Osteomyelitis

Introduction
Osteomyelitis is an infection of the bone, bone marrow, and surrounding soft tissue, caused by pyogenic bacteria, mycobacteria, or fungi. It may be acute or chronic, resulting in progressive inflammatory destruction, bone necrosis, and possible deformity. Prompt recognition and treatment are crucial to prevent permanent damage.

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Classification

1. By duration

• Acute osteomyelitis: Symptoms <2 weeks; marked inflammatory response; better prognosis if treated early.

• Subacute osteomyelitis: Symptoms 2–6 weeks; less severe presentation.

• Chronic osteomyelitis: Symptoms >6 weeks; characterized by dead bone (sequestrum) and new bone formation (involucrum).

2. By pathogenesis

• Hematogenous spread: Common in children; infection seeds bone via bloodstream.

• Contiguous spread: From adjacent infected soft tissue or joint; common in adults.

• Direct inoculation: Open fractures, penetrating injuries, orthopedic surgery.

3. By host status

• Healthy host vs. immunocompromised host (e.g., diabetes, HIV, malignancy).

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Etiology

Bacterial causes:

• Staphylococcus aureus (most common overall, including MRSA).

• Streptococcus pyogenes, Streptococcus pneumoniae.

• Gram-negative bacilli (Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae), especially in puncture wounds or IV drug use.

• Salmonella spp. (notably in sickle cell disease).

• Anaerobes (in bite wounds, diabetic foot infections).

Mycobacterial causes:

• Mycobacterium tuberculosis (Pott’s disease in the spine).

Fungal causes:

• Candida, Aspergillus, Blastomyces, Histoplasma (rare, usually in immunocompromised patients).

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Risk Factors

• Diabetes mellitus (especially with foot ulcers).

• Peripheral vascular disease.

• Immunosuppression (HIV, chemotherapy, corticosteroid use).

• Recent trauma or surgery involving bone.

• Intravenous drug use.

• Presence of orthopedic implants.

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Pathophysiology
Infection triggers an inflammatory response, leading to increased intraosseous pressure, vascular compromise, and ischemia. Bone necrosis (sequestrum) provides a nidus for persistent infection. The body attempts to wall off infection by forming new bone (involucrum). Chronic osteomyelitis often has sinus tract formation to the skin surface.

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Clinical Features

Acute osteomyelitis:

• Fever, chills, malaise.

• Localized bone pain and tenderness.

• Swelling, erythema, warmth over affected area.

• Reduced range of motion in nearby joint.

Chronic osteomyelitis:

• Recurrent pain, swelling.

• Sinus tract drainage.

• Low-grade fever or no systemic symptoms.

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Common sites:

• Children: Long bones (femur, tibia, humerus).

• Adults: Vertebrae, pelvis, foot bones (especially in diabetics).

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Complications

• Pathological fractures.

• Growth disturbances in children (if growth plate involved).

• Septic arthritis.

• Chronic infection with sinus tracts.

• Squamous cell carcinoma arising from chronic sinus tracts.

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Investigations

Laboratory tests:

• CBC: Leukocytosis in acute cases.

• Elevated ESR and C-reactive protein (CRP).

• Blood cultures: Positive in 50–60% of acute hematogenous cases.

Imaging:

• Plain X-rays: May be normal early; later show periosteal elevation, lytic lesions, sclerosis.

• MRI: Most sensitive for early detection; shows marrow edema within 24–48 hours.

• CT: Good for detecting sequestrum and cortical bone detail.

• Bone scan (Technetium-99m): Useful if MRI unavailable.

Definitive diagnosis:

• Bone biopsy and culture (gold standard) for pathogen identification and antibiotic sensitivity.

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Management

1. General principles

• Prompt initiation of targeted antimicrobial therapy.

• Surgical intervention if necessary to remove necrotic bone, drain abscesses, and improve vascular supply.

• Treat underlying conditions (e.g., diabetes control).

2. Antimicrobial therapy

Empirical therapy should cover the most likely pathogens and be adjusted once culture results are available.

a. Acute hematogenous osteomyelitis (children, no prosthetic material)

• Cloxacillin (50 mg/kg IV every 6 hours) or Cefazolin (50 mg/kg IV every 8 hours).

• If MRSA suspected: Vancomycin (15 mg/kg IV every 6–8 hours) or Clindamycin (40 mg/kg/day IV in 3–4 divided doses).

• Duration: Typically 4–6 weeks (initial IV then switch to oral if improving).

b. Acute osteomyelitis in adults

• Nafcillin 2 g IV every 4 hours or Cefazolin 2 g IV every 8 hours.

• MRSA coverage: Vancomycin 15–20 mg/kg IV every 8–12 hours or Daptomycin 6 mg/kg IV daily.

• Duration: 4–6 weeks IV therapy.

c. Gram-negative coverage (e.g., in puncture wounds, IV drug use)

• Cefepime 2 g IV every 8 hours or Ceftazidime 2 g IV every 8 hours.

• Piperacillin–tazobactam 4.5 g IV every 6–8 hours for mixed infections.

d. Chronic osteomyelitis

• Longer antibiotic courses (≥6 weeks IV, often followed by oral suppression).

• Oral agents with good bone penetration include Clindamycin, Fluoroquinolones (e.g., Levofloxacin 750 mg daily, Ciprofloxacin 750 mg twice daily), and Linezolid 600 mg twice daily.

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3. Surgical management

• Indicated for:

  • Chronic osteomyelitis with necrotic bone (sequestrectomy).

  • Draining sinus tracts.

  • Abscess formation.

  • Failure of medical therapy.

• Procedures: Debridement, drainage, dead space management, soft tissue coverage, bone reconstruction.

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4. Adjunctive measures

• Adequate nutrition.

• Analgesia for pain control.

• Physiotherapy to maintain function and prevent contractures.

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Prognosis

• Acute osteomyelitis has a good prognosis with early treatment.

• Chronic osteomyelitis is more difficult to cure, often requiring repeated surgeries and long-term antibiotics.

• Risk of recurrence remains if vascular compromise persists.