By Al Kline DPM

 

Introduction

 

Osteomyelitis is characterized as an acute or chronic inflammatory condition of bone due to secondary infection of bacterial organisms. There are basically two process of contracting osteomyelitis 1) hematogenous infection and 2) direct contiguous infection. Hematogenous osteomyelitis is a secondary bone infection caused by blood bacteriemia seeding infectious bacteria into the bone through the blood stream. This is a common cause of osteomyelitis in children. Over 85% of hematogenous osteomyelitis is reported in children. This infection is most commonly associated with vascular metaphyseal infection in the young, growing bone. Vessels can thrombose and bone will locally necrose from bacterial infection. Direct or contiguous osteomyelitis is the most common cause of bone infection caused by open ulceration in diabetes after a break in the skin barrier. The most common pathogen to cause this infection is staphylococcus aureus. However, ulcerative osteomyelitis is multibacterial in nature with common pathogens such as pseudomonas and streptococcus species as primary and secondary organisms.

 

Prevention

 

It has been shown that early intervention to prevent ulceration by addressing suspected areas of ulceration will decrease the patient’s risk of osteomyelitis and amputation. We advocate early intervention by decreasing areas of hyperkeratosis and skin changes with monthly debridement, if necessary, will help to prevent ulcer complications. This usually includes proper diabetic shoes and accommodative inserts. Identifying pressure points on the bottom of the foot and any structural changes is important. Midfoot and subcuboid ulcers are very common in Charcot arthropathy. These pressure areas should be addressed early. And if the accommodation is not enough, surgical intervention to decrease bone prominence is sometimes necessary.

 

Diagnosis

 

Cultures

Diagnosis of hematogenous osteomyelitis is most commonly confirmed by blood cultures and bone aspiration in children. However, the accuracy of blood and bone cultures is suspect and often unreliable in the presence of previous antibiotic treatment, which is often the case in osteomyelitis. Blood cultures are sensitive in 50% of cases in acute, untreated osteomyelitis. Bone aspiration or surgical biopsy will yield 60-90% specificity) and should be performed in cases of negative blood culture. Direct, contiguous osteomyelitis is more difficult to diagnose by standard culturing techniques. The gold standard to confirm diagnosis was always considered bone biopsy. Over the past decade, more studies have revealed that direct cultures are often unreliable. As early as 1991, Perry, et al reported that operative biopsy is more accurate to identify pathogenic organisms than standard swabbing or needle biopsy in the assessment of osteomyelitis. 60 patients underwent local swabbing and needle biopsies and it was found that there was no statistical significant difference in the two methods for isolating organisms. In 2005, Kessler, et al reported that organisms isolated by needle puncture was significantly lower compared to superficial swabbing in 21 diabetic patients with open ulcers and joint infection. The needle biopsies were performed away from the ulcer with ‘clean’ surrounding skin. However, Kessler found a statistical difference in needle aspiration vs. swabbing and found it more reliable than superficial swabbing. Although swabbing and needle aspiration is rarely required to confirm osteomyelitis in the diabetic patient with an open ulceration, it is a viable alternative in suspected osteomyelitis that is not confirmed by radiograph or MRI. However, needle biopsies are contraindicated in patients with vascular insufficiency or ‘high risk’ diabetes. In fact, direct ulcer swabbing of an ulcer bed is now discouraged and direct tissue biopsy has been shown to give a more accurate diagnosis of tissue and ulcer infection.

 

Imaging

 

Radiographs are an easy method of detecting osteomyelitis. However, it is not accurate in detecting early osteomyelitis. X-ray findings can also be confused with other radiographic changes that appear similar to osteomyelitis such as Charcot arthropathy, gout or septic arthritis just to name a few. Radiographic changes will not typically confirm osteomyelitis until 14-21 days post infection. In 28 days, there is a 90% specificity to bone changes including focal bone loss. In the past decade, MRI has been shown to be highly accurate in the diagnosis of osteomyelitis. The MRI is now considered the gold standard for diagnosing osteomeylitis. MRI has been shown to be most effective in the early detection and localization of osteomyelitis before radiographic confirmation. Sensitivity ranges from 90-100%. Three phase radionucleotide imaging with Technetium 99m has fallen out of vogue for the diagnosis of osteomyelitis. Bone ‘scams’ as Dr. Warren Joseph often called them are often unreliable for the diagnosis of bone infection. On a bone scan, osteomyelitis cannot be distinguished from a soft tissue infection, a neurotrophic lesion, gout, degenerative joint disease, post surgical changes, a healing fracture, a noninfectious inflammatory reaction or a stress fracture. In many cases, a bone scan will be positive despite the absence of bone or joint abnormality.

 

In 1991, Newman et al in the Journal of the American Medical Association found bone biopsy and culture unreliable (68%) in the diagnosis of osteomyelitis in diabetic foot ulcers in 41 diabetic foot ulcers. His team found leukocyte scanning highly sensitive for diagnosing osteomyelitis in diabetic foot ulcers and may be useful for monitoring the efficacy of antibiotic treatment. However, with the advance of magnetic resonance imaging and technology, leukocyte scanning with indium 111 and gallium 67 has also fallen out of favor. CT scanning and ultrasound technology has also been used to diagnose osteomyelitis. CT scanning can be useful in detecting small areas of osteolysis in cortical bone and gas collections in osteomyelitis with gas producing pathogens. Ultrasound is helpful in detecting fluid collections or abscesses associated with osteomyelitis around joints or early periostitis in osteomyelitis.

 

Treatment

 

Historically, the treatment of osteomyelitis falls into two groups: 1) antibiotic therapy or 2) surgical management. Over the past decade, osteomyelitis has been shown to respond favorably to a combination approach of treatment that includes surgical debridement and antibiotic therapy.

 

Antibiosis

 

Appropriate antibiotic therapy is usually dictated by blood and bone cultures results. Empiric therapy is usually initiated on the basis of suspecting organism, patient’s age and clinical presentation. In cases of hematogenous osteomyelitis, treatment protocol dictates 4 to 6 weeks of intravenous antibiotic therapy. Surgical intervention is rarely indicated. In contiguous osteomyelitis, there is ongoing controversy as to the best approach of treatment, whether it is surgical or nonsurgical. I have found that surgical action is required in cases of open ulcer and bone infection in order to debride and remove the source of pathogenicity. Many times, antibiotic therapy has already been initiated orally and more aggressive treatment such as IV antibiotic therapy and surgical debridement is necessary. This is based purely on clinical observation and past experience by the treating physician. There have been many reported instances of treating acute and chronic osteomyelitis with antibiotic therapy alone with success.

 

A few decades ago, common pathogens found in cases of osteomyelitis included pseudomonas, Candida organisms and aspergillus. In 1980, over 60% of osteomyelitis cases isolated s. epidermidis and s. aureus. Puncture wounds were found to isolate pseudomonas in almost all cases of calcaneal osteomyelitis. This trend has not changed after 30 years and s. aureus including methecillin resistant staphylococcal aureas is now the most common pathogen in most forms of osteomyelitis.

The most common pathogen in hematogenous osteomyelitis is staphylococcus aureus. Other common pathogens include enterobacteriaceae organisms, group A and B Streptococcus species, and H influenzae. Treatment should consist of penicillinase-resistant penicillin and a third-generation cephalosporin. This could include treatments using Nafcillin (Unipen), 2 g IV every 6 hours, or Clindamycin phosphate (Cleocin Phosphate), 900 mg IV every 8 hours.

In the past year, there has been a resurgence of Methicillin resistant staphylococcus aureus or MRSA. This has been especially troublesome in the treatment of direct, contiguous MRSA osteomyelitis. Treatment options include administration of Zyvox, vancomycin, clindamycin and a third-generation cephalosporin. Zyvox or linezolid was approved for use by the FDA on April 18th, 2000. Zyvox (linezolid) is the first antibacterial drug in a new class to treat infections associated with vancomycin-resistant Enterococcus faecium (VREF), including cases with bloodstream infection. Zyvox also received approval for treatment of hospital-acquired pneumonia and complicated skin and skin structure infections, including cases due to methicillin-resistant Staphylococcus aureus (MRSA). Due to an increase in microbial resistance, Zyvox should only be used in cases resistant to MRSA after using Vancomycin.

Ciprofloxacin is indicated in the treatment of osteomyelitis associated with enteric gram-negative rod infections and anaerobic organisms. A third-generation cephalosporin can also be administered. In organisms cultured such as Serratia species or Pseudomonas aeruginosa, drugs such as Fortaz (Ceftazidime) 2gm IV every 8 hours or Imipenem (Primaxin), piperacillin-tazobactam (Zosyn) or cefepime (Maxipime) can be used.

 

Surgical debridement

 

Surgical debridement including tissue and bone debridement and limited amputations continues to be an important method of treatment for contiguous osteomyelitis. When abscesses form, rapid decompression of the space will provide the best protection against bone penetration and bone necrosis. Early diagnosis with ultrasound or MRI is essential. Irrigation techniques, both open and closed, have been used with success in the past. In cases of osteomyelitis and implants, removal of the implant and proper antibiotic therapy with limited debridement is indicated. The use of antibiotic impregnated beads are controversial, but remain in use today. In the 1970’s, many orthopedic physicians began using polymethly methacrylate beads impregnated with gentamycin. It was shown to liberate antibiotic in experimental models. This technique continues to be used in cases when implants have become secondarily infected in a joint space. It has also been used in cases of calcaneal osteomyelitis as an adjunct to IV antibiotic therapy in the presence of a large dead space after partial calcanectomy.

 

Hyperbaric therapy of HBO has also been controversial in the treatment of osteomyelitis. Several articles have suggested the it is helpful only as an adjunct to more aggressive therapy including surgical debridement with appropriate antibiosis. In my experience, I have witnessed two cases including osteomyelitis of the calcaneus and first metatarsal head treated with HBO therapy. One patient with calcaneal osteomyelitis underwent an entire year of hyperbaric treatment almost weekly. Both cases resulted in persistant osteomyelitis that required eventual surgical debridement or partial amputation.

The use of antibiotics following surgical debridement or amputation will also differ. Surgical debridement with limited amputation requires continued postoperative antibiotic treatment for up to 4 to 6 weeks. If a distal amputation is performed, for instance in cases of distal phalangeal osteomyelitis, and this portion is surgically removed to non-infective tissue, the patient will not be required to stay on antibiotics very long. Once the clinical signs of infection has resolved post amputation, the patient may be taken off antibiotics, sometimes as soon as one week after surgery.

 

Conclusion

 

Contiguous Osteomyelitis is a common complication of long standing diabetic ulceration. Proper debridement and careful evaluation of the diabetic patient will help decrease the incidence of ulceration. Proper shoe wear and diabetic evaluation in the presence of neuropathy is key in preventing unwanted ulcers that can lead to bone infection. If bone infection is suspected, early detection by MRI is crucial in the successful treatment. Proper identification of pathogen will also aid in the rapid treatment and resolution of osteomyelitis. Proper prevention, diagnosis, antibiotic treatment and surgical debridement all play an important role in the management of osteomyelitis.

 

References

 

King, R, Johnson, D. Osteomyelitis: emedicine, July 2006.

 

Waldovogel, F.A. et al Osteomyelitis: A Review of Clinical Features, Therapeutic Considerations and Unusual Aspects (First of Three Parts) The New England Journal of Medicine, Jan 1979.

 

Perry, C.R. et al Accuracy of Cultures of Material from Swabbing of the Superficial Aspect of the Wound and Needle Biopsy in the Preoperative Assessment of Osteomyelitis JBJS, 1991.

 

Kessler, L. et al Comparison of microbiological results of needle puncture vs. superficial swab in infected diabetic foot ulcer with osteomyelitis. Diabetic Medicine, 23, 99-102. May, 2005.

 

Carek, P. et al Diagnosis and Management of Osteomyelitis American Family Physician, Vol 63/No.12 June, 2001.

 

Newman, et al Unsuspected Osteomyelitis in Diabetic Foot Ulcers: Diagnosis and Monitoring by Leukocyte Scanning With Indium in 111 Oxyquinoline JAMA, Vol 266, No. 9 , Sept. 1991.

 

Waldvogel FA, Vasey, H. Osteomyelitis The Past Decade. N Engl J Med 1980. Hill, J. et al Diffusion of antibiotics from acrylic bone-cement in vitro JBJS, 1977 59:197-9.

 

Smith, D. et al Partial Calcanectomy for the Treatment of Large Ulcerations of the Heel and Calcaneal Osteomyelitis JBJS, 74-A, No. 4, April 1992.

© Al Kline DPM, 2006

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