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Paul Auwaerter, M.D.
02-11-2010
- Osteomyelitis (OM): infection of the bone.
- Acute OM: first presentation of osteomyelitis, < 2 weeks duration, no bony necrosis/sequestrum, usually hematogenously acquired.
- Chronic OM: not clearly defined but may include failure of prior OM treatment, symptoms >3 weeks, presence of necrotic bone/sinus tract or discharge.
- No widely agreed upon definitions or guidelines for treatment of OM in setting of diabetic foot infection (DFI).
- Two general categories of OM: 1) occuring within context of DFI (most common by far); or 2) other sites.
- OM may afflict up to 20% of patients with DFI (Berendt).
- OM due to DFI usually a consequence of neuropathy, callus formation and/or ischemia causing an ulcer that then involves periosteum and then bone.
- Risk factors for OM/DFI: duration of diabetes mellitus >10 years, peripheral neuropathy, abnormal foot structure/maldistribution of weight over the plantar surface, peripheral vascular disease, smoking, poor diabetic control, skin/nail disease (e.g. maceration, puncture wound, tinea pedis, onychomycosis), male gender.
- Acute OM: uncommon, usually hematologic origin; in adults mostly affects the axial skeleton (discitis/vertebral osteomyelitis).
- Chronic OM: predominant bone infection in DM. Usually due to contiguous problem: ulceration > trauma > surgery.
- Microbiology: Staphylococcal species most common (S. aureus including MRSA), streptococcus species (including Group A), Enterobacteriaceae, anaerobes. Enterococci often recovered, role usually uncertain. OM often polymicrobial.
- Suspect when ulcer fails to heal as expected.
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Differential: neuro-osteoarthropathy (may also co-exist, frequently causes positive bone scans without infection present).
- Probing (steel probe) to bone often used. Positive test increases likelihood of OM; negative test reduces likelihood. If lesion spitting bone fragments, OM is definite.
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Imaging: plain radiographs are inexpensive and usually obtained. Many findings such as periosteal reaction, soft tissue swelling, irregularity of cortical bone and demineralization are relatively non-specific and therefore require other testing. More advanced findings such as areas of sclerosis with adjacent radiolucencies or bony destruction are very suggestive. For chronic OM, the overall sensitivity of plain films is high although the specificity is low. For acute OM, a minimum 2-3 weeks to see early changes of OM.
- MRI: preferred test to evaluate bone and soft tissues (especially small bones, for larger bones CT adequate). Occasionally, acute Charcot neuro-osteoarthropathy may be read as OM.
- Bone Scan (Tc-99): Not recommended. Although superior to plain films, many false positives due to non-infectious causes (overlying inflammation, neuro-osteopathy).
- WBC scans: expensive, less sensitive than bone scans. Use mainly when MRI unavailable. PET: role uncertain, limited studies suggest good sensitivity/specificity.
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Lab: ESR > 70mm/hr or elevated CRP suggestive; however, limited bone involvement (e.g., toe) may not be associated with increased ESR or CRP. ESR and CRP elevations are nonspecific, and may be elevated by other active processes (cellulitis, etc.). Blood cultures uncommonly positive.
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Definitive diagnosis: Bone biopsy required, given chronic nature and wide range of possible microbial etiologies. Patient should be off antibiotics for at least 48 hours, preferably longer. One or more pathogens recovered from involved bone (+ compatible histopathology) makes the diagnosis. Obtain by needle biopsy through uninvolved skin or by operative approach. False negatives due to sampling error, fastidious organisms (anaerobes; or uncommonly actinomyces or mycobacterial species) or prior antibiotic therapy. False positives due to contamination from skin flora or other colonizing bacteria of the wound.
- Unfortunately, bone biopsy not widely utilized. If not obtained, important to note that wound swab often does not represent actual pathogens in bone. If wound swab performed, most clinicians can use to guide general selection of antibiotics, especially for S. aureus (MRSA) infection (Mackowiak).
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DFI OM: most commonly toes > metatarsal heads > calcaneum > midfoot (if Charcot neuropathic arthropathy present).
- Acute OM often accompanied by local pain and redness overlying bone + constitutional symptoms + fever.
- Chronic OM often without pain, fever or constitutional symptoms. In DFI, consider if non-healing ulcer, sinus tract, bone observed or probed.
- General approach: secure accurate microbiologic diagnosis (difficult, need surgeon or invasive radiologist) and remove necrotic bone and devitalized surrounding soft tissue in chronic infection.
- Without severe, acute infection, antibiotics can typically be held pending microbiological diagnosis. If severe, empiric antibiotics should be directed against Gram positives (staph, strep), Gram negatives (coverage of P. aeruginosa not needed unless suspicious) and anaerobes (see below). Initial therapy may be with oral or parenteral therapy.
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Antibiotics: Empiric: therapy should cover streptococci, staphylococci and Gram-negative bacteria (GNB), also anaerobes especially if a fetid foot. Examples: vancomycin 15mg/kg IV q12h (MRSA, strep), clindamycin 600mg IV q8 or 450mg PO q6-8 (strep, MSSA, some MRSA, anaerobes), piperacillin-tazobactam 3.375g IV q 4-6h (MSSA, strep, GNB including Pseudomonas aeruginosa, anaerobes), ertapenem 1g IV q24h (MSSA, strep, GNB except P. aeruginosa, anaerobes), ciprofloxacin 400mg IV q8-12h or 750mg PO twice daily (GNB including P. aeruginosa).
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Pathogen-directed therapy: use susceptibilities to guide, combination therapy may be required for polymicrobial infection. See "more" section for details.
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Suppressive or consolidative regimens: use susceptibilities to guide, some commonly used suggestions follow. Staphylococcus: (MSSA or MRSA): trimethoprim/sulfamethoxazole DS 1-2 tabs PO twice daily, minocycline or doxycycline 100mg PO twice daily, clindamycin 300-450mg PO three or four times daily, linezolid 600mg PO twice daily (beware of long-term complications of anemia, thrombocytopenia, peripheral neuropathy or optic neuritis). Some add rifampin 600mg PO once daily. Streptococci, GNB, anaerobes: amoxicillin/clavulanate 500mg PO q8h, moxifloxacin 400mg once daily. GNB: ciprofloxacin 750mg PO twice daily or levofloxacin 500-750mg once daily. Anaerobes: metronidazole 500 mg PO three times daily.
- Duration: acute OM usually treated for 4-6 wks with parenteral antibiotics. Chronic OM more variable and depends upon pathogen, degree of debridement, whether there is intent to cure and/or prevention of relapsing infection. If curative intent, use IV or oral therapy (with good bioavailability) for 6 weeks at a minimum, often longer--12 to 24 wks, some follow ESR/CRP and treat until normalization (assuming removal of any sequestrum). If non-curative intent, may treat a "flare" for six weeks +/- subsequent secondary suppression.
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Surgical: removal of necrotic bone essential for cure of chronic osteomyelitis. Other strategies including tissue or muscle flaps or bone grafting. Whether to amputate depends on whether sufficient medical/surgical options exist or failed. Also, level of amputation should take into consideration functional result desired and likelihood of recurrent ulcer/OM (e.g. AKA or BKA better than TMA).
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Adjunctive therapies: consider revascularization, local delivery of antibiotics via pump to bone or use of antibiotic-impregnated beads, hyperbaric oxygen (controversial).
- Other items deemed important to good outcomes: good glycemic control, smoking cessation, non-weight bearing (if foot involved). Consult with podiatrist, surgeon or wound-care specialist.
- Failure usually due to inadequate debridement, wrong antibiotic (especially if bone biopsy not performed), host problem (e.g., vascular insufficiency, immune suppression) or non-compliance.
- Little good data to suggest that predominantly medical or surgical management of diabetic OM should be favored. Overall success rates reported range 60-90% (Berendt; Calhoun).
- OM increases likelihood that patient may require amputation (if OM due to DFI).
- After successful treatment, dynamics of weight-bearing in the foot often altered. Podiatry involvement encouraged and footwear changes often needed.
- Superficial cultures of ulcers or sinus tracts are unreliable. They should not guide therapy if bone biopsy is possible, except if S. aureus is recovered.
- No antibiotic studies have shown superiority for any agent or combination.
- Antibiotics with excellent bone penetration (based on animal studies): clindamycin, fluoroquinolones and rifampin. Poor bone penetration typical of cefazolin and other beta-lactams. Unclear if this has any impact on human clinical outcomes.
- Several staging systems for OM have been described (Waldvogel, Cierny-Mader) but these are more useful to surgeons than initial diagnostic evaluation or treatment.
- Surgical intervention for foot-salvage individualized. Strategies used include amputation, two-stage debridement with secondary closure, primary debridement to bleeding bone with grafting (muscle, skin).
- Berendt AR, Peters EJ, Bakker K, et al.;
Diabetic foot osteomyelitis: a progress report on diagnosis and a systematic review of treatment.;
Diabetes Metab Res Rev;
2008; Vol.
24 Suppl 1; pp.
S145-61;
ISSN:
1520-7552;
PUBMED: 18442163
Rating:
Basis for recommendation
Comments:Systematic literature review highlights that there is insufficient data regarding medical v. surgical management or antibiotic choice to make firm recommendations.
- Calhoun JH, Manring MM;
Adult osteomyelitis.;
Infect Dis Clin North Am;
2005; Vol.
19; pp.
765-86;
ISSN:
0891-5520;
PUBMED: 16297731
Rating:
Basis for recommendation
Comments:Good overall review of OM including pathogenesis, diagnosis and management--both medical and surgical.
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