Current Diagnosis and Treatment in Orthopedics, 4th Edition

Chapter 8. Orthopedic Infections



Musculoskeletal infections are common; they can affect all parts of the musculoskeletal system; and they can be dangerous and even life threatening. Much has been learned in the last 20 years to treat a wide range of musculoskeletal infections effectively. Often a team including orthopedic surgeons, plastic surgeons, infectious disease specialists, as well as internists, nutritionists, and therapists, must collaborate to orchestrate the multidisciplinary care that may be required to treat these patients optimally. This chapter summarizes the pathogenesis, diagnosis, and treatment of infections relevant to orthopedics. The management of osteomyelitis, septic arthritis, and soft tissue infections is discussed and highlighted with clinical examples.

Because this subject is so important, other chapters in this book include discussions of special aspects of infection. Chapter 3 (Musculoskeletal Trauma Surgery) discusses appropriate management of open fractures, traumatic arthrotomies, and gunshot wounds to minimize the risk of infection. Chapter 5 (Disorders, Diseases, & Injuries of the Spine) describes the clinical identification and management of osteomyelitis of the spine, diskitis, and epidural abscess. Chapter 7 (Adult Reconstructive Surgery) outlines the care of patients with prosthetic joint infections. Chapter 9 (Foot & Ankle Surgery) carefully details the management of diabetic foot ulcers and infections. Chapter 10 (Hand Surgery) discusses the treatment of paronychia, felons, chronic hand infections, human bites, and web space abscesses. Chapter 11 (Pediatric Orthopedic Surgery) reviews acute hematogenous osteomyelitis, septic arthritis especially of the hip joint, puncture wounds of the foot, skeletal tuberculosis, and spinal diskitis.



All clinical infections must be thought of in terms of the attacking microbes and the host's defenses. Infections are more likely to occur if the organisms are more virulent and if the inoculum is larger. Bacteria can gain entry into the body from direct penetrating trauma, by hematogenous spread from adjacent or remote sites of infection, or during surgical exposures. This wide spectrum of clinical possibilities ranges from fight bites to seeding from bacterial endocarditis to intraoperative breaks in sterile technique.

In acute osteomyelitis in children, the metaphysis is commonly involved. It is thought that the end vessels of the nutrient artery empty into much larger sinusoidal veins, causing a slow and turbulent flow of blood at this junction. These conditions predispose bacteria to migrate through adjacent gaps in the endothelium and adhere to the matrix. Also, low oxygen tension in this region may compromise phagocytic activity of white blood cells. Thrombosis caused by infection results in a region of avascular necrosis that may lead to abscess formation. As pus accumulates and pressurizes, it can track through the cortex via the haversian system and Volkmann canals to collect beneath the periosteum. Subperiosteal abscesses may stimulate the formation of a periosteal involucrum. Once out of the cortex, pus can also track through soft tissues to the surface of the skin, forming a draining sinus.

The physis and joint capsule act as barriers to the flow of pus. However, secondary septic arthritis may occur if the infection begins in a region of bone within the confines of a joint capsule. Thus, the hip joint is particularly susceptible to secondary infection arising from a spreading osteomyelitis of the femoral head or neck. Additionally, pus may track through the transphyseal vessels found in infants up to 6 months of age, causing secondary septic arthritis.

In hematogenous septic arthritis, the synovial membrane lacks a basement membrane, facilitating the ingress of hematogenous bacteria into the joint space and resulting in an acute inflammatory reaction. The synovium becomes hyperemic and produces increased amounts of synovial fluid. Acute white blood cells infiltrate the joint space and the synovium hypertrophies. The cartilage may be eroded by the proteolytic enzymes released during phagocytosis. Cytokines and other inductive molecules produced by the leukocytes and synovial tissue recruit a further inflammatory response, which can eventually destroy all articular surfaces. Concurrent bone erosion usually begins in the periarticular folds of synovium at the junction of synovium and cartilage. Arthritis is the end result of articular bone and cartilage loss caused by joint sepsis.


Although the musculoskeletal system may be infected by any infectious agent, the great majority of infections are bacterial. Staphylococcus aureus, Streptococcus, and Haemophilus influenzae are the most common causes of acute hematogenous osteomyelitis in children. The most common causes of septic arthritis are Neisseria gonorrhoeae, S. aureus, and group AStreptococcus. Septic arthritis is less often caused by gram-negative organisms, including Escherichia coli, Pseudomonas aeruginosa, Klebsiella, Enterobacter, Serratia, Proteus, and Salmonella. Uncommon bacterial organisms include Borrelia burgdorferi (Lyme disease), Mycobacterium tuberculosis, Brucella, and the anaerobes Clostridium and Bacteroides. Unusual organisms that may preferentially infect immunocompromised patients include fungi (Blastomyces, Cryptococcus, Histoplasma, Sporotrichum, and Coccidioidomycoses) and atypical mycobacteria (kansasii, avium-intracellulare, fortuitum, triviale, and scrofulaceum). The increase in the immunocompromised population because of iatrogenic causes (eg, transplantation of organs) and other diseases (eg, AIDS and rheumatoid arthritis) has increased the spectrum of bacteria that can cause musculoskeletal infection. Some evidence even suggests that Paget disease is the manifestation of a slow virus infection of bone.

Table 8–1 lists common conditions associated with specific bacterial species. Antibiotic resistance is conferred in these circumstances by spontaneous mutation, transduction of resistance genes via plasmids, and conjugation.

Table 8–1. Bacterial Species Associated with Common Conditions.


Common Occurrence

Staphylococcus aureus 

Most common organism in osteomyelitis, acute hematogenous osteomyelitis (90%), and infected metal implants.

Group B strep

Infants < 1 year old

Haemophilus influenzae 

Children 1–16 years old

Pseudomonas aeruginosa 

Nosocomial, puncture wound through shoe

Pasteurella multocida 

Animal bite

Eikenella corrodens 

Human bite


Sickle cell disease


Diabetic ulcers, fight bites

Candida albicans 




Atypical mycobacteria


Escherichia coli 


Neisseria gonorrhoeae 

Septic arthritis in young sexually active adult


Ahmed S, Ayoub EM: Poststreptococcal reactive arthritis. Pediatr Infect Dis J 2001;20:1081. [PMID: 11734716] 

Bezwada HP et al: Haemophilus influenza infection complicating a total knee arthroplasty. Clin Orthop 2002;402:202.

Brook I: Joint and bone infections due to anaerobic bacteria in children. Pediatr Rehabil 2002;5:11. [PMID: 12396847] 

Dubost JJ et al: No changes in the distribution of organisms responsible for septic arthritis over a 20 year period. Ann Rheum Dis 2002;61:267. [PMID: 11830437] 

Franz JK, Krause A: Lyme disease (Lyme borreliosis). Best Pract Res Clin Rheumatol 2003;17:241. [PMID: 12787524] 

Geyik MF et al: Musculoskeletal involvement of brucellosis in different age groups: A study of 195 cases. Swiss Med Wkly 2002;132:98. [PMID: 11971204] 

Gonzalez TB et al: Acute bacterial arthritis caused by group C streptococci. Semin Arthritis Rheum 2001;31:43. [PMID: 11503138] 

McCarthy JJ et al: Musculoskeletal infections in children: Basic treatment principles and recent advancements. Instr Course Lect 2005;54:515. [PMID: 15948476] 

McLemore MM, Stapleton FB: Atypical septic arthritis due to Neisseria meningitides. J Tenn Med Assoc 1984;77:149.

Press J et al: Leukocyte count in the synovial fluid of children with culture-proven brucellar arthritis. Clin Rheumatol 2002;21:191. [PMID: 12111621] 

Shirtliff ME, Mader JT: Acute septic arthritis. Clin Microbiol Rev 2002;15:527. [PMID: 12364368] 

Tachi M et al: Pathophysiology and treatment of streptococcal toxic shock syndrome. Scan J Plast Reconstr Surg 2002;36:305. [PMID: 12477090] 

Weinstein MA, Eismont FJ: Infections of the spine in patients with human immunodeficiency virus. J Bone Joint Surg Am 2005;87:604. [PMID: 15741629] 


Any host with compromised immunity and wound healing or with an implanted synthetic or allograft material has an increased risk for musculoskeletal infection. Nonspecific factors include the skin as a mechanical barrier. Local host factors include the adequacy of the vascular supply and the presence of tissue injury. Systemic host factors that compromise immunocompetence include nutritional wasting; comorbid diseases such as diabetes mellitus, chronic renal and liver disease, cancer, AIDS, and autoimmune connective tissue diseases; and usage of immunosuppressing medications such as corticosteroids, methotrexate, or tumor necrosis factor inhibitors.

Patients with chronic renal and liver disease, diabetes, cancer, AIDS, autoimmune connective tissue disease, and nutritional wasting and those on immunosuppressive medications are particularly susceptible to infection.

Nutritional depletion with negative nitrogen balance, weight loss, and tissue wasting can easily develop in patients with severe musculoskeletal injuries, as well as in patients who suffer from cancer, gastrointestinal malabsorption syndromes, and other chronic medical conditions. The signs of gross long-standing malnutrition, including profound weight loss, pitting edema, and intercostal wasting, are easily identified, but the signs of acute malnutrition are less apparent and often go undetected. A patient with a major fracture has a 20–25% increase in energy expenditure, and one with multiple trauma or infection has a 30–55% increase. Liver and skeletal muscle glycogen stores can be depleted within 12 hours during severe stress. Even with adequate stores of fat, visceral and skeletal muscle protein may not be spared because fat is not a readily available energy source during severe stress. Therefore, patients who are malnourished have significantly higher infection rates after surgery than patients who have normal nutritional status. Table 8–2 outlines methods to detect malnutrition.

Table 8–2. Tests to Measure Nutritional Depletion.




< 3.5 g/dL


< 10 mg/dL

  Total lymphocyte count

< 1500/L


< 150 mg/dL



  Anergy panel


  Weight loss

> 4.5 kg

  Arm circumference

< 80% standard



Experimental studies indicate that all biomaterials commonly used for total joint arthroplasty increase the incidence of S. aureusinfections. In contrast, biomaterials appear to have no effect on E. coli and S. epidermidis infections except when polymethylmethacrylate is used, in which case the incidence rises markedly.

Adherence of bacteria to the surface of implants is promoted by a polysaccharide biofilm called glycocalyx that acts as a barrier against host defense mechanisms and antibiotics. In addition, this film makes culture of organisms difficult, even with the use of special techniques.

Mixing antibiotics such as vancomycin and gentamicin to methacrylate cement can lower the risk of infection from cemented metal joint replacements, presumably by killing surface bacteria before they can produce glycocalyx.

Implantation of small amounts of allograft bone and connective tissue may slightly increase the risk of postoperative infection, but massive osteoarticular allografts can dramatically elevate the risk (8–12%). Fresh and fresh-frozen allograft bone and soft tissue harvested and processed into implants in an aseptic manner are implicated in clostridium infections because of problems with not detecting contaminated donors and not sterilizing the tissue for spores. In 2001, approximately 875,000 of these implants were used in the United States, with a rate of infection with properly selected donors and treated tissues of much less than 0.1%

Synthetic suture materials such as nylon and polyglycolic acid are less likely to facilitate wound infection than natural suture materials such as silk and cotton. In this regard, monofilaments are superior to braided sutures in preventing infection, and resorbable materials are superior to nonresorbable materials. Therefore synthetic resorbable monofilaments are preferred in wounds that are potentially susceptible to infection.

Archibald LK et al: Update: Allograft-associated bacterial infections—United States, 2002. MMWR Morb Mortal Wkly Rep 2002;51:207. [PMID: 11922189] 

Kainer MA et al: Clostridium infections associated with musculoskeletal-tissue allografts. N Engl J Med 2004;350:2564. [PMID: 15201413] 

Mankin HJ, Hornicek FJ, Raskin KA: Infection in massive bone allografts. Clin Orthop 2005;432:210. [PMID: 15738824] 

Menovsky T et al: Skin closure in carpal tunnel surgery: A prospective comparative study between nylon, polyglactin 910 and stainless steel sutures. Hand Surg 2004;9:35. [PMID: 15368623] 



Transmission of bacterial and viral infections can easily occur in the clinic and hospital setting because health care workers are often in direct contact with patients. The risk of transmission can be reduced by using universal precautions, including hand washing before and after all patient or body fluid contact, and wearing gloves, masks, eye protection, and gowns when in contact with patients with known infections. Proper disposal of patients' waste, dressing materials, and surgical drains should be mandatory. Blades and needles (which should not be recapped) must be disposed of in a dedicated sharps box. Inpatients with easily transmitted infections or infections caused by bacteria resistant to certain antibiotics should be isolated in private rooms, and movement of these patients should be limited to reduce possible contact with other patients or health care workers.


The administration of prophylactic antibiotics immediately before surgery and intraoperatively for cases lasting longer than 3–4 hours is now a uniformly accepted standard of practice. Generally a first-generation cephalosporin is used. Vancomycin, clindamycin, or ciprofloxacin are useful alternatives if the patient has a cephalosporin allergy or an anaphylactic response to penicillin that indicates a potential cross-reactivity. Although the consensus opinion suggests that antibiotic prophylaxis should be administered approximately a half hour prior to skin incision, this may not allow adequate tissue levels to be obtained for some antibiotics in the area of interest. The administration of preoperative antibiotics should be withheld when intraoperative bacterial cultures are to be obtained because they inhibit the in vitro growth of the cultured bacteria and reduce the ability to identify the causative organism(s).


Sterile technique in the operating room is extremely important. The operative site is thoroughly prepped with a variety of topical antiseptics including isopropyl alcohol, chlorhexidine soaps, and iodine-based scrubs and paints. Sterile drapes effectively isolate the operative site from the rest of the patient, and sterile gowns and gloves isolate the surgeons and assistants from the patient. Surgeons may use double gloves, space suits, adherent plastic drapes, pulsatile lavage, and laminar flow operating rooms or rooms with ultraviolet lights as additional techniques that may lower the risk of intraoperative contamination, which is approximately 1% for clean, elective orthopedic cases. Breaks in sterile technique should be dealt with immediately and aggressively even if the operative site has to be reprepped and redraped and the surgeons have to regown and reglove.


Health care workers may be accidentally exposed to infection when poked by a needle or sharp wire, cut by a knife or a sharp bone fracture edge, or splashed in the eye. The primary concern is the possible transmission of hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus (HIV). The estimated risk of acquiring an infection by accidental blood transmission is 6–30% for HBV, 1.8% for HCV, and 0.3% for HIV. Logically, larger inoculations confer an increased risk of infection. If exposure with a potentially infected source occurs, the worker must wash the contact area with disinfectant and immediately report to the occupational health center to document the exposure. The viral status is determined in the exposed worker and the source patient by obtaining serologic tests for HBV, HCV, and HIV. HIV testing requires the source's informed written consent. (Rapid plasma reagent [RPR] for syphilis should also be checked.)

The threat of health care workers acquiring hepatitis B is now dramatically reduced because many health care institutions require their employees to be immunized against HBV. Immunization status is confirmed if the concentration of hepatitis B serum antibody (anti-HBV) is equal to 10 mIU/mL. However, if the worker is unvaccinated or a nonresponder to the vaccine and the source is known to be positive for hepatitis B, the worker should receive hepatitis B immunoglobulin (HBIG) and a series of hepatitis B vaccinations.

Currently there is no vaccination against HCV and no recommended prophylactic therapy for workers exposed to HCV. However, new drugs are being developed to treat active HCV infections and effective prophylaxis may soon be developed. If the source is known to have HIV, the worker should immediately begin a 28-day course of double or triple antiretroviral therapy.

Workers with any viral exposures should be subsequently monitored with serologic tests for HIV, HBV, and HCV at 6 weeks, 3 months, 6 months, and 1 year after exposure. These guidelines are frequently updated, and specific treatment recommendations should be discussed with the institution's occupational health specialist (Table 8–3).

Table 8–3. Testing and Treatment of Exposed Persons, Assuming Source Tests Positive and Exposed Person Tests Negative.


Seroconversion (percutaneous exposure)a

Serologic Test of Exposed Person


Efficacy of Rx

Hepatitis B


Virus antibody-positive

None, immunity intact


Virus antibody-negative

Hepatitis B immunoglobulin



Hepatitis B vaccination series




Hepatitis C

1.8% (0–7%)


Antiretroviral drugs for 4 weeks





Two- or three-drug regimend



aLarger inoculations from increased exposure confer higher risk of seroconversion.

bPatient may benefit from early treatment if symptoms develop.

c0.09% risk of seroconversion from mucosal exposure.

dThree drugs recommended if large exposure or source has AIDS.

Adapted, with permission, from Updated U.S. Public Health Service guidelines for the management of occupational exposures to HBV, HCV and HIV and recommendations for postexposure prophylaxis. MMWR 50(RR11):1–42, 2001. And from Guidelines for using retroviral agents among HIV infected adults and adolescents. Recommendations of the Panel on Clinical Practices for Treatment of HIV. MMWR 51(RR–7):1, 2002.

Clarke MT et al: Contamination of primary total hip replacements in standard and ultra-clean operating theaters detected by the polymerase chain reaction. Acta Orthop Scand 2004;75:544. [PMID: 15513484] 

Gillespie WJ, Walenkamp G: Antibiotic prophylaxis for surgery for proximal femoral and other closed long bone fractures. Cochrane Database Syst Rev 2001;1:CD000244. [PMID: 11279687] 

Owers KL, James E, Bannister GC: Source of bacterial shedding in laminar flow theatres. J Hosp Infect 2004;58:230. [PMID: 15501339] 

Tai CC et al: Antibiotic prophylaxis in surgery of the intervertebral disc. A comparison between gentamicin and cefuroxime. J Bone Joint Surg Br 2002;84:1036. [PMID: 12358368] 



Plain Films

Plain radiographs are useful in establishing a diagnosis of osteomyelitis or chronic septic arthritis. Initially plain radiographs do not show any bony changes in early osteomyelitis. After 7–10 days, an area of osteopenia may appear, heralding cancellous bone destruction. As the infection progresses, a periosteal reaction may be seen, and focal areas of cancellous and cortical bone destruction may become apparent. Chronic osteomyelitis is identified by more extensive bone destruction and the appearance of a reactive rim of bone called the involucrum, which envelops a sclerotic focus of necrotic bone called the sequestrum. The sequestrum is often radiodense compared with the adjacent involucrum.

Plain radiographs are usually normal in early septic arthritis. Only later in the disease do radiographs show cartilage loss and periarticular bone erosion. These radiographic features are not specific for infection and may be present in other arthropathies such as rheumatoid arthritis (RA) and pigmented villonodular synovitis.

Soft-tissue infections are virtually invisible on plain radiographs except for an occasional suggestion of soft-tissue swelling. The striking exception is encountered with air-producing infections causing "gas gangrene." Air in the soft tissues is quite clearly identifiable on plain radiographs as discrete radiolucent areas, analogous to bowel gas in a plain radiograph of the abdomen. Figure 8–1 is a radiograph of air in the calf of a patient with a life-threatening clostridial infection.

Figure 8–1.


Plain radiograph of the knee, showing air in the soft tissues of the calf and thigh arising from a necrotizing clostridial infection.


Ultrasound is useful at identifying a joint effusion and particularly beneficial in the evaluation of pediatric patients with suspected infections of the hip joint. Ultrasound may also aid in the identification and aspiration of soft-tissue abscesses.

Radionuclide Imaging

Radionuclide imaging is not routinely necessary to diagnose acute osteomyelitis and is often falsely negative in acute septic arthritis. This imaging modality is very sensitive but nonspecific in identifying bone disease. Commonly, infection cannot be distinguished from neoplasm, infarction, trauma, gout, stress fracture, postsurgical changes, adjacent soft-tissue infection, neurotrophic joints (Charcot joint), or arthritis. However, in equivocal cases, radionuclide imaging may help identify an infectious process before an invasive procedure is performed.

The most common imaging agents are technetium-99m and indium-111. Technetium-99m is administered intravenously. An early-phase scan is performed in 10–15 minutes. At this time most of the radioisotope is in equilibrium with the extracellular compartment and accumulates in areas of increased blood flow, such as areas associated with cellulitis. The late-phase scan is performed in 3 hours, and the radioisotope is localized to the skeleton in both the organic matrix and the mineral phase of the bone.

Imaging with indium-111 requires collection of 80–90 mL of venous blood, separation of the leukocytes in the sample, and labeling the leukocytes with indium-111 in vitro. The indium-labeled leukocytes are then returned to the patient's bloodstream intravenously, and scanning is done 18–24 hours later. One study found a sensitivity of 91% and a specificity of 62% for detecting osteomyelitis for indium-111 white cell scans.

Imaging with technetium-99m methylene diphosphonate is a highly sensitive technique and useful in cases of suspected acute hematogenous osteomyelitis. In an extensive study of 280 children, the sensitivity of technetium-99m imaging in accurately detecting acute osteomyelitis was 89%, the specificity was 94%, and the overall accuracy was 92%. All soft-tissue infections were correctly identified by this technique, and 37 studies were positive for septic arthritis, although 8 were falsely positive.

Although radionuclide imaging can be sensitive for chronic musculoskeletal infections, it is often nonspecific, and false-positive results may hinder diagnosis. Radionuclide imaging often cannot distinguish a chronic infection from aseptic loosening in patients with painful prosthetic joint replacements, and it is rarely necessary in establishing a diagnosis of septic arthritis.

Computed Tomography

Computed tomography (CT) with sagittal and coronal reformatting is particularly useful in identifying sequestra in cases of chronic osteomyelitis. Routinely discrete sequestra are isolated from the viable bone and are more radiodense than the surrounding involucrum. Also, sagittal and coronal reformatting can be very useful in further assessing the mechanical integrity of the bone and in determining the extent of fracture healing even in the presence of metal fixation hardware. CT can show expansion of a joint capsule and any evidence of bony destruction but is not specific for septic arthritis.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) with T2 and inversion recovery sequencing offers unparalleled visualization of bone marrow and soft-tissue inflammation associated with infection. Intravenous (IV) gadolinium concentrates in areas of increased vascularity and enhances regions of inflammation. Fluid collections are identified as dark signal voids where the gadolinium cannot penetrate because of the absence of vascular ingress. Thus, contrast MRI facilitates the identification of fluid collections within bones, joint spaces, and soft tissues that may represent abscesses and septic effusions.

Acute inflammation in bone and soft tissues is nonspecific. Acute inflammatory arthropathies may reveal synovial and adjacent soft-tissue inflammation, effusion, and periarticular bone inflammation, especially at the synovial-cartilage junction. These findings may be identical with acute septic arthritis, gout, or other inflammatory arthropathies including neuropathic Charcot joints. Pigmented villonodular synovitis may have many of the same features, although it can often be distinguished by areas of decreased signal uptake on T2 images that represent areas of hemosiderin deposition.

As infection progresses in a joint, eroded cartilage and subchondral bone can be seen along with hypertrophic synovium and pronounced effusion. Periarticular erosion usually precedes erosion along weight-bearing surfaces. These changes are accompanied by generalized inflammation in the adjacent bone marrow and soft tissues, including bursas and tendon sheathes. Formation of abscesses, synovial cysts, and sinus tracts are particularly well visualized.

Keat A: Reactive arthritis or post-infective arthritis? Best Pract Res Clin Rheumatol 2002;16:507. [PMID: 12406424] 

Palestro CJ et al: Osteomyelitis: diagnosis with (99m) Tc-labeled antigranulocyte antibodies compared with diagnosis with (111)In-labeled leukocytes—Initial experience. Radiology 2002;223:758. [PMID: 12034946] 

Roddy E, Jones AC: Reactive arthritis associated with genital tract group A streptococcal infection. J Infect 2002;45:208. [PMID: 12387782] 

Sigal LH: Update on reactive arthritis. Bull Rheum Dis 2001;50:1. [PMID: 12386943] 


Whenever possible, antibiotic therapy must be delayed until deep cultures of the infection site are obtained. It is imperative to take appropriate cultures prior to antibiotic administration because antibiotics can often inhibit bacterial growth in vitro. If the cultures fail to grow, the clinician must choose antibiotics empirically. However well informed the clinician may be, the selection of empirical antibiotics is a matter of guesswork, and treatment failure is more likely.

Deep cultures must be obtained percutaneously or intraoperatively using strict sterile technique. The overlying skin must be prepped with antiseptic to decrease the concentration of skin flora that might contaminate the culture sample. In addition to swabs of purulent fluid, bone and soft-tissue samples of the infected site should also be obtained. Additional tissue should be sent for histologic analysis because an acute suppurative infection can be distinguished from a chronic granulomatous infection, and an infection can be distinguished from an unsuspected neoplasm.

Superficial swabs of skin ulcers and draining sinus tracts usually identify colonizing bacteria rather than the pathogenic bacteria that must be eradicated. Therefore, the practice of obtaining superficial cultures of deep-seated infections should be avoided. Also, it is important to employ appropriate techniques for anaerobic cultures because these organisms can be difficult to isolate and may be responsible for a considerable amount of osteomyelitis. This is particularly true for diabetic patients with infected foot ulcers who have a high risk for mixed aerobic/anaerobic infections.

A Gram stain of the culture samples is not diagnostic by itself but may help identify the organism. Therefore, the preliminary information gained from a Gram stain should be used to confirm clinical suspicions such as a staphylococcal osteomyelitis (positive cocci in clusters) or a gonococcal septic arthritis (gram-negative cocci in pairs). Blood cultures should also be obtained in patients who present with acute symptoms of bacteremia, such as fever, chills, and sweats.

Joint aspiration is usually necessary to identify the organisms responsible for septic arthritis, although blood cultures may also be helpful in acute cases. The synovial fluid from an infected joint is opaque, light yellow or light gray, and nonviscous. Cell analysis often reveals a white blood count (WBC) of more than 100,000 and more than 90% polymorphonuclear (PMN) leukocytes (Table 8–4). Similarly, for infected prosthetic knee joints, cell counts and PMN leukocyte percentages were higher, with an average of 18,900/mL and 92% neutrophils compared to 300/mL and 7% neutrophils for joints with aseptic loosening. Iatrogenic contamination of a sterile joint space may occur if the arthrocentesis needle passes through an overlying soft-tissue infection. Therefore, erythematous skin or indurated soft tissue should be avoided when choosing a site for arthrocentesis.

Table 8–4. Analysis of Synovial Fluid.


Normal Results

Noninflammatory Effusion

Inflammatory Effusion

Septic Effusion

Gross Exam 






1–4 mL










Clear/pale yellow









  Mucin clotting





Microscopic Exam 






< 300

< 2000


> 80,000


< 25%

< 25%


> 75%

  Bacterial smear










  Glucose ratio




< 0.5

  Protein g/dL

< 3

< 3









Normal synovial fluid is clear and viscous. Inflammation causes synovial fluid to become more cloudy as the concentration of white cells increases. Traditionally, newsprint can be read through a vial of noninfectious transudate but not through a vial of infectious exudate. The synovial fluid/serum glucose ratio will decrease and the synovial protein concentration will increase. Besides a positive bacterial smear the most helpful indicators of infection are a white blood cell count greater than 50,000 and a percentage of polymorphonuclear leukocytes exceeding 75%. Many acute bacterial infections will generate a white cell count of greater than 100,000 and > 90% PMNs.


Pathologic examination of a tissue sample can help determine the presence of an infection, characterize the type and time frame of the infection histologically, identify the causative organism, and occasionally distinguish an infection from an unsuspected neoplasm.

During revision arthroplasty, samples of periprosthetic tissue may be submitted for frozen section analysis. If less than 5 PMN leukocytes occur per high-powered field, there is a low probability of residual infection. Extensive debridement and prosthetic removal should be considered rather than reimplantation of revision components if there are greater than 10 PMN leukocytes per high-powered field.

Histologic study can distinguish between acute inflammatory responses characterized by the presence of PMN leukocytes and chronic inflammatory responses characterized by plasma cells and lymphocytes. Granulomatous responses with central caseation help establish the diagnosis of Mycobacterium tuberculosis. Noncaseating granulomas can occur with fungal and atypical mycobacterial infections.

Occasionally, the inciting organisms can be identified as well. For example, budding yeast forms of Blastomycesdermatitidis can be visualized with special stains or by using immunohistochemical markers. This is particularly important because mycobacterial and fungal organisms are slow growing in vitro, and they may take 3–6 weeks to identify in culture. Also, histologic analysis can distinguish an infection from an unsuspected tumor such as squamous cell carcinoma arising within a chronic infection or a tumor that radiographically may mimic an infection such as eosinophilic granuloma, Ewing sarcoma, and lymphoma of bone.

Lu TS et al: Concurrent acute gouty and gonococcal arthritis. Lancet Infect Dis 2002;2:313. [PMID: 12062998] 

Trampuz A et al: Synovial fluid leukocyte count and differential for the diagnosis of prosthetic knee infection. Am J Med 2004;117:556. [PMID: 15465503] 



Selection and Use

Whenever possible, antibiotics should be chosen based on the antibiotic sensitivities of the specific organisms that were cultured from the infection site. Consultation with infectious disease experts is prudent for unusual or resistant organisms or if a lengthy course of therapy is anticipated. Because patterns of bacterial resistance to antibiotics vary from region to region, these experts work closely with local clinical laboratories to establish locally specific bacterial sensitivity profiles. Also, infectious disease experts are often more closely attuned to the latest clinical research regarding antibiotic treatment of musculoskeletal infections (information that is not usually encountered in the primary orthopedic literature) and the continually changing patterns of bacterial resistance. For example, Staphylococcus epidermidis is becoming increasingly resistant to methicillin, and certain strains of enterococci and S. aureus are resistant to vancomycin. Resistance to second- and third-generation cephalosporins is emerging in some gram-negative bacilli, and penicillin resistance is increasing in Bacteroides and Clostridium species. Even if an organism is sensitive to a given antibiotic, addition of a second antibiotic may be necessary to lessen the risk of treatment failure because of the development of antibiotic resistance.

Antibiotic therapy is usually continued for 6 weeks for patients with septic arthritis or osteomyelitis. In acute pediatric infections caused by sensitive organisms, a shorter course of therapy may be sufficient. In patients with multiple medical problems, retained orthopedic hardware, or persistent open wounds, a longer course of therapy may be required.

Erythrocyte sedimentation rates (ESRs) and C-reactive protein (CRP) levels should be serially checked weekly or semiweekly to monitor the success of treatment. Quantitative CRP levels usually decrease before ESR levels in adequately treated infections. A patient with persistently elevated ESR and CRP levels toward the end of planned antibiotic treatment may have an incompletely treated infection. Persistence of the infection may be caused by the retention of orthopedic hardware, the incomplete debridement of necrotic tissue, the immunocompromised status of the host, or the development of antibiotic resistance by the causative bacteria. Ideally, surgical reexploration should be performed on these patients and tissue samples should be recultured after the patient is off antibiotics to determine if additional treatment is required.

Occasionally, antibiotics must be given for palliation rather than cure. Chronic suppressive antibiotic therapy may be appropriate in selected patients with severe immunocompromise, those who are not surgical candidates, or those with stable joint prostheses infected by sensitive organisms. Close monitoring of these patients is necessary to detect possible antibiotic resistance.

For example, an 80-year-old woman with a history of a revision total hip arthroplasty 10 years previously underwent a Girdlestone arthroplasty 5 years ago to treat septic loosening of the prosthesis. All components were removed, the bones debrided, and antibiotic beads were placed in the acetabulum (Figure 8–2). During this time, a severe hematologic bleeding disorder was diagnosed that prohibited further surgery. Her lateral hip incision healed incompletely, and she developed a mature deep sinus that tracked down to the cut end of the femur. The antibiotic beads could not be retrieved through this opening. She also developed a new sinus tract in her medial thigh. These wounds were treated with daily absorptive alginate dressings, and occasionally she had debridement of the sinus tracts in clinic to prevent them from closing. When the sinus tracts closed, the undrained pus rapidly created a pressurized abscess that resulted in a prompt increase in local inflammation, bacteremia, and acute febrile illness. Her infection was suppressed using culture-specific oral antibiotics for staphylococcal and enterococcal bacteria. Over the past 5 years she has lived with her infection and controlled her pain with oral narcotics. She is able to stand to transfer and walk short distances with a walker.

Figure 8–2.


Anteroposterior pelvic radiograph depicting the Girdlestone arthroplasty and retained antibiotic beads in the left hip area and a painless malunion of a subcapital fracture of the right hip.

Intravenous Route of Administration

Use of a peripheral intravenous central catheter (PICC) line is now the standard IV access for extended antibiotic therapy. PICC lines can be inserted by qualified nursing personnel in an outpatient setting, and the placement of the line can be confirmed by a chest radiograph. Specialized personnel in the radiology department can also place PICC lines using ultrasound to identify suitable veins and fluoroscopy to ensure appropriate catheter placement with the tip of the catheter in the superior vena cava. A subclavian central line such as a Hickman catheter is used as a backup if peripheral access cannot be established. These catheters are generally placed in an operating room setting with the patient heavily sedated or under general anesthesia.

Most home health agencies are expert in managing PICC lines and administering antibiotics to patients in a home setting. Portable computerized IV pumps with replaceable drug cartridges are often used to automate the delivery of antibiotics throughout a 24-hour period.

Methicillin-Resistant Staphylococcus Aureus/Epidermidis

Methicillin-resistant Staphylococcus aureus (MRSA) is the most common resistant bacteria encountered in orthopedic practice. S. epidermidis is rapidly becoming a concern as isolates start to demonstrate methicillin resistance. This is particularly important because one study showed the methicillin-resistant Staphylococcus epidermidis (MRSE) rate on routine screening for total joint replacement was 55% of samples that grew S. epidermidis. A 6-week course of vancomycin (1 g IV every 12 hours) is the current standard treatment for MRSA. However, this drug has relatively poor bone penetration, and it requires close monitoring because, rarely, it can be the cause of nephrotoxicity and ototoxicity. Establishing therapeutic drug levels by adjusting the dose and interval of treatment should be performed based on drug peak and trough levels. Generally, if the peak level is too high, the dose has to be lowered; and if the trough is too high, the interval between doses has to be lengthened. Dosing has to be adjusted in patients with renal insufficiency based on creatinine clearance, and one daily dose or one dose every other day is not uncommon in this setting. Toxicity is more likely to occur if the trough level remains above the acceptable range. Many infectious disease experts treat MRSA with a two-drug regimen, often adding rifampin to vancomycin. There are reports of vancomycin-resistant MRSA. Newer antibiotics such as linezolid (Zyvox) are now being introduced for MRSA and can be administered orally.


Septic Arthritis

Complete surgical evacuation of a purulent effusion offers the best protection against cartilage destruction in patients with acute infectious pyarthrosis. The greatest risk of cartilage damage comes from proteolytic enzymes produced by the recruited polymorphonuclear leukocytes rather than from direct action of the bacteria. Although serial needle aspirations may accomplish this goal in the acute setting, surgical drainage, irrigation, and drain tube placement are more efficient and better tolerated by the patient. Whenever technically possible arthroscopy is preferred, especially when dealing with septic arthritis of the knee joint. Limited open arthrotomy may also be used because the synovium need not be extensively debrided in acute infections.

In chronic septic arthritis, a pannus of hypertrophic synovium forms that must be surgically debrided to ensure successful treatment. Debridement debulks the bacterial load and decreases the production of inflammatory agents that destroy cartilage.


Successful treatment of bone and soft-tissue infections requires the surgical removal of all nonviable tissue and foreign debris. Necrotic tissue shelters bacteria from access by white blood cells and from therapeutic concentrations of antibiotics. In acute open fractures, all devitalized soft tissue and all free bony fragments that are completely denuded of periosteum must be removed from the wound. Although buckshot and isolated bullets do not need to be removed from gunshot victims, thorough exploration of the bullet wounds is necessary to remove any embedded bullet wadding and clothing fragments. In chronic osteomyelitis, the sequestrum must be completely removed, although the involucrum should be left in place. Involucrum is viable reactive tissue that has a generous vascular supply and contributes to the mechanical stability of the bone.

Skin, subcutaneous fat, and muscle should be sharply debrided until they bleed freely. The appearance of viable cancellous bone is easily discerned by the presence of bleeding trabecular surfaces. It is more difficult to tell the viability of cortical bone because of its normally sparse vascularity. Biologic dyes such as fluorescein and isosulfan blue and flow Doppler examination are used intraoperatively to estimate the vascularity of cortical bone. However, visual inspection for punctate bleeding remains the simplest and most popular method of determining the viability of cortical bone. The so-called paprika sign should be apparent after water-cooled high-speed burring of all exposed cortical surfaces to ensure that all dead bone tissue was removed (Figure 8–3).

Figure 8–3.


Intraoperative photograph of the so-called paprika sign, representing punctate bleeding from the endosteal surface of a tibia that has just undergone aggressive debridement with a high-speed burr.


Infections occasionally are so severe or are located in such unforgiving anatomic locations that amputation is the best method of curing the infection surgically. For example, a 60-year-old man with insulin-dependent diabetes and extensive peripheral vascular disease developed a rapidly worsening heel infection that exposed his calcaneus (Figure 8–4). During physical examination, a cotton swab could easily probe exposed cancellous bone of the calcaneus and subtalar joint. A subtotal calcanectomy with free flap coverage after peripheral arterial bypass would have been necessary for any chance of infection control and limb salvage. The patient elected to proceed with a recommended below-knee amputation.

Figure 8–4.


Calcaneus ulcer with exposed bone and blackened eschar.

Implantable Antibiotics

An excellent method to supplement the IV administration of systemic antibiotics is to implant local antibiotics into the wound using polymethylmethacrylate bone cement as a carrier. Antibiotic "spacers" and "beads" have the added advantage of provisionally filling dead spaces so that bacteria-rich fluids do not accumulate and thwart the host's defenses. Intraoperatively, methacrylate powder is thoroughly mixed with powdered antibiotics and then made into a dough by adding the liquid methacrylate monomer. The antibiotic dough can be fashioned into a string of beads using gauge-5 wire or number 5 nonabsorbable suture (Figure 8–5). Antibiotic-laden cement spacers can be molded into a disk shape like a hockey puck for the knee joint after removal of a total knee prosthesis. Also cement spacers can be molded into the shape of a femoral head and secured to the femur using a rush rod placed in the femur. Alternatively, hip and knee joint prostheses made of antibiotic bone cement are now commercially available. Palacos cement has superior antibiotic elution characteristics when compared with other bone cements. Vancomycin and tobramycin are commonly used in combination to treat presumed staphylococcal infections. A standard recipe in a patient without renal insufficiency is to mix one full bag of Palacos with 2 g of vancomycin and 3.6 g of tobramycin. Scoring the surface of a spacer and using numerous small beads rather than a few large beads increases the overall surface area of the antibiotic cement implant, enhances the elution of the antibiotics, and results in higher local concentrations of antibiotics. Initially the local serum concentrations may be as much as 100 times the minimal inhibitory concentration for Staphylococcus. After 3 weeks the antibiotic concentrations drop below the minimal inhibitory concentration. Although spacers and beads are left in place indefinitely, it is a good practice to remove them after the infection is treated to ensure that the cement does not act as a foreign body and precipitate a new infection.

Figure 8–5.


Two strings of antibiotic beads were molded onto a number 5 braided nonabsorbable suture with the knotted ends incorporated into the outermost beads.

Soft-Tissue and Bone Reconstruction—

Assuming musculoskeletal infections were treated comprehensively with antibiotics and debridement, bone reconstruction can proceed in a standard fashion. Total joints can be reimplanted, and structural bone defects can be filled with bone graft. Intercalary long bone defects can be spanned with bone transport techniques, vascularized structural bone autotransplants supported by external fixators, or even structural allografts secured with intramedullary rods.

Expeditious soft-tissue coverage is the first reconstructive priority in the contemporary management of acute open fractures. Rotation, pedicled, or free flaps are used to accomplish wound closure. Early flap reconstruction also ensures a good vascular supply to the injured area that promotes bone healing and resistance to local infection. If definitive bone fixation must be delayed until after complete debridement and soft-tissue coverage is accomplished, provisional stabilization of the bone can be achieved with orthotics, skeletal traction, or external fixation.

An acute infection occasionally develops after orthopedic fixation of a fracture. Assuming good soft-tissue coverage of the fracture area, the patient is treated with antibiotics, and the implanted hardware is left in place until the fracture heals. Once biologic union of the fracture is achieved, surgical debridement of the wound and removal of the fixation hardware can be performed without having to be concerned about a mechanically unstable bone. Alternatively, debridement of dead bone and removal of hardware with the placement of an external fixator can provide stabilization until the infection is under control. Bone graft for small defects or bone transport for segmental defects can successfully achieve union.


Local Wound Care

Newer alginate dressing materials are more absorbant and may be left in place for 24 hours. Saline wet-to-dry dressings can be used for initial mechanical debridement of wounds that contain necrotic material and must be changed every 6 hours. Antiseptic solutions such as hydrogen peroxide, povidone-iodine, isopropyl alcohol, and sodium hypochlorite (Dakin solution, 5% NaClO) are now used only for the first few days until the bacterial load is reduced and necrotic tissue is debrided. Extended use of these caustic agents inhibits fibrogenesis. Instead, petroleum gel or topical antibiotic cream are placed on the wounds to keep the tissues from desiccating and to promote fibroblast growth.

Treatment of open wounds is now transformed using a new method that employs a sealed sponge dressing to which a negative pressure is applied using a portable pump (Figure 8–6). An open-cell sponge is cut to fit the shape of the wound and secured by an airtight plastic dressing (see Figure 8–12D and E). The sponge is connected to a vacuum pump by way of a plastic tube. When the pump is activated, a partial vacuum is generated within the wound. The porous sponge partially collapses, causing contraction of the walls of the wound. All drainage fluids are sucked out through the sponge and tubing and collected in a container located in the pump unit. The wound is kept quite clean, and the dressing is changed every 2–3 days. The units are portable and can be serviced by visiting nurses in an outpatient setting.

Figure 8–6.


Portable wound suction pump (also known as a wound vacuum-assisted closure device, or VAC). Note the tubing that runs from the pump to a black sponge placed in a patient's ischial decubitus.

Hyperbaric Oxygen

Hyperbaric oxygen (HBO) therapy is used to treat a variety of orthopedic disorders. Specialized diving chambers developed for medical purposes expose patients to 100% oxygen at 2 or more atmospheres of pressure. During an HBO treatment, superphysiologic concentrations of oxygen from the lungs are dissolved into the serum. These high serum oxygen levels stimulate neoangiogenesis, sustain hypoxic tissues, support the activity of phagocytic white blood cells, and inhibit infections caused by anaerobic bacteria. It does not cause oxygen to be absorbed from the skin or wound surface, and it does not revitalize tissue that is already necrotic. Therefore, an adequate vascular inflow to the wound is necessary for HBO to work. When appropriately indicated, HBO can be a useful adjunct to good medical and surgical wound management.

Acute problems that can be helped by HBO include severe crush injury, compromised muscle flaps, and necrotizing fasciitis. Each of these conditions is characterized by soft tissues that have become acutely hypoxic and are at risk for infection. So-called acute HBO protocols usually require higher pressures (2.4–3 atm) and more frequent sessions (two to three times a day) for several days. To be effective, an acute HBO treatment protocol must be started as soon as possible after the injury because a 48-hour delay in initiating HBO can render it ineffective.

Chronic wounds that can be helped by HBO are primarily related to chronic ischemic ulcers that are not caused by peripheral vascular disease, venous stasis disease, or pressure necrosis. Diabetic foot ulcers in particular may benefit from HBO protocols with a reduction in risk for major amputation. The older literature includes uncontrolled studies that expound the use of treating chronic osteomyelitis with HBO. However, newer reconstruction techniques, including free flaps for soft-tissue coverage and bone transport for bone defect restoration, have empowered the surgeon to perform more comprehensive debridement and more aggressive wound closure. Better surgical management results in better cure rates for chronic osteomyelitis.

Nutritional Support

Patients with severe infections and large wounds have increased nutritional and caloric needs. Nutritional depletion can be measured using the following tests: albumin, prealbumin, total protein, total lymphocyte count, and anergy panel (see Table 8–2). Dietary supplementation to restore normal healing in a compromised host may be accomplished using enteral tube feedings or parenteral infusions.

Antony SJ, Diaz-Vasquez E, Stratton C: Clinical experience with linezolid in the treatment of resistant gram-positive infections. J Natl Med Assoc 2001;93:386. [PMID: 11688919] 

Centers for Disease Control and Prevention: Vancomycin-resistant Staphylococcus aureus—Pennsylvania, 2002. JAMA 2002;288:2116.

Connolly LP et al: Acute hematogenous osteomyelitis of children: Assessment of skeletal scintigraphy-based diagnosis in the era of MRI. J Nucl Med 2002;43:1310. [PMID: 12368368] 

Gristina AG et al: The glycocalyx, biofilm, microbes, and resistant infection. Semin Arthroplasty 1994;5:160. [PMID: 10155159] 

Hanssen AD, Spangehl MJ: Practical applications of antibiotic-loaded bone cement for treatment of infected total joint replacements. Clin Orthop 2004;427:79. [PMID: 15552141] 

Herscovici D Jr et al: Vacuum-assisted wound closure (VAC therapy) for the management of patients with high-energy soft tissue injuries. J Orthop Trauma 2003;17:683. [PMID: 14600567] 

Hiramatsu K: Vancomycin-resistant Staphylococcus aureus: A new model of antibiotic resistance. Lancet Infect Dis 2001;1:147. [PMID: 11871491] 

Jenson JE et al: Nutrition in orthopaedic surgery. J Bone Joint Surg Am 1982;64:1263. [PMID: 7142234] 

Jones S et al: Cephalosporins for prophylaxis in operative repair of femoral fractures. Levels in serum, muscle, and hematoma. J Bone Joint Surg Am 1985;67:921. [PMID: 4019541] 

Kartsonis N et al: Efficacy of caspofungin in the treatment of esophageal candidiasis resistant to fluconazole. J Acquir Immune Defic Syndr 2002;31:183. [PMID: 12394797] 

Ledermann HP et al: Pedal abscesses in patients suspected of having pedal osteomyelitis: Analysis with MR imaging. Radiology 2002;224:649. [PMID: 12202694] 

Mazza A: Ceftriaxone as short-term antibiotic prophylaxis in orthopedic surgery: A cost-benefit analysis involving 808 patients. J Chemother 2000;12(Suppl 3):29. [PMID: 11432680] 

Mohanty SS, Kay PR: Infection in total joint replacements: Why do we screen MRSA when MRSE is the problem? J Bone Joint Surg Br 2004;86:266. [PMID: 15046444] 

Neut D et al: Biomaterial-associated infection of gentamicin-loaded PMMA beads in orthopaedic revision surgery. J Antimicrob Chemother 2001;47:885. [PMID: 11389124] 

Perea S, Patterson TF: Antifungal resistance in pathogenic fungi. Clin Infect Dis 2002;35:1073. [PMID: 12384841] 

Petty W et al: The influence of skeletal implants on the incidence of infection: Experiments in a canine model. J Bone Joint Surg Am 1985;67:1236. [PMID: 3802846] 

Roeckl-Wiedmann I, Bennett M, Kranke P: Systematic review of hyperbaric oxygen in the management of chronic wounds. Br J Surg 2005;92:24. [PMID: 15635604] 

Schmidt AH, Swiontkowski MF: Pathophysiology of infections after internal fixation of fractures. J Am Acad Orthop Surg 2000;8:285. [PMID: 11029556] 

Segreti J: Efficacy of current agents used in the treatment of Gram-positive infections and the consequences of resistance. Clin Microbiol Infect 2005;11(Suppl 3):29. [PMID: 15811022] 

Shirtliff ME, Mader JT: Acute septic arthritis. Clin Microbiol Rev 2002;15:527. [PMID: 12364368] 

Stewart PS, Costerton JW: Antibiotic resistance of bacteria in biofilms. Lancet 2001;358:135. [PMID: 11463434] 

Stott NS: Review article: Paediatric bone and joint infection. J Ortho Surg (Hong Kong) 2001;9:83. [PMID: 12468850] 

Stratton RJ et al: Malnutrition in hospital outpatients and inpatients: Prevalence, concurrent validity and ease of use of the "malnutrition universal screening tool" ("MUST") for adults. Br J Nutr 2004;92:799. [PMID: 15533269] 

Stumpe KD et al: FDG positron emission tomography for differentiation of degenerative and infectious endplate abnormalities in the lumbar spine detected on MR imaging. AJR Am J Roentgenol 2002;179:1151. [PMID: 12388490] 

Tarkowski A et al: Current status of pathogenetic mechanisms in staphylococcal arthritis. FEMS Microbiol Lett 2002;217:125. [PMID: 12480095] 

Tomas MB et al: The diabetic foot. Br J Radiol 2000;73:443. [PMID: 10844873] 

Turpin S, Lambert R: Role of scintigraphy in musculoskeletal and spinal infections. Radiol Clin North Am 2001;39:169. [PMID: 11316353] 

van de Belt H: Infection of orthopedic implants and the use of antibiotic-loaded bone cements. A review. Acta Orthop Scand 2001;72:557. [PMID: 11817870] 

Vandecasteele SJ et al: New insights in the pathogenesis of foreign body infections with coagulase negative staphylococci. Acta Clin Belg 2000;55:148. [PMID: 10981322] 

Webb LX: New techniques in wound management: Vacuum-assisted wound closure. J Am Acad Orthop Surg 2002;10:303. [PMID: 12374481] 

Zhuang H et al: Exclusion of chronic osteomyelitis with F-18 fluorodeoxyglucose positron emission tomographic imaging. Clin Nucl Med 2000;25:281. [PMID: 10750968] 

Zhuang H et al: Persistent non-specific FDG uptake on PET imaging following hip arthroplasty. Eur J Nucl Med Mol Imaging 2002;29:1328. [PMID: 12271415] 


Several classification systems are used to describe osteomyelitis. The traditional system divides bone infections according to the duration of symptoms: acute, subacute, and chronic (Table 8–5). Acute osteomyelitis is identified within 7–14 days of onset. Acute infections are most frequently associated with hematogenous seeding of bones in children. However, adults may also develop acute hematogenous infections, especially around implanted metal prostheses and fixation hardware. The duration of subacute osteomyelitis is between several weeks and several months. Chronic osteomyelitis is a bone infection that is present for at least several months. It is associated with an epicenter of bone necrosis called a sequestrum that is generally encased in vascular reactive bone called an involucrum.

Table 8–5. Classification Systems for Osteomyelitis.

Traditional system 


Time of onset 


 2 weeks


Weeks to months


 3 months

Waldvogel system 


Arising from contiguous infection

  No vascular disease

Vascular disease present


Cierny-Mader system 

Anatomic extent of infection

1. Medullary only (acute hematogenous)

2. Superficial cortex (contiguous spread or soft tissue trauma)

3. Localized (cortical and medullary, mechanically stable)

4. Diffuse (cortical and medullary, mechanically unstable)

5. Subtype by host's physiologic status

A Healthy

Bs Compromised because of systemic factors

B1 Compromised because of local factors

B1s Compromised because of both local and systemic factors

C Treatment worse than the disease


Another system, developed by Waldvogel, categorizes bone infections based on etiology and chronicity: hematogenous, contiguous spread (with or without concomitant vascular disease), and chronic (see Table 8–5). Hematogenous and contiguous spreading infections may be acute, although the latter is associated with trauma or preexisting localized soft-tissue infections such as diabetic foot ulcers. Compromise in soft-tissue vascular supply may inhibit the immunological response to an infection. Therefore, Waldvogel created this subcategory to acknowledge the increased difficulty in treating infections in hosts with compromised vascularity.

Cierny and Mader developed a staging system for osteomyelitis that is classified by the anatomic extent of the infection and by the physiologic status of the host rather than by chronicity or etiology (see Table 8–5 and Box 8–1). The four stages are characterized by the pattern of bony involvement of the infection in order of increasing complexity: stage 1—medullary only, stage 2—superficial cortex only, stage 3—localized medullary and cortical, and stage 4—diffuse medullary and cortical (see Box 8–1). The latter two categories are best distinguished by the presence or absence of mechanical compromise of the involved bone. Localized infections have not created an unstable bone. However, diffuse infections have sufficiently weakened the bone that surgical stabilization of the bone is necessary.

Box 8-1. The Cierney and Mader Staging System.


The Cierny and Mader staging system for osteomyelitis is classified by the anatomic extent of the infection and by the physiologic status of the host rather than by chronicity or etiology. The four stages are characterized by the pattern of bony involvement of the infection in order of increasing complexity: stage 1—medullary only, stage 2—superficial cortex only, stage 3—localized medullary and cortical, and stage 4—diffuse medullary and cortical.

Host factors that mitigate healing are subcategorized into three groups: A—healthy host, B—compromised host, and C—"incurable" host (the treatments necessary to cure the disease are worse than living with the symptoms of the disease itself). A good example is an ambulatory diabetic smoker with peripheral vascular disease who has a stage 3 infection in a mechanically stable femur. Appropriate local wound care and suppressive antibiotic therapy may indeed be preferable to extensive surgical debridement that would risk destabilizing the bone, worsening a nonhealing soft-tissue wound, and increasing the risk of an above-knee amputation.

Systemic factors that compromise the host include diabetes mellitus, immunosuppression (eg, corticosteroid or cyclosporin usage), immune disease (eg, AIDS), malnutrition (often associated with alcohol or IV drug abuse), renal or hepatic failure, chronic hypoxia, and extremes of age. Local factors include peripheral vascular disease, venous stasis disease, chronic lymphedema, extensive soft-tissue scarring, radiation fibrosis, arteritis, diabetic dysvascularity of small vessels, neuropathy, and tobacco use.

Belzunegui J et al: Musculoskeletal infections in intravenous drug addicts: Report of 34 cases with analysis of the microbiological aspects and pathogenic mechanisms. Clin Exp Rheumatol 2000;18:383. [PMID: 10895378] 

Casado E et al: Musculoskeletal manifestations in patients positive for human immunodeficiency virus: Correlation with CD4 count. J Rheumatol 2001;28:802. [PMID: 11327254] 

Gilad J et al: Polymicrobial polyarticular septic arthritis: A rare clinical entity. Scand J Infect Dis 2001;33:381.

Lazzarini L, Mader JT, and Calhoun JH: Osteomyelitis of long bones. J Bone Joint Surg Am 2004;86:2305. [PMID: 15466746] 


Acute Hematogenous Osteomyelitis

Acute hematogenous osteomyelitis (AHO) is most frequently encountered in the metaphysis of long bones in children. Clinically, patients have the signs and symptoms of an acute inflammation. Pain is usually localized, although it may radiate to adjacent regions of the body. For example, if a child complains of knee pain, the hip joint must be thoroughly evaluated for the possibility of septic arthritis. If a bone in the leg is infected, the child may limp or stop walking altogether. Children may also demonstrate guarding of an infected arm, refusing to use it and holding it to their side. Exam usually reveals local tenderness and occasionally limited motion of an adjacent joint, but swelling and redness are less frequent. Systemic signs of fever and chills may be present, and infants may be irritable or lethargic and uninterested in eating.

Serology characteristically shows dramatic elevations in the CRP and the ESR. The WBC is usually elevated, and a left shift may be apparent. Peripheral blood cultures grow the offending organism in up to half of acutely infected children.

Plain radiographs taken early in the course of disease are usually negative. After a week or two, radiographs may reveal a radiolucent lesion and periosteal elevation. Reactive sclerosis is absent because it is encountered only in chronic bone infections. Technetium bone scan shows increased activity on soft tissue and delayed bone images. CT may show a radiolucent area in cancellous bone and signs of periosteal elevation. MRI shows early inflammation of bone marrow with inflammation of the periosteum and adjacent soft tissues as the infection progresses. In later stages abscess formation may be seen as a signal void on gadolinium contrast images.

The clinical and radiologic appearance of AHO may be similar to inflammatory neoplasms such as acute lymphocytic leukemia, Ewing sarcoma, and Langerhans cell histiocytosis (also known as eosinophilic granuloma). Therefore, a biopsy may be required to distinguish an infection from a tumor.

Standard evaluation of a patient with suspected AHO includes a needle or open biopsy to obtain tissue for culture and histology and subsequent initiation of empirical antibiotics. If an abscess is identified, thorough irrigation and local debridement through a small cortical window should be performed. Once the culture results and sensitivities are obtained, the final antibiotic regimen may be selected. Six weeks of antibiotic therapy are usually indicated. In pediatric patients with sensitive staphylococcal infections, 2 weeks of parenteral antibiotics may be followed by 4 weeks of oral antibiotic therapy. Close clinical follow-up is necessary to ensure that the patient's inflammatory symptoms are resolving. Serial ESR and CRP should return to normal within the treatment period.

If the patient does not improve, temporary discontinuation of antibiotics may be necessary prior to performing a surgical exploration to culture the infected site. Often antibiotics, even those to which the bacteria are resistant, may suppress the bacteria enough that they will not grow in culture. Although a 2-week waiting period off antibiotics, which is customary for cases of chronic osteomyelitis, may not be tolerated by patients with acute osteomyelitis, even waiting for several days may increase the culture yield. This further highlights the potential problems of beginning an empirical regimen using inappropriate antibiotics and then having difficulty obtaining productive cultures. Either a delay in treatment occurs or the patient has to be placed on several antibiotics to cover all possible organisms.

In patients with stable prosthetic joints who acquire an acute hematogenous infection because of a sensitive organism, thorough soft-tissue debridement, exchange of the polyethylene liner or temporary substitution of the polyethylene with a molded antibiotic spacer, and 6 weeks of IV antibiotic therapy confer a salvage rate approaching 50%.

Clinical Example

A 13-year-old girl complained of acute knee pain beginning 7 days earlier when arising from sleep. Her pain worsened to the point where she had to stay at home from school because she could not walk. On exam her thigh was tender, and her hip and knee motion severely restricted because of pain, but there was no knee effusion. Her temperature was 38.2°C (100.9°F). The serum white blood cell count was 17,000 with a left shift, and the ESR was four times normal. Plain films of the femur were normal. An MRI of the thigh showed significant inflammation of the marrow and adjacent soft tissues on T2-weighted images (Figure 8–7A). Intraoperatively the midfemur was exposed, a hole was drilled in the femur, and a collection of pus was aspirated from the marrow cavity (Figure 8–7B). Irrigation was performed through the drill hole and the wound closed over a drain. Staphylococcus aureus was cultured, and the patient was successfully treated with 6 weeks of IV antibiotics.

Figure 8–7.


A: T2-weighted MRI of the thigh, showing marrow edema in the femur and surrounding musculature. B: Aspiration of the medullary cavity of the femur produces 10 mL of pus in the syringe.

Acute Osteomyelitis Caused by Puncture Wound

Acute osteomyelitis must be considered in the evaluation of a patient who has suffered a deep puncture wound. The feet and hands are the most frequent sites of these injuries. The soft tissue wound may appear insignificant. It may be difficult to detect a foreign body made of wood or plastic on plain radiography, and wound exploration for a foreign body in a clinic setting is frequently unrewarding. Refer to Chapter 9 (Foot & Ankle Surgery) and Chapter 10 (Hand Surgery) for further information.

Clinical Example

An 11-year-old boy punctured his foot when he stepped on a sharp object. Initial radiographs of the foot showed no evidence of a foreign body (Figure 8–8A). In retrospect, a small puncture wound can be visualized in the middistal diaphysis. He was initially treated with a limited irrigation and debridement in the emergency department and discharged on oral antistaphylococcal antibiotics. Two weeks later. the arch of his foot became swollen and drainage emanated from the puncture wound (Figure 8–8B). He was admitted to the hospital and placed empirically on triple IV antibiotics. Superficial swabs of the wound grew Pseudomonas.

Figure 8–8.


A: Initial plain radiograph of the first metatarsal. B: Preoperative view of the puncture wound. C: Bone phase of a technetium bone scan of the feet. D: Follow-up radiograph of the first metatarsal taken 2 weeks after Figure 8–8A.

A technetium bone scan identified a significant uptake of radiotracer in the distal aspect of the first metatarsal compared with the opposite normal foot (Figure 8–8C). New radiographs of the foot depicted a circular region of osteolysis with a slight elevation of the adjacent periosteum (Figure 8–8D). The patient underwent a thorough irrigation and debridement in the operating room. No foreign body was identified. Deep cultures of the wound revealed Mycobacterium fortuitum, a rapidly growing mycobacteria other than tuberculosis (MOTT). He clinically improved within several days of beginning oral clarithromycin and continued this treatment for 9 months.

This case illustrates the need to obtain accurate wound cultures in order to choose appropriate antibiotic therapy. Superficial cultures often reveal skin contaminants that are not representative of the organisms actually causing the infection. When infections do not respond to routine empirical antibiotic therapy, it is always important to consider surgical exploration to obtain deep cultures of the wound for mycobacterium and fungal organisms as well as for aerobic and anaerobic organisms.

Agrawal A et al: Cryptococcal arthritis in an immunocompetent host. J S C Med Assoc 2000;96:297. [PMID: 10933007] 

Babhulkar SS, Pande SK: Unusual manifestations of osteoarticular tuberculosis. Clin Orthop 2002;398:114. [PMID: 11964639] 

Blumberg HM, Leonard MK Jr, Jasmer RM: Update on the treatment of tuberculosis and latent tuberculosis infection. JAMA 2005;293:2776. [PMID: 15941808] 

Caspofungin: New preparation. A last resort for invasive aspergillosis. Prescrire Int 2002;11:142. [PMID: 12378745] 

Centers for Disease Control and Prevention: Trends in Tuberculosis—United States, 2004. MMWR Morb Mortal Wkly Rep 2005;54:149. [PMID: 15772584] 

Dhillon MS et al: Tuberculosis of the sternoclavicular joints. Acta Orthop Scand 2001;72:514. [PMID: 11728080] 

Hansen BL, Andersen K: Fungal arthritis. A review. Scan J Rheumatol 1995;24:248. [PMID: 7481591] 

Nolan CM, Goldberg SV: Treatment of isoniazid-resistant tuberculosis with isoniazid, rifampin, ethambutol and pyrazinamide for 6 months. Int J Tuberc Lung Dis 2002;6:952. [PMID: 12475140] 

Silber JS et al: Insidious destruction of the hip by Mycobacterium tuberculosis and why early diagnosis is critical. J Arthroplasty 2000;15:392. [PMID: 10794239] 


Subacute infections are often associated with pediatric patients. These infections are usually caused by organisms of low virulence and associated with muted symptoms. Ultimately, the infection appears to reach a stalemate with the host's defenses and does not progress. Subacute osteomyelitis shares some of the radiographic characteristics of both acute and chronic infections. Like acute osteomyelitis, regions of osteolysis and periosteal elevation may be present. Like chronic osteomyelitis, a circumferential zone of reactive sclerotic bone may be visualized. When subacute osteomyelitis affects the diaphysis of a long bone, it may be particularly difficult to distinguish from Langerhans cell histiocytosis (also known as eosinophilic granuloma) or Ewing sarcoma.

Clinical Example

A 14-year-old boy presented with a 2-month history of left ankle pain and swelling that occurred when he jumped off a farm trailer. His symptoms persisted, although some improvement was reported. He denied any fever, chills, or night sweats and could walk without assistance. On exam he was still tender and focally erythematous over the anterior region of the ankle. His WBC was normal and the ESR was only slightly elevated.

Anteroposterior (AP) and lateral radiographs of the tibia show mixed areas of radiodensity and radiolucency in the metaphysis and a slightly raised periosteum (Figures 8–9A and B). Axial T2-weighted MRI shows marrow edema and periosteal elevation—identified as the outer dark ring just superficial to the cortex. A halo of inflammation surrounds the raised periosteum (Figure 8–9C). Coronal T2-weighted MRI shows the periosteal elevation along the metadiaphysis and the marrow edema extending as far proximally as the midtibia (Figure 8–9D). During open surgical biopsy, purulent material was encountered within the metaphysis but not along the periosteal surface or in the ankle joint. Thorough irrigation and debridement of the area was performed with primary closure of the incision over a drain. The patient was subsequently cured of his subacute nonresistant S. aureus infection with 6 weeks of IV nafcillin.

Figure 8–9.


A: Anteroposterior radiograph of the distal tibia. B: Lateral radiograph of the distal tibia. Notice focal region of osteopenia immediately above the growth plate. C: Axial T2-weighted MRI of both tibias in the region of the distal metaphysis shows marrow edema and periosteal elevation and inflammation on the affected left side. D: Coronal T2-weighted MRI of both tibias shows extensive marrow edema and periosteal inflammation ascending to the midtibia on the affected side.

Lazzarini L, Lipsky BA, Mader JT: Antibiotic treatment of osteomyelitis: What have we learned from 30 years of clinical trials? Int J Infect Dis 2005;9:127. [PMID: 15840453] 

Mader JT et al: Antibiotic therapy for musculoskeletal infections. Instr Course Lect 2002;51:539. [PMID: 12064145] 

Vinod MB et al: Duration of antibiotics in children with osteomyelitis and septic arthritis. J Paediatr Child Health 2002;38:363. [PMID: 12173997] 


Chronic osteomyelitis is the result of untreated acute or subacute osteomyelitis. It can occur hematogenously, iatrogenically, or as a result of penetrating trauma. Chronic infections are often associated with orthopaedic metal implants used to replace joints, fuse spine segments, or fix fractures. Direct intraoperative inoculation or subsequent hematogenous seeding of metal or dead bone surfaces may provide a haven for the bacteria, protecting them from white blood cells and effective concentrations of antibiotics. Therefore, removal of the metal and dead bone are necessary in addition to appropriate antibiotics to eradicate chronic osteomyelitis.

Surgical debridement of necrotic bone for infection control is akin to curettage of a benign bone tumor. A study validating the Cierny-Mader classification system substaging A and B was reported. Debridements were wide marginal or intralesional.

Clinical Example

A 62-year-old man sustained a closed femur fracture when he fell from a ladder 40 years ago. His fracture was fixed with an intramedullary rod that was subsequently removed after the fracture healed. Unfortunately, the patient's leg became infected postoperatively and a draining sinus tract developed adjacent to the fracture site. He subsequently had several local debridements when oral antibiotics would not resolve his symptoms. He enjoyed extended asymptomatic intervals of up to 14 years between successive debridements. For the last 4 years he had an intermittently draining sinus tract and occasional bouts of pain relieved with brief courses of oral ciprofloxacin.

At the time of presentation he had had a fever of 38.5ºC (101.3ºF) and increasing leg pain and swelling for 1 week. Once the sinus tract opened up and began to drain pus, he defervesced and his leg symptoms modestly improved, although it was still difficult for him to walk. On physical examination the sinus tract was probed with a cotton swab, which easily reached the surface of the femur. Serologic exam yielded these results: CRP, 7.5 (0.5 is normal); ESR, 38 (0–15 mm Hg is normal), and WBC, 7.9 (5–10 k is normal). A sensitive S. aureus was cultured.

Radiographs depict an irregularly expanded callus of sclerotic bone at the prior fracture site (Figure 8–10A). An indium-labeled WBC scan was focally positive (Figure 8–10B). CT showed small free fragments of bone not connected to the main shaft (Figure 8–10C). The main fragment was further outlined using computer-generated sagittal reconstructions and was thought to be a sequestrum (Figure 8–10D). A T1-weighted fat saturation MRI with gadolinium contrast further characterized the infected area outlining the relatively small area of focal inflammation (Figure 8–10E).

Figure 8–10.


A: Lateral radiograph of the femur. B: Indium-labeled white blood count bone scan. C: Axial CT scan of the infected area. D:Computer-reformatted CT with sagittal image of the femur. E: An axial T1-weighted fat-saturated MRI with gadolinium contrast. F:Sequestrum. G: Beads placed in the operative wound. H: Ingredients used to bone graft the bone defect (clockwise from bottom: allograft cancellous bone chips, demineralized bone matrix, autograft iliac crest bone).

Curettage of the femur produced a 3.5-cm sequestrum (Figure 8–10F). A water-cooled high-speed burr was used to debride the adjacent cortical bone extensively until it bled freely. A string of antibiotic beads were made on a number 5 nonabsorbable braided suture using 2 g of vancomycin powder, 3 g of tobramycin powder, and one bag of polymethylmethacrylate bone cement (see Figure 8–5). The beads were counted and snugly placed into the cavity in a way that they could easily be retrieved later (Figure 8–10G). The adjacent soft tissues were curetted to remove necrotic material, but the sinus tract was not closed or excised. Operative cultures grew sensitive S. aureus and a 6-week course of IV nafcillin (2 g every 4 hours) was begun as an outpatient. A visiting nurse administered the antibiotic through a PICC line using a programmable computerized pump.

Three weeks later, the beads were removed and a mixture of posterior iliac crest bone graft, demineralized bone matrix, and allograft cancellous bone chips were placed into the cavity (Figure 8–10H). Further cultures of the wound were sterile. At the conclusion of his antibiotic therapy, the patient's ESR and CRP had returned to normal values, his sinus tract had completely healed, and he was asymptomatic.


Osteomyelitis caused by trauma may present acutely or chronically. In acute cases the signs of infection may be masked by the local open wound and may be delayed by the use of empirical antibiotics and surgical debridement that is not complete. Similar bone changes can be seen on radiographic imaging even in the presence of fractures and fixation hardware. Open wounds where the bone is exposed must undergo comprehensive irrigation and debridement in the operating room. Foreign material, including road dirt, clothing, and bullet shell wadding, must be completely removed, and all necrotic areas of the soft tissues must be excised. If a fracture is present, all fracture fragments completely stripped of their blood supply must also be removed. Viable bone fragments where the periosteum is still attached may be left in the wound but must be carefully monitored. Pulsatile lavage using at least 6 L of saline, with or without antibiotics, is a proven adjunct to sharp surgical debridement. In cases of large soft-tissue defects, early flap coverage is ideal to prevent ongoing contamination of deep tissues and to provide a robust blood supply to the injured area for enhanced antibiotic delivery. Serial debridements every 48 hours may be necessary to establish the viability of injured tissues and to ensure that complete removal of all devitalized tissue is accomplished. In cases where soft-tissue coverage must be delayed, a wound vacuum-assisted closure (VAC) device is an ideal way to manage the wound. This system is easy to apply and only needs to be changed every 2–3 days. Because the pump is portable and the wound is sealed and dry, patient acceptance is high. For these reasons, the wound VAC system has largely replaced open continuous irrigation systems that are more labor intensive to maintain and less well tolerated by the patient.

Fractures can heal even in the presence of a soft-tissue or bone infection. If an acute infection is present in an open wound where a fracture was fixed with a rod or plate, it must be determined if the soft and bony tissues are viable. If they are viable, the fixation hardware should be left in place until the fracture heals. If tissue is necrotic, redebridement to remove all areas of necrosis must first be performed, even if the fixation hardware has to be replaced. If there is a large defect in the bone after comprehensive debridement, the bone should be held to length with an external fixator until the infection is resolved. Placement of temporary antibiotic beads may help provide local antibiotic delivery and eliminate the dead space. Then reconstruction with autograft, vascularized bone graft, or bone transport may be performed.

Chronic osteomyelitis caused by open trauma may often be associated with a healed fracture and an open wound where the bone or fixation hardware may be exposed. The hardware must be removed, and the site of infection must be treated like any chronic osteomyelitis with thorough bone debridement, use of local antibiotic beads, and systemic IV antibiotics. Once the infection is controlled, bone grafting or other reconstruction of the defect may take place, often in association with a local or free flap to reconstruct the soft tissue defect.

Antibiotic therapy for osteomyelitis remains controversial. Antibiotic therapy specific for the offending organism is obvious, but which of several potential agents to use is less clear. Further, use of more than one antibiotics is more effective, according to some studies. Another issue is the length and route of therapy; 6 weeks is the usual empirical recommendation but is not supported by a strong body of literature. With the expense and inconvenience to the patient of IV antibiotics, the length of therapy takes on significant importance. Oral antibiotic therapy could be less burdensome to the patient and the health system, and it was used for pediatric patients in several studies for the final 4 weeks of therapy. Despite years of clinical trials, these questions in the treatment of osteomyelitis remain unanswered.

Clinical Example

A 42-year-old woman sustained an open fracture of the proximal third of her tibia. She underwent debridement and fracture fixation with a 10-hole plate. The fracture healed after 6 months but remained painful and began to drain purulent material from three sinus tracts (Figure 8–11A). A lateral radiograph shows the tibia before and after plate removal and debridement using a water-cooled high-speed burr (Figures 8–11B and C). The tibia was then packed with a string of antibiotic beads and primarily closed. Half way through the 6-week course of IV antibiotic therapy the beads were removed (Figure 8–11D) and the defect bone grafted. Graft incorporation occurred over the next 3 months, at which point unrestricted ambulation was permitted.

Figure 8–11.


A: Leg with draining sinus tracts. B: Preoperative radiograph showing fracture fixation plate. C: Postoperative radiograph showing extent of bony debridement. D: Second surgical exposure of clean tibia and the antibiotic beads that were removed.


Squamous cell carcinoma may arise in the chronically infected granulation tissue that is adjacent to a chronically infected bone. This rare complication can occur in areas of burn scars, chronic pressure ulcers, and ostomies, as well as at sites of chronic draining osteomyelitis. The patient usually has had stable chronic osteomyelitis for an average of approximately 20 years, although the latent period can be as little as 18 months. The tumor can be difficult to distinguish visually from the granulation tissue. The focus of carcinoma appears to be an exuberance of proliferative, lobulated, and friable "granulation tissue." A recent and progressive worsening of the soft-tissue defect in an otherwise stable case of chronic osteomyelitis is a clue that carcinoma has developed. Liberal sampling of the wound can easily be done in a clinic setting with a disposable skin punch biopsy trephine that dermatologists use for skin biopsies. Histologic examination of the biopsy specimens enables the pathologist to distinguish readily between squamous cell carcinoma and chronic granulation.

Staging studies, including contrast CT scan of the chest, abdomen, and pelvis; technetium total body bone scan; and PET scan, are used to detect other sites of disease. PET is particularly helpful in detecting regional and systemic lymphatic spread of the tumor. Wide surgical excision of the primary site and any positive lymph nodes are necessary to render the patient surgically free of disease. Adjunctive radiotherapy for local control and chemotherapy for systemic control are used in conjunction with surgical excision in most cases.

Clinical Example

A 49-year-old man presented with a 30-year history of ischial decubitus ulcers and rectal fistulas. He had spinal meningitis during infancy resulting in severe paraparesis, hypoesthesia, and incontinence of bowel and bladder. Despite a long series of local debridement procedures, muscle flaps, and skin grafts; his buttock region remained open to some degree during this entire time. More recently, he was concerned about a reactivation of his ischial osteomyelitis. On physical exam, a 15-cm region of friable spongelike neogranulation was identified adjacent to a scarred ulcer overlying the ischium (Figure 8–12A). Plain films suggested chronic reactive changes in the ischium caused by infection and prior surgery. Punch biopsies of the concerning area of neogranulation revealed squamous cell carcinoma. CT of the chest abdomen and pelvis were negative except for enlarged inguinal lymph nodes. The patient underwent a permanent diverting colostomy and inguinal and retroperitoneal lymph node dissection. All lymph nodes were negative. The tumor subsequently was radically excised, including a partial excision of the ischium (Figures 8–12B and C). A wound VAC was used for local wound care (Figures 8–12D and E). Eight weeks later, the wound edges had retracted, and normal healthy granulation tissue covered the bony defect (Figure 8–12F). The area was subsequently covered with skin graft to achieve complete healing.

Figure 8–12.


A: Photograph of chronic ulcerative wound with neogranulation tissue laterally. B: Wound and tumor bed after wide excision of the carcinoma. C: Tumor/wound specimen, 18 cm in diameter. D: Wound vacuum-assisted closure (VAC) sponge being measured over wound. E: Wound VAC sponge in place, partially contacting wound. F: Eight weeks after wound VAC and antibiotic therapy. Bed ready for skin grafting.

Copcu E et al: Thirty-one cases of Marjolin's ulcer. Clin Exp Dermatol 2003;28:138. [PMID: 12653697] 

Gonzalez MH, Weinzweig N: Muscle flaps in the treatment of osteomyelitis of the lower extremity. J Trauma 2005;58:1019. [PMID: 15920418] 

Kuokkanen HO et al: Radical excision and reconstruction of chronic osteomyelitis with microvascular muscle flaps. Orthopedics 2002;25:137. [PMID: 11871378] 

Moroni A et al: State of the art review: Techniques to avoid pin loosening and infection in external fixation. J Orthop Trauma 2002;16:189. [PMID: 11880783] 

Strauss MB, Bryant B: Hyperbaric oxygen. Orthopedics 2002;25:303. [PMID: 11918035] 

Thio D et al: Malignant change after 18 months in a lower limb ulcer: Acute Marjolin's revisited. Br J Plast Surg 2003;56:825. [PMID: 14615262] 


There is no formal classification system for septic arthritis. Most joint infections are acute rather than chronic, monoarticular rather than polyarticular, and they arise from a hematogenous source of organisms rather than by direct inoculation or extension from an adjacent infection. The most important clinical question that often arises is whether the patient's inflamed joint is caused by an infection or a noninfectious inflammatory process. Inflammatory arthropathies are numerous, and patients often require systemic medical treatment to control the joint symptoms. They are often categorized as seropositive (for rheumatoid factor) or seronegative. Common conditions include crystal arthropathies (gout and pseudogout) and autoimmune disorders with joint involvement (RA, systemic lupus erythematosus, and inflammatory bowel disease). Finally, arthropathy from osteoarthritis and avascular necrosis may present with inflammatory symptoms and mimic an indolent infection.

Diagnosis of septic arthritis depends much more on arthrocentesis for synovial fluid analysis (see Table 8–4) and culture than it does on radiologic imaging. Early plain radiographs are usually normal. Ultrasound is better at diagnosing increased fluid within a joint space but is not specific as to the cause. Many of the radiographic features of bone scan, CT, and MRI are nonspecific and leave the diagnosis of septic arthritis in question.


Hematogenous septic arthritis commonly affects patients with compromised immunologic defense mechanisms. The underlying source of infection can frequently be determined, and blood cultures are positive in approximately half of patients. Patients at risk include those with specific immune deficiencies from HIV or chemotherapy; those with chronic disease, including RA, gout, renal failure, and sickle cell disease; and IV drug abusers. Patients with known arthropathy from other causes are also at increased risk for superimposed infections. Patients routinely complain of severe pain with passive motion of the affected joint. Rest pain, guarding, swelling, erythema, and heat become more pronounced as the infection progresses. Fever and chills are not sensitive indicators of septic arthritis.

The most common joint affected by hematogenous septic arthritis is the knee. The hip, ankle, wrist, shoulder, and elbow follow in frequency of involvement. The differential diagnosis includes Charcot joint, gout, pseudogout, RA, and other inflammatory arthropathies. The diagnosis is tentatively made on joint fluid analysis (see Table 8–4).

Although infections often spread from joints to affect adjacent metaphyseal bone, tumors seldom do except at the sacroiliac joint. Surgical decompression and irrigation of all large joints is preferred to serial needle aspirations. In the acute setting, arthroscopy is ideal for culturing synovial tissue, thoroughly irrigating the joint space, and for placement of an indwelling drainage tube.

Clinical Example

A 53-year-old woman with RA and a painful left hip presented with a 3-week history of rapidly worsening groin pain, slight fever, and lethargy. Degenerative narrowing of the hip joint is seen on a prior AP radiograph (Figure 8–13A). Although the patient's WBC was normal, the hematocrit was only 18! Her groin was extremely tender, and any motion of the hip joint elicited excruciating pain. The patient was admitted to the hospital directly from the clinic. A bone scan showed intense activity in the region of the hip (Figure 8–13B). A CT of the pelvis outlines a loculated soft-tissue mass anterior to the femoral head displacing the femoral artery and vein medially (Figure 8–13C). Using CT guidance, the region was aspirated, and a pigtail catheter was inserted to drain the abscess cavity. MRI with T1 fat-saturated sequences and gadolinium contrast further characterized the infection, revealing significant inflammation in the femoral head and an effusion of the hip joint (Figure 8–13D). A plain radiograph at that time showed a dramatic collapse of the femoral head (Figure 8–13E). A Girdlestone arthroplasty was performed, and the remainder of the femoral head was submitted for histologic analysis (Figure 8–13F). An antibiotic spacer was orthotopically placed to stabilize the femur, and the wound was closed over drains (Figure 8–13G). A 6-week course of IV antibiotics was given. Afterward, the hip was surgically reexamined, and no evidence of persistent infection was seen grossly or by frozen section analysis. At that time a total hip prosthesis was successfully implanted.

Figure 8–13.


A: Initial anteroposterior radiograph of hip joint with narrowed cartilage caused by rheumatoid arthritis. B: Technetium bone scan shows intense activity in region of left hip. C: CT scan shows loculated soft-tissue mass anterior to the femoral head displacing the femoral artery and vein medially. D: T1-weighted fat-saturated MRI with gadolinium contrast shows intense inflammation around hip joint and in acetabulum and femoral head. A retroperitoneal abscess is depicted in the enlarged iliopsoas muscle by a dark central area of signal void surrounded by a halo of bright inflammation. E: Preoperative plain radiograph showing extensive collapse of the weight bearing portion of the femoral head. F: Surgical specimen showing flattened femoral head (upper portion). Note the cut surface of the neck (lower right). G: Radiograph of an antibiotic spacer molded around a rush rod that was implanted in the femoral canal.


Unlike acute septic arthritis, which is intensely painful, chronic septic arthritis presents with indolent joint symptoms that are often muted by oral or intraarticular injections of antiinflammatory medications and may be attributed to coexistent chronic joint arthritis. Immunocompromised patients are susceptible to less virulent and slower growing organisms such as atypical mycobacteria and fungus. These organisms may solicit a subdued chronic inflammatory response that generates less pain and joint effusion, resulting in a delay in diagnosis.

Clinical Example

A 52-year-old man with AIDS on retroviral therapy presented with a 4-month history of arthritic pain and effusion in his knee and a 1-week history of an enlarging painful mass on the medial aspect of his knee (Figure 8–14A). One year earlier he was diagnosed with a large popliteal abscess in the same leg caused by S. epidermidis that was successfully treated with surgical drainage and 6 weeks of IV antibiotics. Exam revealed focal swelling, warmth, erythema, and restricted motion because of pain. During arthrotomy, the medial swelling was found to communicate directly with the knee joint. Intraoperative findings included a large quantity of pus, extensive erosion of cartilage, and chronic proliferative synovial tissue (Figure 8–14B). After irrigation and debridement, the wound was primarily closed over drainage catheters. Cultures grew Candida albicans, and the patient was treated with fluconazole (Diflucan).

Figure 8–14.


A: A large focal erythematous soft-tissue swelling and a longitudinal scar from prior surgical drainage of a popliteal abscess are seen along the medial aspect of the knee. B: With the patella everted to the left, the articular surfaces of the femur are seen at the top and the hypertrophic synovium is seen below. Note the complete loss of cartilage on the medial femoral condyle to the right.

Even though this patient's symptoms appeared acute, he actually had chronic septic arthritis that likely began 4 months previously when he began having arthritic pain. Because he was immunocompromised, his inflammatory symptoms were muted, causing a delay in clinical presentation. Unusual pathogens are a hallmark of immunocompromised patients. Therefore, it is essential to acquire mycobacterial and fungal cultures in addition to aerobic and anaerobic bacterial cultures. Unless the cause of immunosuppression is known, a comprehensive diagnostic survey must be undertaken to identify the underlying causes, including cancer, severe malnutrition, immune disorders, and chronic viral infection.

Aubry A et al: Sixty cases of Mycobacterium marinum infection: Clinical features, treatment, and antibiotic susceptibility of the causative isolates. Arch Intern Med 2002;162:1746. [PMID: 12153378] 

Biviji AA et al: Musculoskeletal manifestations of human immunodeficiency virus infection. J Am Acad Orthop Surg 2002;10:312. [PMID: 12374482] 

Le Dantec C et al: Occurrence of mycobacteria in water treatment lines and in water distribution systems. Appl Environ Microbiol 2002;68:5318. [PMID: 12406720] 

Laine M, Luukkainen R, Toivanen A: Sindbis viruses and other alpha viruses as a cause of human arthritic disease. J Intern Med 2004;256:457. [PMID: 15554947] 

Mylonas AD et al: Natural history of Ross River virus-induced epidemic polyarthritis. Med J Aust 2002;177:356. [PMID: 12358577] 

Stahl HD et al: Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis. Ann Rheum Dis 2000;59:342. [PMID: 10784515] 


Contiguous spread of infection to a joint most commonly occurs in pediatric patients with AHO or in adults with chronic wounds such as ischial decubiti and diabetic foot ulcers. Chronic soft-tissue and bone infections may extend into joints in adults as well. Of particular concern is occurrence in patients who are immunocompromised or insensate.

Clinical Example

A 28-year-old man with paraplegia and a long-standing history of sacral and ischial decubiti presented with a 2-week history of fevers, anemia, and increased spasticity of the lower extremities. Two large fist-sized decubiti, one over the sacrum and one over the right ischium, were observed (Figure 8–15A). The underlying bone was easily palpated at the base of both of these ulcers. Further examination with a probing finger revealed a deep sinus that tracked to the posterior aspect of the femoral head. Plain films revealed a chronically dislocated hip with cephalad migration of the femur and concomitant destruction of the ilium (Figure 8–15B). Axial CT scan showed air within and surrounding the dislocated femoral head (Figure 8–15C). MRI with inversion recovery sequencing depicted extensive inflammation of the femur, the ilium, and the surrounding gluteal musculature (Figure 8–15D). An extensive surgical debridement of the acetabulum and removal of the proximal femur was performed through the lateral ulcer. A wound VAC was placed on both ulcers, and culture-specific antibiotics were administered. The patient refused a hip disarticulation with an anterior thigh flap that would close both ischial and sacral decubiti, and he was subsequently treated with chronic oral antibiotic suppression and daily wound packing.

Figure 8–15.


A: Large sacral and right ischial ulcer. B: Anteroposterior radiograph of the pelvis. C: CT scan of pelvis. D: MRI with inversion recovery sequence of the pelvis.

Goergens ED et al: Acute osteomyelitis and septic arthritis in children. J Pediatr Child Health 2005;41:59. [PMID: 15670227] 

Li SF et al: Laboratory tests in adults with monoarticular arthritis: Can they rule out a septic joint? Acad Emerg Med 2004;11:276. [PMID: 15001408] 

Salter RB, Bell RS, Keeley FW: The protective effect of continuous passive motion on living articular cartilage in acute septic arthritis. Clin Orthop 1981;159:223. [PMID: 7285461] 

Shirtliff ME, Mader JT: Acute septic arthritis. Clin Microbiol Rev 2002;15:527. [PMID: 12364368] 

Swan A, Amer H, Dieppe P: The value of synovial fluid analysis in the diagnosis of joint disease: A literature survey. Ann Rheum Dis 2002;61:493. [PMID: 12006320] 

Yu KH et al: Concomitant septic and gouty arthritis—An analysis of 30 cases. Rheumatology (Oxford) 2003;42:1062. [PMID: 12730521] 


Skin infections are common, and it is important to distinguish cellulitis from noninfectious rashes and from deeper infections that have a component of cellulitis, such as osteomyelitis, septic arthritis, myositis, and necrotizing fasciitis. Stasis dermatitis may visually mimic cellulitis. Patients often present with a rash over areas of increased peripheral edema. Unlike patients with cellulitis, these patients do not have a fever or elevated WBC.

Clinical Example

A 43-year-old man fell 3 weeks ago, injuring his leg. He presented with progressively worsening pain and swelling in his thigh. On examination, cellulitis of the anterior and lateral thigh was manifested by erythema, diffuse and tense swelling with shiny skin, and dramatic pain with knee flexion and tenderness with light palpation (Figure 8–16A). No swelling or erythema of the calf or foot was noted, and distal pulses and sensation were intact. Plain radiographs of the femur were normal. Doppler ultrasound ruled out a deep venous thrombosis but identified diffuse swelling of the muscle compartment. A T2-weighted MRI depicted characteristic expansion of the subcutaneous tissues with feathery streaks of increased water content circumferentially. It also revealed an underlying fluid collection within the vastus lateralis and intermedius (Figure 8–16B). Surgical inspection of this fluid revealed pus from an underlying myositis. An intramuscular hematoma from nonpenetrating trauma to the thigh had become hematogenously seeded with S. aureus.The infection caused an expanding abscess with myositis and superficial cellulitis. Culture acquisition, serial irrigation and debridement with open packing, and antibiotic therapy were started. Delayed primary closure and 6 weeks of culture-sensitive IV antibiotics cured the patient's infection. It should be noted in this case that the cellulitis was manifested after the leg began to swell, indicating clinically that the cellulitis was a secondary finding. In this circumstance a search for an underlying cause was necessary to understand the source of infection.

Figure 8–16.


A: Cellulitis and diffuse thigh swelling. B: Axial T2-weighted MRI of the thigh.


Pyomyositis is usually caused by hematogenous spread of bacteria rather than direct inoculation via penetrating trauma. Usually there is very limited muscle necrosis, and a very vascular fibrous reactive capsule contains the abscess. Open exploration with copious irrigation, limited debridement, and primary wound closure over a surgical drain is the surgical treatment of choice. Evaluation for contiguous spread to bone or joint must be performed. Aspiration for culture and insertion of a pigtail catheter for drainage can be done with ultrasound or CT guidance.

Clinical Example

A 6-year-old boy presented with a 2-week history of a posterior thigh mass. Focal tenderness and swelling were present, but no erythema was noted (Figure 8–17A). Further inspection revealed numerous insect bites around his ankle and leg that had become open pustules because of vigorous scratching. A T1-weighted fat-saturated MRI with gadolinium clearly characterized a fluid collection represented by a black signal void (Figure 8–17B). A halo of increased signal uptake along the rim of the fluid collection represents intense localized inflammation. The patient underwent surgical exploration, and pus was easily expressed from the thigh. The wound was debrided, irrigated, and a surgical drainage tube was placed. The wound was primarily closed. Staining revealed gram-positive cocci in clusters, and cultures grew a sensitive S. aureus. IV antibiotics were initiated, and the patient's symptoms rapidly improved. A week later he was discharged to home with 5 weeks of oral antibiotics that cured his infection.

Figure 8–17.


A: Prone patient with focal swelling of the posterior region of the midthigh. Note the insect bites scarring the skin. B: T1-weighted MRI with gadolinium contrast showing dark signal void in center of abscess.


A bursa occasionally becomes infected by hematogenous spread or because of open trauma to the overlying skin. The patient complains of pain and stiffness and possibly a fever. A tender, inflamed bursal region is seen clinically with significant erythema and swelling. Because these findings may also occur in acute exacerbations of rheumatism and flare-ups of gout, the patient must be carefully questioned regarding a possible history of these diagnoses. For example, aspiration of a soft, inflamed olecranon tophus may yield fluid that is strikingly similar to pus. Gram stain and polarized microscopy are necessary to identify negatively birefringent crystals.

If infectious bursitis is identified within the first several days, an oral course of antibiotics may successfully treat the infection. If skin erythema spreads and the bursa fills with fluid, the patient must be admitted to the hospital to aspirate and culture the bursal fluid and to begin empirical IV antibiotics. If the infection does not begin to resolve clinically within 48 hours, surgical bursectomy and primary closure of the wound over a drain should be performed.

Clinical Example

An 18-year-old woman skinned her knee on the gym floor during a game of basketball 1 week prior to presentation. She was noted on exam to have a dramatically painful, swollen, and erythematous prepatellar region with only slight loss of knee motion. A small central eschar, indicative of a floor burn, was observed (Figures 8–18A and B). Gram stain of the aspirate from the prepatellar bursa revealed gram-positive cocci in clusters. Despite 2 days of IV antistaphylococcal antibiotic therapy, the inflammation worsened. A complete bursectomy was performed (Figure 8–18C). A layer of normal appearing fatty tissue was left to cover the surface of the patella (Figure 8–18D), and the wound was closed over a surgical drain. The inflammation quickly improved within 3 days, and the patient was sent home with 3 weeks of culture-specific antibiotics.

Figure 8–18.


A: Anterior view of acute prepatellar bursitis. Notice small dark eschar. B: Lateral view of swollen prepatellar bursa. C: Bursa sectioned sagittally. Note the white-appearing rind of reactive fibrosis surrounding the central cavity. D: Intraoperative view of knee after bursectomy. Notice that the adipose tissue covering periosteum of patella was retained.


Necrotizing fasciitis is a rare but extremely aggressive, life-threatening soft-tissue infection of the subcutaneous and fascial tissues often encountered in diabetic patients. The muscle tissues are generally spared. Clinical examination of the skin reveals streaking erythema and sometimes small blisters, arising in the region of an incidental puncture wound. Local induration is always found, and occasionally subcutaneous crepitation caused by gas in the soft tissues is encountered. Air in the soft tissues can usually be seen on plain radiographs in gas-producing clostridial infections (see Figure 8–1). Serial exams are necessary to track the leading edge of the infection, which rapidly progresses in the direction of venous drainage. Emergent surgical debridement of devitalized tissues (sometimes necessitating amputation) along with antibiotics and intensive care treatment for hypotension are required to prevent death.

Clinical Example

A 38-year-old woman with a history of insulin-dependent diabetes mellitus sustained a penetrating trauma to the dorsum of her wrist while using scissors. Two days later she presented to the emergency room with a very painful arm and an infected stab wound that was draining serous fluid, an erythematous rash that extended from the wound to her elbow, and an increase of her forearm circumference of 6 cm compared with the other arm. She had a temperature of 38.6ºC (101.5ºF), a serum WBC of 22,000 with a left shift, and normal plain radiographs of the forearm.

The patient was admitted to the hospital and started empirically on a ticarcillin with clavulanate potassium (Timentin) and gentamicin. After 24 hours, however, the arm pain progressively worsened, and the rash advanced above the elbow (Figure 8–19A). MRI showed significant soft-tissue edema in the subcutaneous tissues but not in the muscle compartments (Figures 8–19B and C). Concerned about an uncontrolled necrotizing fasciitis, surgical exploration was emergently performed. Although most of the skin and all of the muscle tissues were viable, necrosis of the subcutaneous tissues and fascia was extensive (Figures 8–19D and E). All necrotic tissue was sharply excised. The necrotic tissue could easily be distinguished because it was friable to palpation. Normal-appearing tissue was firmer, and a finger could not easily dissect the plane between the subcutaneous tissue and the fascia. The wound was copiously irrigated with a pulsatile lavage device and packed open with moist gauze dressings secured with sterile rubber bands and staples in a shoelace fashion (Figure 8–19F). Gram-positive cocci in chains were identified intraoperatively, and the antibiotics were switched to oxacillin and clindamycin. Hyperbaric oxygen treatments using an acute protocol of 2.4 atm for 90 minutes three times daily was begun, and daily surgical debridements were performed for 3 days (Figure 8–19G). Some skin died and was debrided. The patient's infection cleared, and the wound was left to heal by delayed primary closure with use of split-thickness skin grafts where necessary (Figure 8–19H).

Figure 8–19.


A: A small draining puncture wound is noted at the middorsum of the hand, and an extensive erythematous rash covers the forearm. B: Axial MRI inversion recovery sequence showing circumferential subcutaneous inflammation. C: Sagittal MRI inversion recovery sequence showing subcutaneous inflammation but absence of inflammation in muscle tissue. D: Dorsal forearm incision revealing extensive subcutaneous necrosis. E: Necrosis in subcutaneous tissues but not in muscle tissue. F: Open packing of wound with saline-dampened gauze sponges secured with staples and sterile rubber bands in a shoelace fashion. G: Appearance of viable wound after 1 week of serial debridements, antibiotics, and hyperbaric oxygen treatments. H: Delayed primary closure with interrupted retention sutures.

Tiu A et al: Necrotizing fasciitis: Analysis of 48 cases in South Auckland, New Zealand. ANZ J Surg 2005;75:32. [PMID: 15740513]