Epidemiology


  • Hematogenous osteomyelitis
    • More common in children and adolescents
    • Incidence is increasing in adults, driven by a rise in vertebral osteomyelitis
  • Exogenous osteomyelitis: more common in adults

Etiology


Routes of infection

  • Hematogenous osteomyelitis (endogenous osteomyelitis): caused by hematogenous dissemination of a pathogen
  • Exogenous osteomyelitis: caused by a spread of bacteria (typically multiple pathogens) from the surrounding environment
    • Posttraumatic: infection following deep injury (penetrating injury, open fractures, severe soft tissue injury)
    • Contiguous: spread of infection from adjacent tissue
      • Secondary to infected foot ulcer in patients with diabetes
      • Iatrogenic (e.g., postoperative infection of a prosthetic joint implant)

Pathogen

  • Overall: Staphylococcus aureus
  • Sexually active young adults: Neisseria gonorrhoeae (presents as septic arthritis, tenosynovitis, dermatitis).
  • Sickle cell disease: Salmonella species, S. aureus. c
  • IV drug users (IVDU): Pseudomonas aeruginosaCandidaS. aureus (often involves vertebral spine, clavicle).
  • Prosthetic joint/hardware: Staphylococcus epidermidis.
  • Puncture wound through shoe: Pseudomonas aeruginosa. c
    • P. aeruginosa thrives in warm, moist, hydrophobic environments—specifically the foam/rubber inner soles of athletic shoes (sneakers).
  • Cat/dog bites: Pasteurella multocida.
  • Diabetic foot ulcer (polymicrobial): S. aureus, Gram-negatives, anaerobes.
  • Vertebral osteomyelitis (Pott disease): Mycobacterium tuberculosis.

Pathophysiology


Clinical features


Diagnostics


  • Initial / Screening LabsESR & CRP (highly sensitive; CRP tracks response to Tx). CBC (leukocytosis w/ left shift).
  • Initial ImagingPlain Radiographs (X-ray).
    • May be normal in early disease (first 10-14 days).
    • Early changes: Soft tissue swelling, periosteal reaction/elevation.
    • Late changes: Cortical erosion, lytic bone lesions, sequestrum (necrotic bone fragment), involucrum (thick layer of new periosteal bone).
  • Most Sensitive ImagingMRI w/ gadolinium (best test for early detection, soft tissue/epidural involvement; indicated if X-ray is negative but clinical suspicion remains high).
  • Confirmatory / Gold StandardBone biopsy and culture (CT-guided needle biopsy or open surgical biopsy).
    • Must perform before initiating Abx unless pt is hemodynamically unstable or septic.
    • Superficial wound/sinus tract swabs are unreliable (reflect skin flora; exception: S. aureus).

Treatment

  1. Obtain Diagnostic Samples: Bone biopsy/culture prior to Abx initiation (unless septic/unstable).
  2. Empiric Antibiotics (broad-spectrum, prolonged IV 4-6 weeks):
    • Standard empiricVancomycin (MRSA coverage) + 3rd/4th-gen Cephalosporin (e.g., Cefepime) OR Piperacillin-Tazobactam (Gram-negative & anaerobic coverage).
    • Sickle cell: Coverage for Salmonella & S. aureus (e.g., Ceftriaxone + Vancomycin). c
    • Puncture wound (shoe): Coverage for Pseudomonas (e.g., Cefepime or Ciprofloxacin).
  3. Targeted Antibiotics: De-escalate based on bone culture & sensitivity results.
  4. Surgical Intervention: Surgical debridement indicated for sequestrum removal, sinus tract excision, intraosseous/subperiosteal abscess, or failure to respond to Abx.
  5. Monitoring: Serial CRP/ESR levels to track response to therapy.