Osteomyelitis¶
Chapter 136 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Osteomyelitis is classified by etiology (hematogenous, contiguous, or vascular insufficiency), duration (acute/chronic), and anatomical location (vertebral, long bones, periarticular).
- The Cierny-Mader classification system is critical for surgical planning, stratifying long-bone osteomyelitis based on anatomical site, comorbidity, and radiographic findings.
- Acute osteomyelitis without bone necrosis is treated with antibiotics alone, while chronic cases require surgical debridement and prolonged antimicrobial therapy.
- MRI is the gold standard for diagnosis, with PET/CT as an alternative in patients with implants or when MRI is contraindicated.
- Antibiotic selection depends on pathogen susceptibility, with rifampin and fluoroquinolones effective against staphylococcal biofilms, and combination therapy often required for implant-associated infections.
1. DEFINITION & OVERVIEW¶
Osteomyelitis is an infection of bone, caused by microorganisms entering via hematogenous, contiguous, or vascular routes. It is classified as acute (short duration, <3 weeks) or chronic (long duration, >3 weeks) and further stratified by anatomical location (vertebral, long bones, periarticular). The Cierny-Mader system is used for trauma/surgical planning, emphasizing anatomical site, comorbidity, and radiographic findings.
Table 136-1: Antibiotic Therapy for Osteomyelitis in Adults without Implants¶
| Microorganism | Antimicrobial Agent (Dose, Route) |
|---|---|
| Staphylococcus spp. (Methicillin-susceptible) | Nafcillin or oxacillin (2 g IV q6h) followed by Rifampin (300–450 mg PO q12h) + Levofloxacin (750 mg PO q24h) |
| Staphylococcus spp. (Methicillin-resistant) | Vancomycin (15 mg/kg IV q12h) or Daptomycin (8–10 mg/kg IV q24h) followed by Rifampin (300–450 mg PO q12h) + Levofloxacin (750 mg PO q24h) |
| Streptococcus spp. | Penicillin G (5 million units IV q6h) or Ceftriaxone (2 g IV q24h) |
| Enterobacteriaceae (Quinolone-susceptible) | Ciprofloxacin (750 mg PO q24h) |
| Pseudomonas aeruginosa | Cefepime or Ceftazidime (2 g IV q8h) + Aminoglycoside followed by Ciprofloxacin (750 mg PO q12h) |
1.1 Pathogenesis¶
Hematogenous spread (most common in adults, especially vertebral osteomyelitis), contiguous spread from adjacent infections (e.g., post-surgical or trauma), and vascular insufficiency/nerve damage (e.g., diabetic foot). Biofilm formation by pathogens like S. aureus or C. acnes is a key factor in chronicity.
1.2 Classification¶
Cierny-Mader system: Long-bone osteomyelitis (acute/chronic), vertebral osteomyelitis (acute/chronic), and periarticular osteomyelitis. Acute vs. chronic based on duration, presence of sequestra, and response to treatment.
2. EPIDEMIOLOGY¶
Incidence varies by region and population. Vertebral osteomyelitis: 2.2–5.8 cases/100,000 person-years (age-dependent, higher in males ≥ 70 years). Long-bone osteomyelitis: posttraumatic or postsurgical, with risk factors including open fractures, diabetes, and immunocompromise. Subacute/chronic cases are more common in endemic regions (e.g., tuberculosis, brucellosis).
2.1 Risk Factors¶
Diabetes, peripheral neuropathy, vascular insufficiency, immunocompromise (HIV, transplant recipients), and prior surgery/trauma. IV drug use and poor wound healing increase risk of implant-associated infections.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Common pathogens: S. aureus (acute), coagulase-negative staph, C. acnes (chronic), and gram-negative bacilli. Hematogenous spread (vertebral osteomyelitis), contiguous spread (post-surgical/trauma), and vascular insufficiency (diabetic foot). Biofilm formation and host factors (e.g., diabetes, immunosuppression) contribute to chronicity.
3.1 Microbiology¶
S. aureus (most common), coagulase-negative staph, C. acnes, gram-negative bacilli, and rare pathogens (tuberculosis, brucellosis, fungi). In diabetic foot, P. aeruginosa and enterococci are common in chronic infections.
4. CLINICAL FEATURES¶
Nonspecific symptoms: fever, back pain (85% of vertebral cases), localized pain, and neurological deficits (radiculopathy, weakness). Chronic cases may present with sinus tracts, non-healing wounds, or systemic inflammation. Diabetic foot osteomyelitis often lacks classic signs due to neuropathy.
4.1 Complications¶
Epidural abscesses (15–20% of cases), septic arthritis, spinal instability, and chronic osteonecrosis. In diabetic foot, amputation risk is high if untreated.
5. DIFFERENTIAL DIAGNOSIS¶
Pyelonephritis, pancreatitis, viral syndromes, and non-infectious conditions (e.g., spondylitis, spinal stenosis). In vertebral osteomyelitis, differentiate from erosive osteochondrosis, gouty spondylitis, or metastatic disease.
6. INVESTIGATIONS & DIAGNOSIS¶
MRI is the gold standard for detecting osteomyelitis, especially in vertebral and long bones. PET/CT is useful in patients with implants or when MRI is contraindicated. Blood tests (CRP, ESR) are sensitive but nonspecific. Bone biopsy and cultures are critical for confirming pathogens, especially in chronic cases.
Table 136-2: Antibiotic Therapy for Osteomyelitis with Orthopedic Devices¶
| Microorganism | Antimicrobial Agent (Dose, Route) |
|---|---|
| Staphylococcus spp. (Methicillin-susceptible) | Rifampin (450 mg PO/IV q12h) + Nafcillin or Oxacillin (2 g IV q6h) |
| Staphylococcus spp. (Methicillin-resistant) | Rifampin (450 mg PO/IV q12h) + Vancomycin (15 mg/kg IV q12h) or Daptomycin (8–10 mg/kg IV q24h) |
| Streptococcus spp. | Penicillin G (18–24 million units/d IV) or Ceftriaxone (2 g IV q24h) for 4 weeks followed by Amoxicillin or Clindamycin |
| Enterobacteriaceae | b-lactam (based on susceptibility) for 2 weeks followed by Ciprofloxacin (750 mg PO q12h) |
6.1 Imaging¶
MRI: High sensitivity for detecting bone marrow edema and sequestra. CT: Useful for assessing bone destruction and guiding biopsy. Bone scans (SPECT/CT) help in chronic cases but are less sensitive in the first year post-surgery.
7. MANAGEMENT & TREATMENT¶
Acute cases: IV antibiotics (6–8 weeks) with surgical debridement if necrosis is present. Chronic cases: Long-term antibiotics (3–6 months) with surgical debridement. Implant-associated infections require device removal or prolonged suppressive therapy. Rifampin and fluoroquinolones are key for biofilm disruption.
7.1 Surgical Management¶
Debridement, implant retention (if stable), or removal (in chronic/implant-associated cases). Early infections (<3 weeks) may be treated with debridement and antibiotics, while late infections require prolonged therapy.
8. PROGNOSIS & COMPLICATIONS¶
Mortality: 6–20% in secondary sternal osteomyelitis. Chronic complications include spinal instability, septic arthritis, and amputation in diabetic foot. Prognosis is poor in immunocompromised patients or those with multidrug-resistant pathogens.
9. SPECIAL CONSIDERATIONS¶
Diabetic foot osteomyelitis: Requires strict glycemic control, offloading, and early surgical debridement. In pregnancy, antibiotic selection must avoid teratogens. Elderly patients with vascular insufficiency face higher risks of chronicity and complications.
10. KEY POINTS & CLINICAL PEARLS¶
- MRI is the gold standard for diagnosing osteomyelitis.
- Acute vs. chronic classification guides treatment duration and surgical intervention.
- Rifampin and fluoroquinolones are essential for biofilm disruption.
- Diabetic foot osteomyelitis requires multidisciplinary management to prevent amputation.
- Early surgical debridement is critical in implant-associated infections.