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Osteomyelitis
Osteomyelitis is inflammation of bone and marrow, virtually always secondary to infection. It may complicate any systemic infection or present as a solitary primary focus.
— Robbins Pathologic Basis of Disease, p. 989
1. Pathogenesis & Routes of Infection
Three mechanisms underlie osteomyelitis:
- Haematogenous spread — bacteria seed bone during bacteraemia; the most common route in children and for vertebral osteomyelitis in adults
- Contiguous spread — from adjacent infected soft tissue, or after surgery/trauma (open fractures, joint replacement, sternal surgery)
- Vascular insufficiency / neuropathy — chronic progressive deep soft tissue infection, most commonly diabetic foot
— Harrison's Principles of Internal Medicine 22e, p. 1105
Why the Metaphysis?
In haematogenous osteomyelitis, the metaphysis of long bones is preferentially infected because slow blood flow through looped sinusoidal vessels combined with microtrauma encourages bacterial seeding during bacteraemia. In neonates, metaphyseal vessels penetrate the growth plate, allowing spread to the epiphysis and adjacent joint. After growth plate closure in adults, anastomoses between metaphyseal and epiphyseal vessels facilitate bacterial spread to subchondral regions.
Figure: Pathogenesis of haematogenous osteomyelitis — bacteraemia seeds the artery supplying the metaphysis; microtrauma causes thrombosis of the sinusoidal vessel, and bacterial colonies establish. (Bailey & Love, p. 656)
2. Microbiology
| Setting | Common Organism(s) |
|---|
| All ages (most common) | Staphylococcus aureus (80–90% of culture-positive cases) |
| Neonates | Group B Streptococcus, E. coli |
| Children | S. aureus, Streptococcus pyogenes, H. influenzae |
| Sickle cell disease | Salmonella spp. (+ S. aureus) |
| Vertebral (acute) | S. aureus (40–50%), Gram-negative bacilli (E. coli, Pseudomonas), Streptococci |
| IV drug users / Candida | Candida spp., Pseudomonas aeruginosa |
| Subacute/chronic (endemic regions) | Mycobacterium tuberculosis, Brucella spp. |
| Implant-associated | Coagulase-negative staphylococci, Cutibacterium acnes |
S. aureus cell wall proteins bind bone matrix collagen, facilitating bacterial adherence.
— Robbins, p. 991; Harrison's, p. 1106
3. Classification
By Duration
| Type | Characteristics |
|---|
| Acute | Days to weeks; predominantly neutrophilic; no bone necrosis → antibiotics alone may suffice |
| Subacute | Weeks to months; includes Brodie's abscess; may present insidiously |
| Chronic | Bone necrosis (sequestrum) present; requires combined antibiotics + surgery |
The presence or absence of bone necrosis (sequestrum), not a specific duration, is the critical determinant guiding management.
— Harrison's, p. 1106
Cierny-Mader Classification (Long Bone Osteomyelitis)
The most widely used surgical staging system, classifying by anatomic type and host physiology:
Anatomic Stage:
- Type I — Medullary (endosteal) infection
- Type II — Superficial (cortical surface only)
- Type III — Localized (full-thickness cortex, stable bone)
- Type IV — Diffuse (segmental instability, worst prognosis)
Host Class:
- Class A — Normal immune system and vascularity
- Class B — Locally (BL) or systemically (BS) compromised
- Class C — Treatment worse than disease; suppressive therapy only
Systemic factors: malnutrition, diabetes, renal/hepatic failure, immunosuppression, tobacco/alcohol, extremes of age
Local factors: lymphoedema, venous stasis, major vessel compromise, neuropathy, radiation fibrosis
— Rockwood & Green's Fractures in Adults, 10e
4. Pathological Stages & Morphology
Acute Phase
- Bacteria proliferate → neutrophilic infiltration
- Necrosis of bone cells and marrow within 48 hours
- Infection spreads via Haversian canals to periosteum
- Subperiosteal abscess formation (especially in children)
- Periosteal elevation → impairs blood supply → amplifies necrosis
- Pus formation → pus passes through cortical bone; if periosteum is breached → soft tissue abscess → sinus tract to skin
Chronic Phase
- Sequestrum — devascularised dead bone (hallmark of chronic osteomyelitis)
- Involucrum — periosteal new bone formed around the sequestrum; may encase it → "bone-within-a-bone" appearance
- Brodie's abscess — a subacute form; well-defined lytic lesion with sclerotic rim on imaging; typically in young males
- Sinus tracts — pus tracks through gaps in involucrum to the skin surface
— Robbins, p. 991–992; Bailey & Love, p. 656; Grainger & Allison, p. 1637
5. Clinical Features
Acute Haematogenous Osteomyelitis (Children)
- Fever, malaise, toxaemia
- Localised bone pain, tenderness, erythema, warmth, swelling over the affected metaphysis
- Pseudoparalysis / refusal to bear weight / move limb
- May coexist with sympathetic joint effusion or frank septic arthritis
Vertebral Osteomyelitis (Adults)
- Back pain (most common presenting symptom, >85%)
- Lumbar spine 60%, thoracic 30%, cervical 10%
- Fever in only ~50% of patients (analgesic use blunts this)
- Neurological deficit if epidural abscess complicates
- Primary foci: urinary tract, skin/soft tissue, intravascular catheter, endocarditis
Chronic Osteomyelitis
- Persistent or recurrent pain, discharging sinus tracts, systemic malaise
- Intermittent flares after years of quiescence
6. Investigations
| Investigation | Findings |
|---|
| WBC, CRP, ESR | Elevated in acute; CRP is the best marker for treatment response |
| Blood cultures | Positive in ~50% of haematogenous cases — must be obtained before antibiotics |
| Bone biopsy / aspiration | Gold standard for organism identification; always attempt before antibiotics in non-septic patients |
| Plain X-ray | Changes lag 10–14 days behind disease onset; shows soft tissue swelling, cortical irregularity, periosteal reaction, lytic lesions |
| Ultrasound | Best first-line in children; shows subperiosteal fluid, guides aspiration |
| CT | Best for defining cortical destruction and detecting sequestra |
| MRI | Highest sensitivity and specificity; shows bone marrow oedema (T2 hyperintensity), abscess (penumbra sign in subacute), soft tissue involvement, epidural extension; investigation of choice for vertebral osteomyelitis |
| Bone scintigraphy / PET-CT | Useful for multifocal disease; PET-CT increasingly used for implant-associated infection |
Radiographic signs of improvement lag behind clinical recovery even on appropriate therapy.
— Grainger & Allison's Diagnostic Radiology, p. 1638
7. Treatment
General Principles
- Obtain microbiological diagnosis before starting antibiotics (blood cultures + bone biopsy) — unless sepsis mandates immediate treatment
- Drain pus whenever present
- Rest and splintage of the affected limb
- Treat underlying conditions (diabetes, malnutrition, sickle cell disease)
Antibiotic Therapy
Empirical therapy targets S. aureus as the most likely pathogen:
- Flucloxacillin (or nafcillin) IV for MSSA
- Vancomycin IV for MRSA or unknown organism in high-risk settings
- Adjust based on culture and sensitivity results
Duration:
- Acute without necrosis: 4–6 weeks total (IV then oral step-down)
- Chronic / with sequestrum: 6+ weeks combined with surgery
- Vertebral osteomyelitis: 6 weeks (RCT evidence — 6 weeks = 12 weeks, cure rate ~91% both groups)
- Implant-associated, early (<30 days): debridement + implant retention + 3 months antibiotics
- Implant-associated, late (>30 days): implant removal + 6 weeks antibiotics
IV vs. Oral:
Evidence from a landmark RCT shows oral antibiotics are non-inferior to IV when: correct spectrum, excellent oral bioavailability, normal GI function, no vomiting. High-bioavailability agents (fluoroquinolones, linezolid, co-trimoxazole) are suitable for oral step-down. A short initial IV course may reduce fluoroquinolone resistance emergence.
— Harrison's, p. 1107; PubMed PMID 40280255
Surgical Treatment
| Indication | Procedure |
|---|
| Abscess / subperiosteal collection | Incision and drainage |
| Chronic osteomyelitis with sequestrum | Sequestrectomy + debridement of dead bone (saucerisation) |
| Large bone defect after debridement | Bone grafting, Masquelet technique, distraction osteogenesis |
| Implant-associated infection (late) | Implant removal |
| Vertebral osteomyelitis (most acute haematogenous) | Usually does NOT require surgery |
| Vertebral with neurological deficit, spinal instability, undrained abscess | Surgical decompression / stabilisation |
8. Special Forms
Brodie's Abscess
- Subacute haematogenous osteomyelitis, mainly in young males
- Well-defined lytic cavity with sclerotic rim, most common in tibial metaphysis
- Penumbra sign on MRI (peripheral high-signal granulation tissue surrounding low-signal abscess)
Vertebral / Spinal Osteomyelitis (Spondylodiscitis)
- Most common form of haematogenous osteomyelitis in adults
- MRI shows T2 hyperintensity in disc and adjacent vertebrae + gadolinium enhancement
- Complications: epidural abscess, spinal cord compression, vertebral collapse, psoas abscess
Diabetic Foot Osteomyelitis
- Arises from progressive deep soft tissue infection
- Diagnosis: "probe-to-bone" test (positive = bone felt through ulcer), MRI
- Treatment: prolonged antibiotics ± surgical debridement ± amputation
Tuberculous Osteomyelitis (Pott's Disease)
- Haematogenous spread from primary pulmonary focus
- Predilection for thoracolumbar vertebrae; insidious onset
- Gibbus deformity, psoas abscess, cord compression
- Tuberculosis dactylitis — "spina ventosa" (cyst-like cavities with diaphyseal expansion)
9. Complications
| Complication | Mechanism |
|---|
| Septic arthritis | Direct spread from adjacent metaphysis into joint |
| Growth plate damage | Epiphyseal vessel involvement in neonates/infants → limb length discrepancy, angular deformity |
| Pathological fracture | Cortical destruction weakens bone |
| Sinus tracts | Chronic suppuration tracking to skin |
| Squamous cell carcinoma | Rare malignant transformation in long-standing sinus tracts (Marjolin's ulcer) |
| Amyloidosis | Secondary (AA) amyloidosis in chronic infection |
| Epidural abscess / cord compression | Vertebral osteomyelitis |
10. Summary
"Not the duration of infection, but the presence or absence of bone necrosis is crucial. Acute osteomyelitis without bone necrosis can generally be treated with antibiotics alone. In contrast, for chronic osteomyelitis antibiotic treatment should be combined with debridement surgery."
— Harrison's Principles of Internal Medicine 22e, p. 1106
Key clinical pearls:
- Always obtain blood cultures and bone biopsy before antibiotics (unless septic)
- MRI is the imaging gold standard
- S. aureus is the cause in ~80–90% of culture-positive cases
- Oral antibiotics are non-inferior to IV when bioavailability is adequate (2025 meta-analysis, PMID 40280255)
- Surgery is required for chronic osteomyelitis with sequestrum, implant-associated infection, and vertebral disease with neurological compromise
Sources:
- Robbins Pathologic Basis of Disease, p. 989–993
- Harrison's Principles of Internal Medicine 22e, pp. 1104–1109
- Bailey & Love's Short Practice of Surgery, 28e, pp. 655–657
- Grainger & Allison's Diagnostic Radiology, p. 1620–1644
- Rockwood & Green's Fractures in Adults, 10e (Cierny-Mader Classification)
- Schwartz's Principles of Surgery, 11e