Osteomyelitis: Keys To Diagnosis And Treatment
The ESR, however, is not beneficial in gauging a response to treatment as the kinetics are too slow. The CRP is better in this regard as values will increase within a few hours of infection and will trend toward baseline values after a week of appropriate therapy.9,10 When evaluating for osteomyelitis in children, ESR and CRP have the best sensitivity and specificity when one uses them in combination.10
Procalcitonin is a relatively new laboratory marker for the determination of osteomyelitis. Secreted by the thyroid gland, procalcitonin is a precursor peptide to calcitonin. Procalcitonin is elevated during an acute infective process and studies have well documented its utility in the prediction of soft tissue infection.10,11 However, one study refuted procalcitonin’s usefulness in diagnosing osteomyelitis within the diabetic population, finding it to be an unreliable indicator.11
One must cautiously consider sinus tract cultures in those with chronic osteomyelitis. When Staphylococcus aureus is the cultured organism from the sinus tract, the results are more reliable. However, sensitivity is still only 60.5 percent and specificity is 45 percent with a positive predictive value of 72.2 percent.12 Generally, sinus tract organisms are much lower in sensitivity (50.9 percent) and specificity (20 percent) when Staph aureus is not the causative agent. Intraoperative bone culture remains more predictive in identifying the causative organisms.
Pertinent Insights On The Microbiology Of Osteomyelitis
Staphylococcus aureus continues to be the most common pathogen occurring in both traumatic and diabetic bone infections. It can be extremely difficult to treat for a number of reasons. Staphylococcus aureus adhesions interact with thrombin, vitronectin, fibrinogen, fibronectin, collagen, laminin, von Willebrand factor, elastin and bone sialoprotein. It is through these adhesions that colonization occurs.
Additionally, S. aureus contains protein A, toxins and capsular polysaccharides that allow for evasion of host defenses. Exotoxins and hydrolases also promote extracellular matrix destruction and intracellular penetration. Biofilm production also adds to the virulence of this microbe, making it very difficult for antimicrobials to attack and kill.13
Other pathogens commonly cultured in the diabetic foot infection include Streptococcus, Enterococcus, coagulase-negative staphylococci, gram-negative aerobic bacilli and anaerobes. Pseudomonas aeruginosa commonly arises in puncture wounds to the heel, especially in those that develop osteomyelitis. Pathogens such as Staphylococcus aureus, polymicrobial infections, gram-negative aerobic bacilli and anaerobes most commonly occur with traumatic osteomyelitis.13
Antimicrobial therapy remains the primary treatment for most cases of juvenile hematogenous osteomyelitis whereas in chronic osteomyelitis, a focal nidus of infection is often impenetrable to antibiotic therapy. In this instance, pharmaceutical treatment becomes secondary and surgical debridement with irrigation becomes primary. Despite adequate treatment, recurrence rates continue to range between 20 and 30 percent.14 Some recent studies have disputed that surgical intervention is always necessary and suggest that antibiotic therapy alone may be a viable treatment option even for complicated bone infections.15,16 What the literature does not dispute is that deep bone culture is necessary to guide definitive antibiotic therapy.13
Empiric antimicrobial coverage for diabetic osteomyelitis should always include coverage of methicillin resistant Staphylococcus aureus (MRSA). Clinicians can then tailor pharmaceutical therapy toward specific organisms once they acquire culture results. Intravenous therapy should continue for six to 12 weeks unless definitive debridement of infected bone has occurred. At this time, one may shorten the antibiotic course to two weeks.17