> Table of Contents > Osteomyelitis
Tricia Elaine VanWagner, MD
image BASICS
  • An acute or chronic infection and inflammation of the bone; can occur as a result of hematogenous seeding, contiguous spread of infection, or direct inoculation into intact bone (trauma or surgery)
  • Two major classification systems:
    • Lew and Waldvogel classification
      • Classified according to duration (acute or chronic) and the mechanism of infection (hematogenous, contiguous)
    • Cierny-Mader classification
      • Based on the portion of bone affected, the physiologic status of the host, and other risk factors
      • Stage 1: medullary bone (typically monomicrobial)
      • Stage 2: bony surface (deep soft tissue infection or ulcer)
      • Stage 3: advance local infection (polymicrobial); often associated with open fracture or infected orthopedic hardware
      • Stage 4: Extensive disease (multiple tissue layers) requires combination medical and surgical therapy.
      • Class A host: otherwise normal
      • Class B host: immunocompromised
      • Class C host: Treatment risk outweighs benefit.
  • Special situations
    • Vertebral osteomyelitis
      • Acute, subacute, or chronic
      • May result from hematogenous seeding, direct inoculation, or contiguous spread
      • Back pain is most common initial symptom.
      • Lumbar spine is most commonly involved, followed by thoracic spine.
    • Infections of prosthetic joints
      • Obtaining specific diagnosis and targeted therapy quicker (easy access)
      • X-ray, then 3-phase bone scan, as MRI/CT is limited use in this circumstance
      • Treat with combination of antibiotics, including rifampin.
    • Posttraumatic infections
      • Depends on type of fracture, level of contamination, and severity of tissue injury
      • Tibia is the most commonly involved.
  • System(s) affected: musculoskeletal
  • Predominant age: more common in older adults
  • Predominant sex: male > female
  • Hematogenous osteomyelitis
    • Adults (most >50 years of age): vertebral
    • Children: long bones
  • Contiguous osteomyelitis: related to trauma and surgery in younger adults and decubitus ulcers and infected total joint arthroplasties in older adults
Generally low; normal bone is resistant to infection.
Up to 66% of diabetics with foot ulcers
  • Infection is caused by biofilm bacteria (protects bacteria from antimicrobial agents and host immune responses).
  • Acute: suppurative infection of bone with edema and vascular compromise leading to sequestra
  • Chronic: presence of necrotic bone or sequestra or recurrence of previous infection
  • Hematogenous osteomyelitis (typically monomicrobial)
    • Staphylococcus aureus (most common)
    • Coagulase-negative staphylococci and aerobic gram-negative bacteria
    • Salmonella sp. (sickle cell disease)
    • Mycobacterium tuberculosis and fungi (rare) in endemic areas or in immunocompromised hosts
  • Contiguous focus osteomyelitis (commonly polymicrobial)
    • Diabetes or vascular insufficiency
      • Coagulase-positive and coagulase-negative staphylococci
      • Streptococci, gram-negative bacilli, anaerobes (Peptostreptococcus sp.)
    • Prosthetic device
      • Coagulase-negative staphylococci and S. aureus
  • Diabetes mellitus
  • Recent trauma/surgery
  • Foreign body (e.g., prosthetic implant)
  • Neuropathy and vascular insufficiency
  • Immunosuppression
  • Sickle cell disease
  • Injection drug use
  • Previous osteomyelitis
  • Antibiotic prophylaxis
    • Clean bone surgery
      • Administer IV antibiotics within an hour of skin incision and continue no longer than 24 hours after the procedure.
    • Closed fractures
      • Cefazolin, cefuroxime, clindamycin (&bgr;-lactam allergy), or vancomycin (&bgr;-lactam allergy or MRSA infection)
    • Open fractures
      • In patients who can receive antibiotics within 3 hours of injury with prompt operative treatment, 1st-generation cephalosporins are preferred (clindamycin or vancomycin if allergy exists). Add aminoglycoside if type III fracture and penicillin for anaerobic coverage if farm injury or possible bowel contamination.
  • All diabetic patients should have an annual foot examination.
See “Risk Factors.”
  • Fever
  • Restriction of movement of the involved extremity or refusal to bear weight
  • Pain or tenderness in the infected area
  • Signs of localized inflammation
  • Motor and sensory deficits (vertebral infection)
  • Visible defect: probe to bone
  • Ulcer >2-cm wide and >2-cm deep increases likelihood in diabetic foot ulcers.
  • In patients with diabetes, classic signs and symptoms of infection may be masked due to vascular disease and neuropathy.
  • Systemic infection from other source
  • Aseptic bone infarction
  • Localized inflammation or infection of overlying skin and soft tissues (e.g., gout)
  • Brodie abscess (subacute osteomyelitis)
  • Neuropathic joint disease (Charcot foot)
  • Fractures/trauma
  • Tumor
Initial Tests (lab, imaging)
  • WBC is not reliable (can be normal with infection).
  • CRP is usually elevated but nonspecific.
  • ESR is high in most cases:
    • ESR >70 mm/hr increases likelihood.
  • Antimicrobial agents given prior to culture may alter culture results.
  • Disorders that may alter lab results: immunosuppression (including diabetes), chronic inflammatory disease, other/adjacent sites of infection (1)[C]
  • Routine radiography is first-line imaging: Classic triad for osteomyelitis is demineralization, periosteal reaction, and bone destruction:
    • Bone destruction is not apparent on plain films until after 10 to 21 days of infection.
    • Bone must undergo 30-50% destruction before damage is evident on films.
    • Bone scan is typically first test after plain x-ray in setting of joint prosthesis.
  • Radionuclide scanning (e.g., technetium, indium, or gallium) is useful when diagnosis is ambiguous or extent of disease is in question but is limited by low sensitivity and specificity.
  • MRI
    • Best for visualization of septic arthritis, spinal infection, and diabetic foot infections (1)[C]
    • T1-weighted image: low signal intensity
    • T2-weighted image: high signal intensity
    • MRI with gadolinium: sensitivity and specificity range from 60-100% to 50-90%, respectively
    • MRI is not helpful in assessing the response to therapy due to persistence of bony edema.
  • CT
    • Better than standard radiography in fragments and sequestration, but inferior to MRI in soft tissue and bone marrow assessment
    • Helps define soft tissues and identify sequestra

Follow-Up Tests & Special Considerations
  • A persistently elevated CRP (4 to 6 weeks) can be associated with persistent osteomyelitis.
  • Patients receiving prolonged antimicrobial therapy should be monitored with:
    • Weekly CBC
    • Liver and kidney function tests
Diagnostic Procedures/Other
  • Cultures
    • Definitive diagnosis is made by blood culture (hematogenous) or by needle aspiration/bone biopsy, with identification of the microorganism by culture and sensitivity or histology.
    • Patients with positive blood cultures and with radiographic evidence of osteomyelitis may not need bone culture.
    • Wound swabs and sinus tract cultures correlate well with the presence of S. aureus in deep cultures.
  • Image-guided bone biopsy for vertebral osteomyelitis (unless positive blood culture and positive radiographic evidence)
Test Interpretation
Inflammatory process of bone with pyogenic bacteria, necrosis
  • Adequate nutrition
  • Smoking cessation
  • Control diabetes
  • Direct empiric therapy toward probable organism and tailor once culture results are available.
  • Optimal antimicrobial concentration at infection site is essential (consider vascular perfusion to site).
  • Antibiotic dosing altered for renal function
  • Duration of therapy 4 to 6 weeks for acute osteomyelitis and generally >8 weeks for chronic osteomyelitis or MRSA infection
  • In children, early transition from IV to oral therapy, (after 3 to 4 days if responding well) followed by oral therapy for 3 weeks may be as effective as longer courses for uncomplicated acute osteomyelitis (2)[B].
First Line
  • S. aureus or coagulase-negative staphylococci
    • MSSA: &bgr;-lactam at high dose (nafcillin or oxacillin 2 g IV q4h) or cefazolin 2 g IV q8h
    • MRSA: vancomycin 15 mg/kg IV q8-12h (use q8h interval if CrCI >70 mL/min) with target trough of 15 to 20 &mgr;g/mL
  • Streptococcus sp.
    • Ceftriaxone 2 g IV q24h or cefazolin 2 g IV q8h
  • Enterobacter sp.
    • Fluoroquinolone (levofloxacin 750 mg IV/PO q24h) or ceftriaxone 2 g IV q24h
  • Pseudomonas aeruginosa
    • Ciprofloxacin 750 mg PO BID or levofloxacin 750 mg PO q24h
  • Anaerobes
    • Clindamycin 600 mg IV q8h (300 to 450 mg PO q6-8h)
Second Line
  • S. aureus
    • MSSA: fluoroquinolone plus rifampin (levofloxacin 750 mg IV/PO q24h plus rifampin 300 mg PO q12h or 600 mg PO q24h)
    • MRSA: linezolid 600 mg PO/IV q12h or daptomycin 6 mg/kg IV q24h
  • Streptococcus sp.
    • Penicillin G 4 million U q4-6h
  • Enterobacter sp. (quinolone-resistant, including extended-spectrum &bgr;-lactamase-producing Escherichia coli)
    • Carbapenem (imipenem/cilastatin) 500 mg IV q6h
  • P. aeruginosa
    • Cefepime or ceftazidime 2 g IV q8h (consider adding aminoglycoside)
  • Anaerobes
    • Metronidazole 500 mg IV/PO q6-8h
  • Hyperbaric oxygen therapy may be a useful adjunct.
  • Negative pressure wound therapy is a possible adjunctive treatment.
Surgical drainage, dead space management, adequate soft tissue coverage, restoration of blood supply, and removal of necrotic tissues improve cure rates.
Pediatric Considerations
Medullary osteomyelitis (stage 1) in children may be treated without surgical intervention (2)[B].
Admission Criteria/Initial Stabilization
Correct electrolyte imbalances, hyperglycemia, azotemia, and acidosis; control pain.
Bed rest and immobilization of the involved bone and/or joint
Discharge Criteria
Clinical and laboratory evidence of resolving infection and appropriate outpatient therapy
Patient Monitoring
Blood levels of antimicrobial agents, ESR, CRP, and repeat plain radiography as clinical course dictates
Diabetic glycemic control and foot care
  • Superficial and medullary osteomyelitis treated with antimicrobial and surgical therapy have a response rate of 90-100%.
  • Up to 36% recurrence rate in diabetics
  • Increased mortality after amputation
1. Malhotra R, Chan CS, Nather A. Osteomyelitis in the diabetic foot. Diabet Foot Ankle. 2014;5. doi:10.3402/dfa.v5.24445.
2. Howard-Jones AR, Isaacs D. Systematic review of duration and choice of systemic antibiotic therapy for acute haematogenous bacterial osteomyelitis in children. J Paediatr Child Health. 2013;49(9):760-768.
Additional Reading
  • Bhavan KP, Marschall J, Olsen MA, et al. The epidemiology of hematogenous vertebral osteomyelitis: a cohort study in a tertiary care hospital. BMC Infect Dis. 2010;10:158.
  • Dinh MT, Abad CL, Safdar N. Diagnostic accuracy of the physical examination and imaging tests for osteomyelitis underlying diabetic foot ulcers: metaanalysis. Clin Infect Dis. 2008;47(4):519-527.
  • Fraimow HS. Systemic antimicrobial therapy in osteomyelitis. Semin Plast Surg. 2009;23(2):90-99.
  • Stumpe KD, Strobel K. Osteomyelitis and arthritis. Semin Nucl Med. 2009;39(1):27-35.
  • Vardakas KZ, Kontopidis I, Gkegkes ID, et al. Incidence, characteristics, and outcomes of patients with bone and joint infections due to communityassociated methicillin-resistant Staphylococcus aureus: a systematic review. Eur J Clin Microbiol Infect Dis. 2013;32(6):711-721.
  • Zimmerli W. Clinical practice. Vertebral osteomyelitis. N Engl J Med. 2010;362(11):1022-1029.
  • M86.9 Osteomyelitis, unspecified
  • M86.00 Acute hematogenous osteomyelitis, unspecified site
  • M86.10 Other acute osteomyelitis, unspecified site
Clinical Pearls
  • Hematogenous osteomyelitis is usually monomicrobial, whereas osteomyelitis due to contiguous spread or direct inoculation is usually polymicrobial.
  • Acute osteomyelitis typically presents with gradual onset of pain.
  • Treatment of osteomyelitis often requires both surgical débridement and at least 6 weeks of antimicrobial therapy.