% of all osteomyelitis cases
- Biofilm formation on necrotic bone prevents antibiotic penetration
- Sequestrum = necrotic bone, Involucrum = new bone shell around infection
- Chronic osteomyelitis requires surgical debridement - antibiotics alone insufficient
- Antistaphylococcal penicillin (flucloxacillin/nafcillin/cefazolin) is first-line for MSSA bone infection worldwide
Clinical Pearls
- "Cierny-Mader combines anatomic location with host physiologic status
- "CRP more sensitive than ESR for monitoring treatment response
- "MRI has 90% sensitivity for osteomyelitis detection
- "Minimum 6 weeks total antibiotic therapy required for cure
Critical Osteomyelitis Exam Points
Pathophysiology
Biofilm formation is the key to chronicity. Bacteria adhere to necrotic bone in a glycocalyx matrix that prevents antibiotic and immune cell penetration. This is why surgery is mandatory for chronic osteomyelitis.
Classification
Cierny-Mader is the gold standard. Type I-IV describes anatomy, A-C describes host status. Type IV-C host (diffuse infection, compromised host) has worst prognosis.
Diagnosis
MRI is the investigation of choice - 90% sensitive, shows marrow oedema, abscess, and soft tissue extension. Plain XR takes 10-14 days to show changes. Always culture before antibiotics.
Treatment
Surgery plus antibiotics is synergistic. Debride all necrotic tissue, obtain cultures, dead space management, then 6 weeks of pathogen-directed therapy. First-line for MSSA is an antistaphylococcal penicillin (flucloxacillin/nafcillin) or cefazolin. The OVIVA trial showed oral is non-inferior to IV once the patient is stable.
At a Glance
Osteomyelitis is bacterial bone infection with Staphylococcus aureus responsible for 80% of cases. The key to chronicity is biofilm formation—bacteria adhere to necrotic bone within a glycocalyx matrix that prevents antibiotic and immune cell penetration. A sequestrum (necrotic bone fragment) acts as a nidus for persistent infection, while the involucrum (new bone shell) forms around the infected segment. The Cierny-Mader classification combines anatomic type (I-IV: medullary, superficial, localized, diffuse) with host status (A-C). MRI is the investigation of choice (90% sensitivity) showing marrow edema and abscess; plain X-ray changes take 10-14 days to appear. Treatment requires surgery plus antibiotics—debride all necrotic tissue, then a pathogen-directed course of roughly 6 weeks (antistaphylococcal penicillin or cefazolin first-line for MSSA). The landmark OVIVA RCT (N=1054) established that oral antibiotics are non-inferior to intravenous therapy once the patient is clinically stable. CRP is superior to ESR for monitoring response.
SPINSCommon Causative Organisms by Clinical Scenario
| S | Staphylococcus aureus 80% of all cases - most common in all age groups |
| P | Pseudomonas aeruginosa Puncture wound through shoe, IV drug users |
| I | IV drug user organisms S. aureus, Pseudomonas, Candida in vertebral osteomyelitis |
| N | Nail through shoe Pseudomonas in calcaneal osteomyelitis |
| S | Salmonella species Sickle cell disease patients |
| S | Staphylococcus aureus 80% of all cases - most common in all age groups | N | Nail through shoe Pseudomonas in calcaneal osteomyelitis |
| P | Pseudomonas aeruginosa Puncture wound through shoe, IV drug users | S | Salmonella species Sickle cell disease patients |
| I | IV drug user organisms S. aureus, Pseudomonas, Candida in vertebral osteomyelitis |
Hook:When bacteria SPINS into bone, think of the clinical scenario to predict the organism!
CWEInflammatory Markers for Diagnosis and Monitoring
| C | CRP (C-reactive protein) Most sensitive - rises in 6-12 hours, falls with treatment |
| W | WCC (White cell count) Often normal in chronic cases - less useful |
| E | ESR (Erythrocyte sedimentation rate) Slower to rise and fall - use CRP for monitoring |
| C | CRP (C-reactive protein) Most sensitive - rises in 6-12 hours, falls with treatment |
| W | WCC (White cell count) Often normal in chronic cases - less useful |
| E | ESR (Erythrocyte sedimentation rate) Slower to rise and fall - use CRP for monitoring |
Hook:CWE - CRP Wins Every time for monitoring osteomyelitis treatment response!
Overview/Introduction
Osteomyelitis is an infection of bone that can be caused by bacteria, fungi, or mycobacteria. The clinical presentation, microbiology, and management differ significantly between acute and chronic forms. Understanding the pathophysiology—particularly biofilm formation on necrotic bone—is fundamental to effective treatment.
Key Definitions:
- Sequestrum: Segment of necrotic, avascular bone that becomes colonized by bacteria and serves as a nidus for chronic infection
- Involucrum: Reactive new bone that forms around a sequestrum as the body attempts to wall off the infection
- Cloaca: Opening in the involucrum through which pus drains, often leading to a sinus tract
The fundamental principle is that chronic osteomyelitis cannot be cured with antibiotics alone—surgical debridement is mandatory because biofilm-coated sequestrum prevents antibiotic penetration.
Concepts and Mechanisms
Biofilm Formation - The Key to Chronicity
Biofilm is a structured community of bacteria enclosed in a self-produced polysaccharide matrix (glycocalyx). This matrix:
- Provides physical barrier against antibiotics
- Prevents neutrophil phagocytosis
- Allows bacteria to enter a dormant, metabolically inactive state
- Enables quorum sensing between bacteria
Bacteria within biofilm are 1000x more resistant to antibiotics than planktonic (free-floating) bacteria. This is the fundamental reason why surgical debridement—not antibiotics—is the cornerstone of chronic osteomyelitis treatment.
Vascular Anatomy and Susceptibility
Different bones have unique vascular patterns that influence infection susceptibility:
- Metaphysis of long bones: Sinusoidal blood flow with hairpin loops creates stagnant zones for bacterial seeding
- Vertebral bodies: Batson's valveless venous plexus allows retrograde seeding from pelvic/abdominal infections
- Cortical bone: Supplied by periosteal vessels—damage leads to avascular sequestrum formation
Host-Pathogen Interaction
The outcome of bone infection depends on the balance between bacterial virulence and host immune response. Local factors (vascular supply, foreign material) and systemic factors (diabetes, immunosuppression) determine whether infection resolves, becomes chronic, or disseminates.
Pathophysiology of Osteomyelitis
Routes of Infection
Haematogenous
- Metaphysis in children - slow sinusoidal blood flow
- Vertebral bodies in adults - Batson's plexus
- Bacteraemia seeds bone during transient episodes
- S. aureus most common organism
Contiguous Spread
- Post-surgical infection - hardware, fracture fixation
- Diabetic foot ulcers - direct inoculation
- Polymicrobial in trauma and diabetic cases
- Often involves soft tissue and bone together
Direct Inoculation
- Open fractures - contamination at injury
- Puncture wounds - nail through shoe (Pseudomonas)
- Combat injuries - high-energy trauma
- Implant surgery - low virulence organisms (Staph epidermidis)
Stages of Infection
Progression from Acute to Chronic
Bacterial invasion and inflammatory response. Vascular congestion leads to intraosseous pressure increase. Pus formation under periosteum causes subperiosteal abscess. Purulent material tracks along Volkmann canals.
Vascular compromise develops. Elevated intraosseous pressure compresses vessels causing ischaemia. Necrotic bone (sequestrum) forms. Body attempts to wall off infection with new bone shell (involucrum).
Biofilm formation on sequestrum. Bacteria enter dormant state within glycocalyx matrix. Sinus tracts form to skin. Recurrent flares despite antibiotics. Requires surgical debridement for cure.
Biofilm Significance
The biofilm is the fundamental problem in chronic osteomyelitis. Bacteria within the glycocalyx matrix are 1000x more resistant to antibiotics than planktonic forms. Biofilm also prevents neutrophil phagocytosis. This is why antibiotics alone cannot cure chronic osteomyelitis - surgical removal of the biofilm-colonized sequestrum is mandatory.
Microbiology
Organism by Patient Population and Site
| Patient Group | Site | Organism | Key Feature |
|---|---|---|---|
| Neonate under 4 months | Long bone metaphysis | Group B Streptococcus, E. coli | Crosses physis - can cause septic arthritis |
| Child 4 months to 4 years | Metaphysis of long bones | S. aureus, Kingella kingae | Metaphyseal vessels cross physis |
| Child over 4 years | Metaphysis | S. aureus 90% | Physis acts as barrier |
| Adult | Vertebral bodies | S. aureus, E. coli, Mycobacterium TB | Batson's plexus spread |
| Diabetic foot | Metatarsals, calcaneus | Polymicrobial, anaerobes, MRSA | Contiguous spread from ulcer |
| Sickle cell disease | Diaphysis, vertebrae | Salmonella more common than S. aureus | Only scenario where Salmonella predominates |
| IV drug user | Vertebrae, long bones | S. aureus, Pseudomonas, Candida | Haematogenous seeding |
| Post-surgical implant | Fracture site | S. aureus, S. epidermidis, Propionibacterium | Low virulence biofilm formers |
Cierny-Mader Classification
Anatomic Classification (Type I-IV)
| Type | Location | Characteristics | Treatment |
|---|---|---|---|
| Type I - Medullary | Intramedullary canal | Endosteal surface, hematogenous | Reaming, antibiotics, nail |
| Type II - Superficial | Surface of bone | Exposed cortex, soft tissue loss | Debridement, flap coverage |
| Type III - Localized | Full thickness, stable | Cortical sequestrum, stable bone | Debride, maintain stability |
| Type IV - Diffuse | Permeative, unstable | Loss of structural integrity | Resection, bone transport, arthrodesis |
Type III vs Type IV Distinction
The key distinction: Type III leaves the bone stable after debridement (can just excise the localized infected segment). Type IV becomes unstable after debridement (requires reconstruction with bone transport, free fibula, or arthrodesis). This fundamentally changes the surgical plan.
Clinical Relevance and Diagnosis
Imaging Hierarchy
Plain Radiographs (first line):
- Changes take 10-14 days to appear
- 30-50% bone loss needed to see lysis
- Look for: periosteal reaction, lytic lesions, sequestrum, involucrum
MRI (gold standard):
- 90% sensitive, 80% specific
- Shows marrow oedema (T2 hyperintense)
- Differentiates abscess from cellulitis
- Gadolinium enhances inflamed tissue
Nuclear medicine:
- Bone scan sensitive but not specific
- Labelled WCC scan more specific for infection
Microbiological Diagnosis
Tissue culture is the gold standard:
- Multiple deep samples (not sinus tract)
- Send for aerobic, anaerobic, fungal, TB cultures
- Minimum 3 samples increases yield
Blood cultures:
- Positive in 50% of acute haematogenous cases
- Usually negative in chronic osteomyelitis
Antibiotic timing:
- Hold antibiotics until cultures obtained
- Exception: septic patient requires empiric therapy
Sinus Tract Swabs are Unreliable
Cultures from sinus tract openings have only 50% concordance with deep bone cultures. Do NOT base antibiotic choice on superficial swabs - they grow skin commensals and colonizers, not the true pathogen. Always obtain intraoperative bone and tissue cultures before starting definitive antibiotics.
Brodie's Abscess (Subacute Osteomyelitis)
Diabetic Foot Osteomyelitis
Differential Diagnosis
Osteomyelitis is a notorious mimic - and is mimicked by - several aggressive lesions. The cardinal rule is that a lytic, painful bone lesion with periosteal reaction must be biopsied before assuming infection, because Ewing sarcoma and osteosarcoma can look identical.
Distinguishing Osteomyelitis from Key Mimics
| Condition | Typical Patient | Discriminating Features | Resolving Step |
|---|---|---|---|
| Ewing sarcoma | Child/adolescent | Onion-skin periosteal reaction, fever and raised inflammatory markers can mimic infection, diaphyseal | Biopsy (small round blue cells, EWSR1 translocation) |
| Osteosarcoma | Adolescent/young adult | Sunburst/Codman triangle, metaphyseal, soft-tissue mass with ossification | Biopsy and staging MRI/CT |
| Eosinophilic granuloma (LCH) | Child | Well-defined lytic lesion, vertebra plana, may be painful | Biopsy |
| Charcot neuroarthropathy | Diabetic, neuropathic foot | Midfoot, joint-centred destruction and deformity, less focal cortical erosion | MRI pattern plus probe-to-bone; bone biopsy if uncertain |
| Bone infarct (e.g. sickle cell) | Sickle cell disease | Serpentine sclerosis, no soft-tissue abscess; vs Salmonella osteomyelitis | MRI, aspiration/culture |
| Gout/septic arthritis (adjacent) | Variable | Joint-centred rather than intraosseous; crystals or pus on aspiration | Joint aspiration and culture |
The Mimic Rule
A permeative, painful bone lesion with periosteal reaction in a child is Ewing sarcoma until proven otherwise. Fever, raised CRP/ESR and a lytic diaphyseal lesion overlap completely with osteomyelitis - never debride such a lesion as "infection" without a diagnostic biopsy first.
Controversies & Areas of Uncertainty
Antibiotic Duration
Traditional 6 weeks is dogma more than data. OVIVA standardised 6 weeks but did not test shorter courses; paediatric RCTs support around 3 weeks. The optimal duration in adults, and whether it differs by Cierny-Mader type, remains unresolved.
Oral vs IV Route
OVIVA shifted practice toward early oral switch, but uptake varies and concerns persist for poorly bioavailable agents, non-adherent patients and certain organisms. Route is now individualised rather than reflexively IV.
Single- vs Two-Stage Surgery
Single-stage debridement with immediate soft-tissue cover and local antibiotic carriers (e.g. calcium sulfate) challenges the classic staged Lautenbach/bead approach, with promising but largely observational outcome data.
Diabetic Foot Osteomyelitis
Whether forefoot diabetic osteomyelitis needs surgery or can be cured medically is debated; IWGDF accepts antibiotic-only management in selected cases, but recurrence and amputation risk remain high.
Management Algorithm
Treatment Algorithm for Chronic Osteomyelitis
Confirm osteomyelitis: Clinical (pain, draining sinus), imaging (MRI), inflammatory markers (CRP). Hold antibiotics pending cultures. Plan surgical intervention.
Radical debridement of all necrotic tissue. Remove all sequestra, open medullary canal, excise sinus tracts. Obtain minimum 3 deep tissue cultures. Send specimen for histology. Dead space management (antibiotic beads, muscle flap, bone graft).
Organism-specific therapy guided by intraoperative cultures. MSSA: flucloxacillin/nafcillin 2g 6-hourly or cefazolin (BOA/AAOS/IDSA-aligned). MRSA: vancomycin or daptomycin. Adjust to sensitivities. Monitor CRP weekly - should fall by roughly 50% at 2 weeks. The OVIVA trial supports early oral switch when the patient is stable.
Switch to oral antibiotics once clinically improving and CRP falling, supported by OVIVA-level evidence. Total duration approximately 6 weeks. High-bioavailability agents: fluoroquinolones (often with rifampicin for staphylococcal biofilm), clindamycin, linezolid. Continue until CRP normalizes and patient asymptomatic.
Definitive reconstruction if needed. Bone transport for segmental defects. Free fibula for massive defects. Arthrodesis for joint involvement. Only proceed once infection controlled (normal CRP, no drainage).
Pathogen-Directed Antibiotic Selection (Global Reference)
These agents reflect convergent IDSA, BOA-BOAST, AAOS and EFORT/European practice. Exact agent and dose vary with local resistance patterns and renal function; the principle (narrow, high-bioavailability, pathogen-directed) is universal.
First-Line Antibiotic Choices by Organism
| Organism | First-Line Parenteral | Oral Step-Down | Duration |
|---|---|---|---|
| MSSA | Flucloxacillin/nafcillin 2g 6-hourly or cefazolin 2g 8-hourly | Flucloxacillin 1g 6-hourly; add rifampicin for biofilm | Approximately 6 weeks |
| MRSA | Vancomycin 15-20 mg/kg 12-hourly or daptomycin | Linezolid 600mg 12-hourly or doxycycline | Approximately 6 weeks |
| Streptococcus | Benzylpenicillin 1.8g 4-hourly | Amoxicillin 1g 8-hourly | Approximately 6 weeks |
| Gram-negative (Enterobacterales) | Ceftriaxone 2g daily | Ciprofloxacin 750mg 12-hourly | Approximately 6 weeks |
| Pseudomonas aeruginosa | Piperacillin-tazobactam 4.5g 6-hourly or ceftazidime | Ciprofloxacin 750mg 12-hourly | 6-8 weeks |
Evidence Base
Short vs Long Antibiotic Course - Childhood AHOM (Peltola RCT)
- Prospective RCT of 131 culture-positive acute haematogenous osteomyelitis cases in children
- 20 days vs 30 days of clindamycin or first-generation cephalosporin (IV only first 2-4 days)
- S. aureus caused 89% of cases; all strains methicillin-susceptible
- Except for 1 mild sequela per arm, all patients fully recovered - no difference between arms
- 24% needed no surgery; most had only diagnostic aspiration or drilling
Osteomyelitis and the Role of Biofilms in Chronic Infection
- Reviews biofilm attachment, development and maturation using S. aureus as the model organism
- Self-produced glycocalyx matrix shields bacteria from antibiotics and host immune cells
- Biofilm-embedded bacteria are orders of magnitude more tolerant of antibiotics than planktonic forms
- Explains the persistence of chronic bone infection and rationale for surgical source control
Surgical Management of Chronic Osteomyelitis
- Review of surgical techniques for chronic osteomyelitis (most commonly post-traumatic tibial)
- Cure requires pathogen isolation, radical debridement of all necrotic/infected tissue, then dead-space and soft-tissue reconstruction
- Discusses debridement, dead space management, Ilizarov bone transport and vascularised reconstruction
- Host morbidity strongly influences propagation and outcome - individualise treatment
A Clinical Staging System for Adult Osteomyelitis (Cierny-Mader)
- Seminal paper formalising the Cierny-Mader staging system for adult osteomyelitis
- Combines anatomic type (I medullary, II superficial, III localised, IV diffuse) with host physiologic class (A, B-local/systemic, C)
- Stage directs both the extent of surgery and the prognosis
- Type IV in a class-C host carries the worst outlook and may favour amputation over reconstruction
Oral versus IV Antibiotics for Bone and Joint Infection (OVIVA)
- Multicentre non-inferiority RCT across 26 UK centres, 1054 adults with bone or joint infection
- Oral vs intravenous antibiotics for the first 6 weeks after surgery or start of treatment
- Oral therapy was non-inferior to IV for definitive treatment failure at 1 year (margin 7.5 percentage points)
- Oral arm had fewer intravenous-catheter complications and shorter hospital stay
Osteomyelitis (Lew & Waldvogel Seminal Review)
- Authoritative review establishing the contiguous-focus / vascular-insufficiency / haematogenous framework
- Bone biopsy for microbiology and histology is key to targeted, long-lasting therapy
- Chronic osteomyelitis with sequestrum requires surgical debridement for cure; acute disease may respond to antibiotics alone
- Multidisciplinary care (orthopaedics, infectious diseases, plastic and vascular surgery) underpins success
Exam Viva Scenarios
Use these scenarios to practise clinical reasoning and management decisions
Scenario 1: Chronic Tibial Osteomyelitis Classification
"A 45-year-old male presents 18 months after open tibial fracture ORIF. He has persistent drainage from the anterior shin. MRI shows intramedullary signal abnormality with cortical sequestrum but the tibia appears structurally intact. CRP 45. How would you classify and manage this?"
Scenario 2: Pediatric Acute Osteomyelitis Pathophysiology
"Explain why acute haematogenous osteomyelitis in children typically affects the metaphysis of long bones, and why it can lead to septic arthritis in some cases but not others."
Scenario 3: Antibiotic Strategy and the OVIVA Evidence
"A 58-year-old man has had radical debridement and a local muscle flap for chronic tibial osteomyelitis. Intraoperative cultures grow methicillin-susceptible Staphylococcus aureus. The medical team plans 6 weeks of intravenous flucloxacillin via a PICC line. The patient is systemically well and keen to go home. How would you advise on antibiotic route and duration, and what evidence supports your view?"
MCQ Practice Points
Most Common Organism Question
Q: What is the most common causative organism in all age groups for osteomyelitis? A: Staphylococcus aureus - causes 80-90% of all osteomyelitis cases regardless of age. The exception is sickle cell disease where Salmonella is more common than S. aureus.
Biofilm Resistance Question
Q: Bacteria within biofilm are how many times more resistant to antibiotics than planktonic bacteria? A: 1000 times more resistant - this is why surgical debridement is mandatory for chronic osteomyelitis. Antibiotics cannot penetrate the glycocalyx matrix.
MRI Sensitivity Question
Q: What is the sensitivity of MRI for diagnosing osteomyelitis? A: 90% sensitive - MRI is the gold standard imaging modality, showing marrow oedema and soft tissue extension. Plain radiographs take 10-14 days to show changes.
Oral vs IV Antibiotics (OVIVA) Question
Q: For complex bone and joint infection, is oral antibiotic therapy inferior to intravenous therapy? A: No - the OVIVA RCT (Li et al, NEJM 2019, N=1054) showed oral antibiotics are non-inferior to IV for the first 6 weeks once the patient is clinically stable, with fewer line complications. First-line MSSA agent remains an antistaphylococcal penicillin (flucloxacillin/nafcillin) or cefazolin; MRSA needs vancomycin or daptomycin.
Guidelines, Registries & Global Practice
Global Epidemiology
- Acute haematogenous osteomyelitis is predominantly a paediatric disease; reported incidence is roughly 1 in 5,000 children per year in high-income settings, higher in low- and middle-income countries where presentation is often delayed.
- Chronic and contiguous osteomyelitis is increasingly an adult disease driven by open fractures, internal fixation, diabetic foot disease and prosthetic joints. Diabetic foot osteomyelitis is rising globally in parallel with the diabetes pandemic.
- Staphylococcus aureus remains the dominant pathogen worldwide across all settings; MRSA prevalence varies markedly by region (high in parts of the Americas and Asia, lower in much of Scandinavia and the Netherlands due to search-and-destroy policies).
- In regions with high tuberculosis burden, skeletal TB (including spinal Pott disease) is an essential differential for subacute/chronic bone infection.
Side-by-Side Society Guidance
How Major Bodies Frame Osteomyelitis Management
| Body (Region) | Emphasis | Distinctive Position |
|---|---|---|
| IDSA (US) | Vertebral osteomyelitis and diabetic foot guidelines | Image-guided/open biopsy before antibiotics; culture-directed therapy approximately 6 weeks |
| BOA-BOAST / BONE & JOINT (UK) | Combined ortho-plastic single-stage management | Specialist-centre, ortho-plastic teams; radical debridement plus immediate soft-tissue cover |
| AAOS (US) | Musculoskeletal infection principles | Surgical source control plus pathogen-directed therapy; MDT model |
| AO Foundation (Global) | Fracture-related infection (FRI) consensus | Standardised FRI definition (confirmatory vs suggestive criteria); debridement, stabilise, soft-tissue cover |
| EFORT / EBJIS (Europe) | Peri-implant and bone-joint infection definitions | Biofilm-focused; structured diagnostic criteria; rifampicin combinations for staphylococci |
| IWGDF (Global) | Diabetic foot osteomyelitis | Probe-to-bone test; conservative (medical) management viable for selected forefoot disease |
Practice Variation: High- vs Limited-Resource Settings
High-Resource Settings
- MRI, image-guided biopsy and molecular diagnostics readily available
- Single-stage ortho-plastic reconstruction with free flaps and local antibiotic carriers (calcium sulfate/Cerament)
- Early oral switch supported by OVIVA-level evidence
- OPAT services enable outpatient parenteral therapy
Limited-Resource Settings
- Later presentation; chronic sequestrum and large involucrum more common
- Reliance on plain radiographs and clinical diagnosis
- Sequestrectomy plus local bone-cement beads and staged management
- Higher TB-osteomyelitis burden mandates routine mycobacterial work-up
Universal Quality and Safety Principles
Applicable in every health system:
- Obtain deep tissue cultures before definitive antibiotics (unless the patient is septic)
- Justify and document antibiotic choice, dose and duration; review against culture at 48-72 hours under antimicrobial stewardship
- Informed consent for surgery must discuss recurrence risk (chronic osteomyelitis recurrence approximately 10-30%)
- Multidisciplinary input (infectious diseases, microbiology, plastic surgery for soft-tissue cover)
Common pitfalls and litigation themes: starting antibiotics before cultures, inadequate debridement, and relying on sinus-tract swabs instead of deep tissue.
OSTEOMYELITIS PATHOPHYSIOLOGY
Clinical summary
Key Pathophysiology
- •Biofilm on sequestrum = 1000x antibiotic resistance
- •Metaphyseal sinusoidal flow = seeding site in children
- •Sequestrum = dead bone, Involucrum = new bone shell
- •Elevated intraosseous pressure causes vascular compromise
Cierny-Mader Classification
- •Type I = Medullary, Type II = Superficial
- •Type III = Localized (stable after debridement)
- •Type IV = Diffuse (unstable after debridement)
- •A = Normal host, B = Compromised, C = Treatment worse than disease
Microbiology
- •S. aureus = 80% all cases
- •Pseudomonas = puncture wound through shoe
- •Salmonella = sickle cell disease
- •Polymicrobial = diabetic foot, trauma
Diagnosis
- •MRI = 90% sensitive - gold standard
- •CRP better than ESR for monitoring treatment
- •Deep tissue culture (NOT sinus tract swab)
- •Plain XR needs 10-14 days to show changes
Treatment
- •Surgery + antibiotics synergistic
- •Debride all necrotic tissue and sequestra
- •Approximately 6 weeks antibiotics; OVIVA = oral non-inferior to IV when stable
- •MSSA: flucloxacillin/cefazolin; MRSA: vancomycin/daptomycin