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Osteomyelitis Treatment & Management

  • Author: Stephen Kishner, MD, MHA; Chief Editor: Harris Gellman, MD  more...
Updated: Aug 24, 2015

Approach Considerations

Surgery is indicated for osteomyelitis if the patient has not responded to specific antimicrobial treatment, if there is evidence of a persistent soft tissue abscess or subperiosteal collection, or if concomitant joint infection is suspected. Debridement of necrotic tissues, removal of foreign materials, and sometimes skin closure of chronic unhealed wounds are necessary in some cases.

Although vertebral osteomyelitis does not usually necessitate surgical treatment, indications include failure to respond to antimicrobial therapy, neural compression, spinal instability, or drainage of epidural or paravertebral abscesses.

The Infectious Diseases Society of America has published clinical practice guidelines for the diagnosis and treatment of native vertebral osteomyelitis in adults, including recommendations regarding antibiotic therapy and surgical intervention.[31]


Medical Therapy

Antibiotic treatment should be based on the identification of pathogens from bone cultures at the time of bone biopsy or debridement.[1, 4] Bone cultures are obtained first, and suspected pathogens are then covered by initiation of a parenteral antimicrobial treatment. However, treatment may be modified once the organism is identified. Parenteral and oral antibiotics may be used alone or in combination depending on microorganism sensitivity results, patient compliance, and infectious disease consultation.

Prophylactic treatment with the bead pouch technique has been suggested in open fractures to reduce the risk of infection, with systemic antibiotics supplemented with antibiotic beads compared to using systemic antibiotics alone.

Local antibiotic therapy with gentamicin-impregnated Septopal beads, though available in Europe, is controversial.[32]  Factors involved in the debate include the length of implantation, the need for removal, and the choice of nonabsorbable versus bioabsorbable delivery vehicles. Prolonged implantation of antibiotic beads and spacers remains controversial owing to the risk of secondary infection and development of resistant organisms. Secondary infection stems from the beads, which may serve as a foreign body upon complete elution of antibiotic.

Traditionally, antibiotic treatment of osteomyelitis consists of a 4- to 6-week course.[4] Animal studies and observations show that bone revascularization after debridement takes about 4 weeks.

Oral antibiotics that have been proven to be effective include clindamycin, rifampin, trimethoprim-sulfamethoxazole, and fluoroquinolones. Clindamycin is given orally after initial intravenous treatment for 1-2 weeks and has excellent bioavailability. It is active against most gram-positive bacteria, including staphylococci. Linezolid is active against methicillin-resistant staphylococci and vancomycin-resistant Enterococcus. It inhibits bacterial protein synthesis, has excellent bone penetration, and is administered intravenously or orally.

Oral quinolones are often used in adults for gram-negative organisms. Quinolones have excellent oral absorption and may be used as soon as patient is able to take them. Rifampin has an optimal intercellular concentration and a good sensitivity profile for methicillin-resistant staphylococci. It is used in combination with cell wall active antibiotics to achieve synergistic killing and to avoid rapid emergence of resistant strains.

Empiric therapy is necessary when it is not possible to isolate organisms from the infection site.[1] Hospital-acquired infections are usually derived from methicillin-resistant staphylococci. Infections contracted outside the hospital are often polymicrobial with the presence of gram-negative bacteria.

Parenteral antibiotics should be administered for several weeks, often requiring patients to remain in the hospital for an extended duration. At this time, oral therapy is indicated only in children whose compliance is certain. Infection may fail to improve owing to the ability of bacteria to resist antibiotics. Some bacteria, such as S epidermidis in prosthesis infections, adhere to a biofilm that protects the organism from phagocytosis and impedes delivery of the antibiotic.

Rifampin must always be used in combination with other antibiotics for prosthesis infections because it acts on the biofilm and avoids recurrence. Infection may recur if rifampin is not used within a few weeks to a month of treatment.

Suppressive antibiotic therapy should also be directed by bone culture and is given orally when surgery is contraindicated.[4] Good bioavailability, low toxicity, and adequate bone penetration are important factors in treatment. If the infection recurs after 6 months of suppressive antibiotic treatment, a new, lifelong regimen of suppressive therapy may be tried.

Extensive studies of suppressive therapy with administration of rifampin, ofloxacin, fusidic acid, and trimethoprim-sulfamethoxazole for 6-9 months have been performed in patients with infected orthopedic implants. Studies have shown that, after discontinuation of antibiotics, no recurrence of infection occurred in 67% of patients treated with trimethoprim-sulfamethoxazole, 55% of patients treated with rifampin and fusidic acid, and 50% of patients treated with rifampin and ofloxacin.[4]


Surgical Therapy

Preoperative planning

The Cierny-Mader classification system (see Workup) plays an important role in guiding treatment. As described above, stage 1 and 2 disease usually do not require surgical treatment, whereas stage 3 and 4 respond well to surgical treatment. In Cierny-Mader class C hosts, treatment may be more harmful than the osteomyelitis itself.[5]

Operative treatment consists of adequate drainage, extensive debridement of necrotic tissue, management of dead space, adequate soft-tissue coverage, and restoration of blood supply.[4] When a fracture and stable hardware are involved, surgery is used to treat a residual infection after suppressing the infection until the fracture heals. Techniques involve second-stage hardware removal followed by treatment of an infected nonunion, often with an external fixator. External fixators, plates, screws, and rods may be used to restore skeletal stability at the infection site.[4] Since hardware tends to become secondarily infected, external fixation is preferred over internal fixation.

Remission or cure is most likely with extensive debridement, obliteration of dead space, removal of any hardware, and appropriate antibiotic therapy.

Debridement of all nonviable or infected tissue is critical because retained necrotic or infected debris can result in osteomyelitis recurrence. Bone debridement is performed until punctuate bleeding is noted.[4] The remaining tissue is still considered contaminated even after adequate debridement of necrotic tissue. Studies have shown that marginal resection may be sufficient in normal hosts. However, in compromised hosts, extensive resection seems to be much more important.

“Dead space” refers to the soft tissue and bony defect left behind after debridement.[4] Appropriate management of this space is necessary to reduce the risk of persistent infection from poor vascularization of the area and to maintain the integrity of the skeletal part. Dead space must be filled with durable vascularized tissue, sometimes from the fibula or ilium. Antibiotic-impregnated beads may be used for temporary sterilization of dead space. Vancomycin, tobramycin, and gentamicin are some of the common antibiotics used in these beads. Within 2-4 weeks, the beads may be replaced with cancellous bone graft.

Because two major aims of surgical treatment include resection of necrotic bone and thorough debridement of intraosseous and soft tissue fistula, CT scanning is sometimes performed when planning a surgical intervention and for guiding surgery. Preoperatively, CT scanning is helpful to characterize bone quality, demonstrate intraosseous fistula, and detect devitalized bone areas, or cortical defects that lead to soft tissue sinus tracts.[2]

When osteomyelitis involves a fracture, it is also important to include a workup to be sure the fracture has healed. Antibiotic-impregnated beads may be used as an effective measure to maintain sterile dead space until a definitive surgical procedure can be performed.

In order to apply the Ilizarov method successfully and to prevent damage to vital nerves and blood vessels, preoperative planning is helpful with careful attention to "safe zones" during wire insertion. It is important to adjust the skin to prevent tension on the skin-wire interface. Correction of the deformity or lengthening is better achieved by appropriately constructing the Ilizarov frame.[33]

Ilizarov method

The Ilizarov method, developed by G. A. Ilizarov in 1951, promotes bone growth through distraction osteogenesis using a specialized device and systematic approach. This technique has facilitated limb lengthening, decreased the incidence of many complications, and decreased the level of surgical intervention necessary.

The Ilizarov method involves the use of a tissue-sparing, cortical osteotomy-osteoclasis technique that preserves the osteogenic elements in the limb. To create a preliminary callus that can be lengthened, Ilizarov advocated a delay of several days before initiating distraction. A high-frequency, small-step distraction rhythm permits regeneration of good-quality bone and less soft-tissue complications such as nerve and vessel injury. An advantage of using this procedure is that it minimizes the prevalence of nonunion and thus further bone grafting by producing good-quality bone formation.

The risk of repeat osteotomy and osteoclasis is also decreased owing to less-premature consolidation of the lengthened segment.[34] However, Ilizarov techniques are often not tolerated well by patients, and other options, including amputation, may be preferred.

The Ilizarov external fixator is a popular device that is composed of wires, fixation bolts, rings, threaded rods, hinges, and plates, together allowing customized assemblies. Although this apparatus is stiff for bending and torsion, it is less stiff for axial loading. This feature is thought to help promote osteogenesis.[33]

The Ilizarov method is based on the concept of "tension stress," in which gradual distraction stimulates bone production and neogenesis. The Ilizarov device is attached to the distal or proximal portion of the affected bone. Bone regenerates as the screw and wire mechanism moves the healthy bone fragment at a maximal rate of approximately 0.25 mm 4 times per day for an overall rate of 1 mm per day. Gentle distraction allows bone formation and decreases the need for supplemental bone grafting and internal fixation. The distraction force permits tissue fibers and cells to become oriented in the same direction as the distraction vector, which is thought to mimic the process of natural bone growth.[33]

Nonunions, malunions, or defects of any length can be treated and may also be corrected using the Ilizarov method. At the same time, the Ilizarov technique is labor-intensive and may require at least 8 months of treatment. In addition, the fixator pins can be uncomfortable and often become infected. Amputation is an option if reconstruction is not suitable.

Wound closure

To arrest infection, it is necessary to provide adequate soft-tissue coverage.[4] Over small soft-tissue defects, a split-thickness skin graft may be placed, whereas large soft-tissue defects may be covered with local muscle flaps and free vascularized muscle flaps. Rotation of a local muscle with its neurovascular supply must be possible anatomically for that procedure to be successful.

These flaps bring in a blood supply, which is important for host defense mechanisms, new bone regeneration, delivery of antibiotics, and healing. They also may be used in combination with antibiotics and surgical debridement of necrotic and infected tissues. The fibula and iliac crest are common donor sites for free flaps.

Adjunctive hyperbaric oxygen therapy

Adjunctive hyperbaric oxygen therapy can promote collagen production, angiogenesis, and healing in an ischemic or infected wound.[4]


The Ilizarov technique is usually well tolerated by the patient, with little associated pain. A few complications that have been reported include pin-tract infections and cellulitis, flexion contractures above and below the frame, limb edema, and bone fragment rotation with malunion.[35]

The complication rate may be decreased by future trends to improve the Ilizarov method.[34] Some goals include improving the technique to prevent pin-track infections and osteomyelitis, premature or delayed consolidation of bone, angular or axial deviation of the new bone, joint contracture or instability, neurovascular compromise, and psychological adjustment reactions.


Long-Term Monitoring

After a corticotomy is made for bone lengthening, a latency period is required before distraction. Once distraction has begun using the Ilizarov technique, new bone should be apparent within 3-4 weeks. After obtaining the appropriate length or correcting the angular deformity, the apparatus remains in place until completion of the consolidation phase. During the postoperative period, it is necessary to adjust or modify the assembly, and the apparatus is removed when the goal is achieved.[33]

Because the apparatus may be in place for an extended period, even up to a year, special postoperative considerations are important.[33] Pain management may be a challenge because of the duration of mild to moderate postoperative pain. To prevent flexion contractures of the surrounding joints, a key element is intensive physical therapy and splinting techniques. Successful treatment also requires psychological support and family counseling. Some problems to be cautious of during the postoperative period include pin-track infections, premature or delayed consolidation, joint contractures, and pin breakage that may require replacement.

Imaging studies in the follow-up period are most useful in patients who have equivocal or worse clinical status at the end of therapy.

Contributor Information and Disclosures

Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans

Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.


James Monroe Laborde, MD, MS Clinical Assistant Professor, Department of Orthopedics, Louisiana State University Health Sciences Center and Tulane Medical School; Board of Advisors, Department of Biomedical Engineering, Tulane University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical School

James Monroe Laborde, MD, MS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Farheen Arshia Khan, DO Resident Physician, Department of Physical Medicine and Rehabilitation, Louisiana State University Health Science Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine, Clinical Professor, Surgery, Nova Southeastern School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, Arkansas Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

Steven I Rabin, MD Clinical Associate Professor, Department of Orthopedic Surgery and Rehabilitation, Loyola University, Chicago Stritch School of Medicine; Medical Director, Orthopedic Surgery, Podiatry, Rheumatology, Sports Medicine, and Pain Management, Dreyer Medical Clinic; Chairman, Department of Surgery, Provena Mercy Medical Center

Steven I Rabin, MD is a member of the following medical societies: AO Foundation, American Academy of Orthopaedic Surgeons, American Fracture Association, Orthopaedic Trauma Association

Disclosure: Nothing to disclose.

  1. [Guideline] Concia E, Prandini N, Massari L, Ghisellini F, Consoli V, Menichetti F. Osteomyelitis: clinical update for practical guidelines. Nucl Med Commun. 2006 Aug. 27(8):645-60. [Medline].

  2. Gross T, Kaim AH, Regazzoni P, Widmer AF. Current concepts in posttraumatic osteomyelitis: a diagnostic challenge with new imaging options. J Trauma. 2002 Jun. 52(6):1210-9. [Medline].

  3. Newman LG, Waller J, Palestro CJ, Schwartz M, Klein MJ, Hermann G. Unsuspected osteomyelitis in diabetic foot ulcers. Diagnosis and monitoring by leukocyte scanning with indium in 111 oxyquinoline. JAMA. 1991 Sep 4. 266(9):1246-51. [Medline].

  4. Calhoun JH, Manring MM. Adult osteomyelitis. Infect Dis Clin North Am. 2005 Dec. 19(4):765-86. [Medline].

  5. Paluska SA. Osteomyelitis. Clinics in Family Practice. 2004. 6:127-56.

  6. Shaw B A, Kasser J R. Acute septic arthritis in infancy and childhood. Clinical Orthopaedics & Related Research. August 1990. 257:212-225. [Medline].

  7. Vincent GM, Amirault JD. Septic Arthritis in the Elderly. Clinical Orthopaedics and related research. February/1990. 251:241-245. [Medline].

  8. Belthur MV, Birchansky SB, Verdugo AA, et al. Pathologic Fractures in Children with Acute Staphylococcus aureus Osteomyelitis. J Bone Joint Surg Am. 2012 Jan 4. 94(1):34-42. [Medline].

  9. Böhm E, Josten C. What's new in exogenous osteomyelitis?. Pathol Res Pract. 1992 Feb. 188(1-2):254-8. [Medline].

  10. Laughlin RT, Reeve F, Wright DG, Mader JT, Calhoun JH. Calcaneal osteomyelitis caused by nail puncture wounds. Foot Ankle Int. 1997 Sep. 18(9):575-7. [Medline].

  11. Mader JT, Cripps MW, Calhoun JH. Adult posttraumatic osteomyelitis of the tibia. Clin Orthop Relat Res. 1999 Mar. (360):14-21. [Medline].

  12. Roesgen M, Hierholzer G, Hax PM. Post-traumatic osteomyelitis. Pathophysiology and management. Arch Orthop Trauma Surg. 1989. 108(1):1-9. [Medline].

  13. Weber EJ. Plantar puncture wounds: a survey to determine the incidence of infection. J Accid Emerg Med. 1996 Jul. 13(4):274-7. [Medline].

  14. Beronius M, Bergman B, Andersson R. Vertebral osteomyelitis in Göteborg, Sweden: a retrospective study of patients during 1990-95. Scand J Infect Dis. 2001. 33(7):527-32. [Medline].

  15. Digby JM, Kersley JB. Pyogenic non-tuberculous spinal infection: an analysis of thirty cases. J Bone Joint Surg Br. 1979 Feb. 61(1):47-55. [Medline].

  16. Tseng CH, Huang WS, Muo CH, Kao CH. Increased risk of dementia among chronic osteomyelitis patients. Eur J Clin Microbiol Infect Dis. 2014 Aug 7. [Medline].

  17. Bernard L, Lübbeke A, Stern R, Bru JP, Feron JM, Peyramond D. Value of preoperative investigations in diagnosing prosthetic joint infection: retrospective cohort study and literature review. Scand J Infect Dis. 2004. 36(6-7):410-6. [Medline].

  18. Spangehl MJ, Masri BA, O'Connell JX, Duncan CP. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am. 1999 May. 81(5):672-83. [Medline].

  19. Abiri MM, Kirpekar M, Ablow RC. Osteomyelitis: detection with US. Radiology. 1989 Aug. 172(2):509-11. [Medline].

  20. Howard CB, Einhorn M, Dagan R, Nyska M. Ultrasound in diagnosis and management of acute haematogenous osteomyelitis in children. J Bone Joint Surg Br. 1993 Jan. 75(1):79-82. [Medline].

  21. Wheat J. Diagnostic strategies in osteomyelitis. Am J Med. 1985 Jun 28. 78(6B):218-24. [Medline].

  22. Howard CB, Einhorn M, Dagan R, Yagupski P, Porat S. Fine-needle bone biopsy to diagnose osteomyelitis. J Bone Joint Surg Br. 1994 Mar. 76(2):311-4. [Medline].

  23. Perry CR, Pearson RL, Miller GA. Accuracy of cultures of material from swabbing of the superficial aspect of the wound and needle biopsy in the preoperative assessment of osteomyelitis. J Bone Joint Surg Am. 1991 Jun. 73(5):745-9. [Medline].

  24. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: a review of clinical features, therapeutic considerations and unusual aspects. 3. Osteomyelitis associated with vascular insufficiency. N Engl J Med. 1970 Feb 5. 282(6):316-22. [Medline].

  25. Cierny G 3rd, Mader JT, Penninck JJ. A clinical staging system for adult osteomyelitis. Clin Orthop Relat Res. 2003 Sep. (414):7-24. [Medline].

  26. Gordon L, Chiu EJ. Treatment of infected non-unions and segmental defects of the tibia with staged microvascular muscle transplantation and bone-grafting. J Bone Joint Surg Am. 1988 Mar. 70(3):377-86. [Medline].

  27. Mader JT, Shirtliff M, Calhoun JH. Staging and staging application in osteomyelitis. Clin Infect Dis. 1997 Dec. 25(6):1303-9. [Medline].

  28. Ger R. Muscle transposition for treatment and prevention of chronic post-traumatic osteomyelitis of the tibia. J Bone Joint Surg Am. 1977 Sep. 59(6):784-91. [Medline].

  29. Weiland AJ, Moore JR, Daniel RK. The efficacy of free tissue transfer in the treatment of osteomyelitis. J Bone Joint Surg Am. 1984 Feb. 66(2):181-93. [Medline].

  30. Kelly PJ. Infected nonunion of the femur and tibia. Orthop Clin North Am. 1984 Jul. 15(3):481-90. [Medline].

  31. [Guideline] Berbari EF, Kanj SS, Kowalski TJ, Darouiche RO, Widmer AF, Schmitt SK, et al. 2015 Infectious Diseases Society of America (IDSA) Clinical Practice Guidelines for the Diagnosis and Treatment of Native Vertebral Osteomyelitis in Adultsa. Clin Infect Dis. 2015 Sep 15. 61 (6):e26-46. [Medline].

  32. Zalavras CG, Patzakis MJ, Holtom P. Local antibiotic therapy in the treatment of open fractures and osteomyelitis. Clin Orthop Relat Res. 2004 Oct. (427):86-93. [Medline].

  33. Louie KW. Ilizarov method. West J Med. 1991 Aug. 155(2):170. [Medline].

  34. Rosenfeld SR. The Ilizarov method. West J Med. 1995 Dec. 163(6):568. [Medline].

  35. Gateley DR, Irby SJ, Martin DL, Simonis RB. Ilizarov bone transport for the treatment of chronic osteomyelitis: a rare complication. J R Soc Med. 1996 Jun. 89(6):348P-50P. [Medline]. [Full Text].

  36. May JW Jr, Jupiter JB, Weiland AJ, Byrd HS. Clinical classification of post-traumatic tibial osteomyelitis. J Bone Joint Surg Am. 1989 Oct. 71(9):1422-8. [Medline].

Osteomyelitis of T10 secondary to streptococcal disease. Photography by David Effron MD, FACEP.
Rarefaction and periosteal new-bone formation around the left upper fibula in a 12-year-old patient. This was caused by subacute osteomyelitis.
Osteomyelitis, chronic. Image in a 56-year-old man with diabetes shows chronic osteomyelitis of the calcaneum. Note air in the soft tissues.
Osteomyelitis, chronic. Three-phase technetium-99m diphosphonate bone scans (static component) show increased activity in the heel and in the first and second toes and in the fifth tarsometatarsal joint.
Osteomyelitis, chronic. T1- and T2-weighted sagittal MRIs show bone marrow edema in L1 and obliteration of the disk space between L1 and L2.
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