Acute osteomyelitis
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acute osteomyelitis pathology radiology
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Acute Osteomyelitis
Definition & Classification
Acute osteomyelitis is bone infection diagnosed within 2 weeks of symptom onset. Subacute osteomyelitis exceeds 2 weeks; chronic osteomyelitis presents months after onset. — Grainger & Allison's Diagnostic Radiology
Pathophysiology
Infection reaches bone via three routes:
- Haematogenous spread — most common in children and in adult vertebral disease
- Contiguous spread — from adjacent soft-tissue infection or sinusitis
- Direct implantation — trauma, open fractures, surgical instrumentation, animal bites
Infection preferentially seeds the metaphysis due to its rich, sluggish blood supply. From there it can:
- Spread laterally through Volkmann canals → breach cortex → lift periosteum → subperiosteal abscess
- Perforate periosteum → soft-tissue abscess
- Spread to epiphysis/joint (especially in neonates and adults after physeal fusion) → septic arthritis
Age-specific vascular anatomy drives this pattern:
- Neonates: metaphyseal capillaries connect to epiphyseal plate → easy joint extension, multifocal involvement in ~50%
- Children (>1 year): transphyseal vessels atrophy, cortex thickens → subperiosteal abscesses predominate
- Adults: after physeal ossification, metaphyseal-epiphyseal anastomoses reform → joint seeding possible again, but periosteum is firmly adherent, limiting subperiosteal abscess
Bacteria in bone form biofilm, where organisms exist in planktonic, slow-growing, and dormant states. Antibiotics target only metabolically active (planktonic) bacteria, explaining treatment difficulty and the rationale for surgical débridement in established infection. — Rosen's Emergency Medicine
Epidemiology & Risk Factors
- Acute haematogenous osteomyelitis (AHO) is most common in children <5 years; 2–3× more common in boys
- Long bones (femur, tibia, humerus) account for ~80% of cases
- Risk factors: diabetes mellitus, sickle cell disease, HIV, IV drug use, chronic corticosteroids, rheumatoid arthritis, prosthetic devices, immunosuppression
Microbiology
S. aureus is the leading organism in all age groups except neonates. MRSA is now the most common cause of AHO in children.
| Age Group | Key Organisms |
|---|---|
| Neonates | Group B Streptococcus, E. coli, S. aureus, S. epidermidis |
| Infants/children | S. aureus (MRSA dominant), Group A Strep, Kingella kingae |
| Adolescents/adults | S. aureus, Gram-negative rods (diabetics/elderly) |
| IV drug users | S. aureus, Pseudomonas aeruginosa |
| Sickle cell disease | Salmonella spp., S. aureus |
| Puncture wounds (foot) | P. aeruginosa |
| Animal/human bites | Pasteurella multocida, Eikenella, oral flora |
| War injuries/MDR | MRSA, Enterobacteriaceae, Acinetobacter |
Kingella kingae is fastidious, can mimic Haemophilus, and often requires PCR for diagnosis. H. influenzae type b has essentially disappeared as a cause in vaccinated children. — Rosen's Emergency Medicine, Grainger & Allison's
Clinical Features
Children (typically ages 1–10 years):
- Pain and reluctance to use the affected limb (sudden limp, inability to bear weight)
- Localized warmth, swelling, erythema — may develop later
- Systemic: fever, chills, malaise, vomiting — usually not toxic-appearing
- Point tenderness over the infected metaphysis is the most consistent finding
Adults:
- Fever, rigors; may appear toxic in severe cases
- Fatigue, malaise, anorexia (less consistent)
- Point tenderness is the hallmark; palpable warmth and soft-tissue swelling variable
- Vertebral osteomyelitis: back pain in ~90%, tenderness over spinous process; neurological deficits in <40%; only 10% appear septic at presentation — diagnosis often delayed up to 4 months
Neonates:
- Often not severely ill; presents as failure to thrive
- Minimal systemic signs; diagnosis frequently delayed
- Multiple sites involved in ~50%; concurrent septic arthritis common
Investigations
Laboratory
- ESR and CRP are elevated in virtually all cases (ESR/CRP 98–100% in vertebral osteomyelitis)
- Leukocytosis is common but non-specific
- Blood cultures: positive in ~40% of children with AHO; tissue cultures positive in ~86% — obtain before antibiotics
- Gram stain of bone aspirate: often negative (biofilm effect)
Imaging
Plain radiographs — first-line:
- Normal in early disease; osseous changes appear only after 10–21 days (loss of ~30–50% bone mineral density)
- Useful to exclude fractures, Perthes disease, SFCE, malignancy
- Early finding: soft-tissue swelling; late: periosteal reaction, lytic lesions, cortical destruction
Ultrasound:
- Detects subperiosteal abscess as hypoechoic fluid along bone surface
- Useful to guide aspiration for culture; increased Doppler flow around soft-tissue abscesses
MRI — investigation of choice:
- High sensitivity and specificity for acute, subacute, and chronic osteomyelitis
- T1: low signal (bone marrow oedema, marrow replacement)
- T2/STIR: high signal (oedema, fluid)
- Post-gadolinium: enhancing walls of abscesses; non-enhancing pus collection
- Fat globule sign on T1 is pathognomonic for acute osteomyelitis
- Identifies physeal involvement, subperiosteal/intraosseous/soft-tissue abscesses, and septic arthritis
- For vertebral disease: MRI whole spine with and without contrast; T2-weighted sequences most diagnostic; sensitivity ~90%
CT:
- Good for cortical destruction and guided needle aspiration; less useful than MRI in children (radiation); helpful when MRI unavailable
Bone scintigraphy (³⁹mTc-MDP):
- Useful in early disease and for detecting multifocal involvement; non-specific (positive in trauma, tumour)
- Largely replaced by MRI for vertebral osteomyelitis
MRI Appearance
MRI of pediatric knee: T1 images (A, B) show hypointense metaphyseal lytic lesions (red arrows); T2 image (C) shows corresponding hyperintensity. Yellow arrows show transphyseal extension, demonstrating how infection can cross the physis in children.
Complications
- Chronic osteomyelitis (sequestrum, involucrum, Brodie abscess, sinus tracts)
- Septic arthritis (especially in neonates and adults)
- Bacteraemia and sepsis
- Pathological fracture through areas of bone destruction
- Growth disturbance in children if physis is involved (shortened or deformed limb)
- Vertebral: epidural abscess, spinal cord compression, paralysis (<15% of vertebral cases); paraspinal/psoas abscess, empyema
Management
Principles
Aggressive treatment of acute osteomyelitis reduces progression to chronic osteomyelitis. — Textbook of Family Medicine
1. Blood cultures before antibiotics
2. Empirical antibiotic therapy (tailor once cultures return):
| Scenario | Empirical Choice |
|---|---|
| Children (community-acquired AHO) | Anti-staphylococcal agent ± MRSA cover (clindamycin or vancomycin if MRSA prevalent) |
| MRSA suspected/confirmed | Vancomycin IV (first-line); linezolid, daptomycin as alternatives |
| Neonates | Anti-staphylococcal + cover for Group B Strep & Gram-negatives |
| IV drug user | Cover Pseudomonas: piperacillin-tazobactam or ciprofloxacin |
| Vertebral (adults) | Vancomycin + broad Gram-negative cover until cultures available |
Duration: typically 4–6 weeks total (IV followed by oral step-down when clinical improvement and falling inflammatory markers); children with uncomplicated AHO may do well with shorter courses if treated early.
3. Surgical indications:
- Failure to respond to antibiotics within 48–72 hours
- Subperiosteal or soft-tissue abscess requiring drainage
- Necrotic bone / sequestrum requiring debridement
- Septic arthritis complicating osteomyelitis
- Spinal cord compression in vertebral osteomyelitis
- Prosthetic joint involvement (complete surgical débridement essential — biofilm)
4. Orthopaedic involvement is mandatory for suspected osteomyelitis in children, neonates, and vertebral disease.
Key Differentials
- Septic arthritis, Ewing sarcoma, osteosarcoma, Langerhans cell histiocytosis, stress fracture, Perthes disease, SFCE, cellulitis
Sources: Grainger & Allison's Diagnostic Radiology; Rosen's Emergency Medicine, 10th ed.; Textbook of Family Medicine, 9th ed.; Sherris & Ryan's Medical Microbiology, 8th ed.
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