Chapman’s Orthopaedic Surgery
3rd Edition

CHAPTER 133
MANAGEMENT OF ACUTE AND CHRONIC OSTEOMYELITIS
Michael J. Patzakis
M. J. Patzakis: Department of Orthopaedic Surgery, University of Southern California School of Medicine, Los Angeles, California, 90033.
The portals of entry for osteomyelitis, or inflammation of the bone, can result from hematogenous seeding, from direct inoculation (i.e., following open fractures or open reduction and internal fixation of fractures), or from the contiguous spread of bacteria from infected structures. Early diagnosis and effective surgical and antibiotic management can control the infection; suppression of infection may last a lifetime.
Since the early 1980s, limb salvage with good functional outcome has been enhanced by the addition of microvascular and local muscle transfers, bone grafting techniques, bone transport for large bone defects, newer antibiotics, and local antibiotic delivery systems. The treatment of osteomyelitis requires the work of a team,
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consisting of the orthopaedic surgeon, an infectious disease physician, and, in complex cases involving soft-tissue defects or inadequate soft-tissue coverage, a plastic surgeon. In many institutions, some orthopaedic nurses are specially trained in the care of patients with orthopaedic infections.
PATHOGENS
The organisms that cause osteomyelitis vary depending on the portal of entry and the type, age, and associated medical conditions of the host. Unfortunately, it is usually not possible to accurately predict the specific pathogen on the basis of clinical presentation alone. In the past, the most common causes of osteomyelitis were Staphylococcus aureus and various streptococcal species. Gustilo et al. (22) and Patzakis et al. (48) reported that S. aureus and coagulase-negative staphylococci were the most common organisms causing infections in open fractures. However, the microbiology of musculoskeletal sepsis has been changing in recent years. While S. aureus remains the predominant cause of osteomyelitis, there has been an increase in the frequency of infections caused by gram-negative organisms (52,53).
The portal of entry is an important consideration in the determination of the microbiology. Hematogenous osteomyelitis is most commonly caused by S. aureus. In the past, Haemophilus influenzae type B (HiB) was a common organism in children, but the advent of HiB vaccine has made it a rare cause (3). Causes of osteomyelitis due to direct inoculation, such as into an open fracture, will be influenced by the environment in which the injury occurred. For example, injuries occurring in water may lead to infection with Aeromonas or Plesiomonas. Nail puncture wounds of the foot, particularly through a tennis shoe, are associated with infection with Pseudomonas aeruginosa (28,50).
Underlying medical conditions of the host also influence the expected microbiology. Intravenous drug users may have P. aeruginosa and other gram-negative bacilli as causes of their osteomyelitis (18,39,61). Patients with sickle cell disease are prone to the development of Salmonella osteomyelitis. Osteomyelitis caused by fungal infections is more likely to be seen in immunocompromised hosts. Diabetic foot infections leading to osteomyelitis often are polymicrobial, often involving anaerobes and gram-positive and gram-negative aerobic bacilli. Patients infected with the human immunodeficiency virus (HIV) are at risk for a variety of unusual infections, including atypical mycobacteria.
One of the greatest problems for the future is the growing frequency of antimicrobial resistance in bacteria. Methicillin-resistant S. aureus has been known for decades, but its incidence is growing, even among nonhospitalized patients. Multidrug-resistant gram-negative bacteria are increasingly becoming a problem, limiting treatment options. Vancomycin-resistant Enterococcus faecium has become a major problem in nosocomial infections in the United States, but thus far has been rarely seen in osteomyelitis. The greatest concern is the development of vancomycin-resistant S. aureus, which has now been identified in patients in Japan, the United States, and Europe. Although this has not yet been reported as a cause of osteomyelitis, bone infections with this organism could be catastrophic, as no effective antibiotics for this infection are yet available.
SYSTEMIC ANTIBIOTIC THERAPY
Antibiotic therapy is an adjunct to good surgical management, which includes adequate debridement and wound management. There has been a recent surge in the number of antibiotics available for the treatment of osteomyelitis. The beta-lactam antibiotics, such as penicillin and cephalosporin, are effective and relatively safe antimicrobials that can cover a wide range of gram-positive and gram-negative infections. The quinolones, however, have changed the treatment of osteomyelitis by providing oral drugs that achieve excellent serum levels and have good bone penetration.
The questions most often asked about the use of antimicrobials concern the choice of agent, the optimal route (intravenous, oral, or local), and the length of administration. The Gram stain, culture, and antimicrobial sensitivity tests are important guides in determining the specific antimicrobials to be used. Sensitivity testing not only helps to identify resistant organisms but also to guide the selection of the most active antimicrobial for the specific infection.
Staphylococcus aureus remains the most common cause of osteomyelitis. A semisynthetic penicillin (such as nafcillin) is the drug of choice for most staphylococcal infections. Alternative choices could include a first-generation cephalosporin [such as cefazolin (Ancef)], clindamycin, or a quinolone. Vancomycin is less active against S. aureus than the penicillins and should not be used except in the case of patient allergy to the beta-lactams or for the treatment of methicillin-resistant S. aureus. Rifampin may be used in combination with one of the other agents for synergy.
Infections with the gram-negative bacilli can be treated with a penicillin plus beta-lactamase inhibitor combination [such as piperacillin-tazobactam (Zosyn)], a cephalosporin [such as cefotaxime (Claforan) or ceftriaxone (Rocephin)], an aminoglycoside, or a quinolone. For infections with P. aeruginosa, treatment with an antipseudomonal beta-lactam (such as piperacillin, ceftazidime, or cefipime) together with an aminoglycoside (such as tobramycin,
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which is the most effective against Pseudomonas) still represents the gold standard of therapy. Although successful treatment with a single agent, such as ceftazidime, has been reported (1,16), treatment failures with single-agent therapy have been noted, including some cases associated with the emergence of resistance.
The quinolones are a major addition to the antimicrobials available for the treatment of osteomyelitis. Currently available quinolones that may be useful in the treatment of osteomyelitis include ciprofloxacin, ofloxacin, and levofloxacin. They have a broad spectrum of activity including S. aureus and streptococci (with the newer quinolones such as levofloxacin having much better activity against the gram-positive organisms than ciprofloxacin), the aerobic gram-negative enteric bacilli, and P. aeruginosa.
One of the most important advantages of the quinolones is the fact that oral administration results in levels similar to those obtained with intravenous administration, suggesting that oral therapy can replace intravenous therapy, at least in some instances (17,58). Since the incidence of adverse reactions to these drugs is low, they may be used in place of more toxic antimicrobials such as the aminoglycosides.
The treatment of osteomyelitis caused by Mycobacterium tuberculosis has been influenced by the rise in drug-resistant organisms. The current treatment recommendations are starting with three or four drugs (isoniazide, rifampin, pyrazinamide, and ethambutol), depending on the level of isoniazide resistance in the community. If cultures show that the organism is sensitive to isoniazide and rifampin, therapy can continue with isoniazide and rifampin for a minimum of 6 months, although longer regimens (9–12 months) are probably required (55).
Fungal infections have traditionally been treated with amphotericin B, which was the only agent effective against deep fungal infections. Although it is often effective, there are significant adverse effects associated with the administration of amphotericin B, including fever, chills, and nausea during administration, and renal insufficiency or failure with potassium and magnesium wasting. Newer agents such as fluconazole and itraconazole have excellent activity against many of the fungal organisms and far fewer side effects.
Because of the large number of new antimicrobials available, the problem of increasing resistance among organisms, and the potential for significant adverse reactions with many of the drugs, it is imperative that an infectious disease consultant help with the selection of specific antibiotic therapy and the monitoring of the patient for adverse reactions. Table 133.1 lists commonly used antimicrobials (also see Chapter 132).
Table 133.1. Commonly Administered Antimicrobials
TOPICAL ANTIBIOTIC THERAPY
Topical antibiotic therapy is an old concept. Hippocrates and later Galen used medicinal ointments that included honey, a bactericidal agent, in the treatment of open fractures. In the early 1900s, Lord Lister, with good success, used phenol-soaked compresses to combat the microorganisms believed to be responsible for infection (35). He later introduced the use of carbolic acid as an antiseptic. Following the discovery of the sulfonamides, sulfa powder in wounds was popular among war surgeons. The major
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changes of today are the choice of the agent used and the development of new vehicles for delivery.
Most orthopaedic surgeons use a topical antibiotic solution for irrigation of infected wounds at the time of surgery. Although any antimicrobial could be used, the most commonly used agents are polymyxin (1 million units/L of saline) and bacitracin (50,000 units/L of saline).
Closed-suction antibiotic, high-volume irrigation systems have been used for ingress and egress, usually administered for a period of 3 to 21 days. The main deterrent to this mode of administration has been the emergence of new organisms, usually hydrophilic gram-negative organisms (10,29,47). The overall success for antibiotic irrigation has been shown to be the same as for antibiotic-impregnated polymethylmethacrylate (PMMA) beads (62). Therefore, tube-suction irrigation has been abandoned by many surgeons. If this system is used, adhere to every means possible to prevent contamination. The risk of secondary contamination increases with the length of usage of the irrigation system. It is advisable to use Silastic drains and to place the tubes on suction or egress for 24 hours before removing the system. This procedure will remove all of the fluid and hematoma present and will collapse the dead space, thereby precluding the possibility of abscess formation. I do not recommend the use of suction-irrigation systems.
Antibiotic-impregnated PMMA can be used to achieve local delivery of high concentrations of antibiotics. Among the advantages of antibiotic beads are low systemic levels of antibiotics, resulting in a lower potential of systemic toxicity, decreased need for systemic intravenous therapy, and decreased length of hospital stay. The disadvantages are that it requires a closed wound for the development of high local levels of antibiotics. Moreover, it may act as a foreign body, especially in the presence of resistance to the antibiotic in the vehicle, such as gentamicin or tobramycin.
The use of antibiotic-impregnated PMMA in total hip implants has been advocated (4,5,41). Klemm and other investigators have reported good results with the use of gentamicin-impregnated methylmethacrylate beads (Septopal) for the treatment of chronic osteomyelitis (30,31). Unfortunately, the United States Food and Drug Administration (FDA) approval of factory-made gentamicin beads (Septopal) has been indefinitely delayed, leading many surgeons to make their own beads using bead molds (13).
Numerous studies have evaluated the in vitro elution characteristics of PMMA combined with antibiotics. The
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majority of studies have evaluated gentamicin, but as it is no longer commercially available in powder form for injection in the United States, physicians now use tobramycin and vancomycin since they are active against the most common organisms leading to prosthetic joint infections and osteomyelitis. Antibiotic elution from antibiotic-impregnated PMMA is proportional to the surface area of the cement (68,69) and affected by the type and concentration of the antibiotic used, the brand of PMMA cement, and the amount and turnover of the surrounding fluid (66). Studies have shown that antibiotics elute better from beads than from spacers, and better from palacos cement than from simplex cement, and tobramycin achieves better levels than vancomycin (20,33,36).
Overall, the results of treatment with antibiotic-impregnated PMMA beads are encouraging, so the use of these in selected cases seems appropriate (Fig. 133.1). A different vehicle for the delivery of local antibiotic therapy may improve results and lessen the disadvantages associated with this therapy. Various biodegradable antibiotic delivery systems are now being evaluated but are still in the investigational stage.
Figure 133.1. Anteroposterior roentgenograms of a 46-year-old man with chronic osteomyelitis. The patient was treated with debridement followed by insertion of aminoglycoside-impregnated methylmethacrylate beads and a local muscle flap.
CLASSIFICATION OF OSTEOMYELITIS
Cierney et al. proposed a staging system for adult osteomyelitis based on anatomic type and physiologic class (7,8). The four anatomic types are type I, medullary osteomyelitis; type II, superficial osteomyelitis; type III, localized osteomyelitis; and type IV, diffuse osteomyelitis.
The three physiologic classes deal with the condition of the host. An “A” host has good systemic defenses with good local vascularity and a normal physiologic response to infection and surgery. A “B” host is a compromised host with either local, systemic, or combined deficiency in wound healing and infection response. A “C” host is a patient who is not a surgical candidate, requires suppressive or no treatment, who has minimal disability, or for whom the treatment or results of treatment are more compromising than the disability caused by the disease itself.
DIAGNOSIS
A diagnosis of acute osteomyelitis should be considered an emergency. The presenting signs and symptoms may vary with the severity of the infection. Symptoms include fever and chills, general malaise, irritability, pain, and swelling. With lower extremity involvement, there is either a limp or an inability to bear weight. An infant with upper extremity involvement may exhibit pseudoparalysis; older children and adults with upper extremity involvement complain of pain on movement or use of the extremity.
It is important to localize the point of maximum tenderness, which is usually warm and swollen. In children it is generally in the metaphyseal region. It is also important to evaluate the adjoining joint for evidence of septic arthritis, which can occur as an extension of the adjoining osteomyelitis. Osteomyelitis involving the neck of the femur, talus, and humeral head often leads to sepsis of the joint because these foci are located within the joint capsule.
Once the point of maximum tenderness is localized, aspirate the area, and send the pus or fluid obtained for Gram stain, culture, and sensitivity studies. If tuberculosis or a fungal infection is suspected, obtain an acid-fast stain and tuberculosis and fungal cultures. When a joint effusion is present or joint involvement is suspected, aspirate the joint and confirm with an arthrogram. The arthrogram helps document the location of the aspiration and is useful for positive as well as for negative aspirations, since it may also identify joint capsule rupture. Aspiration of the hip joint under ultrasound guidance is very helpful in children and adults.
The white blood cell count is generally elevated, depending on the severity of the infection, with an increase in immature or band cells. The erythrocyte sedimentation rate and the C-reactive protein are usually elevated. Obtain blood cultures in all cases of acute hematogenous osteomyelitis and in chronic osteomyelitis exacerbated by fever and bacteremia.
Roentgenograms taken early in the disease process generally show soft-tissue swelling. Bony changes are not present until 7–10 days after the onset of infection. Radionuclide bone scanning using radioactive-labeled isotopes, such as technetium-99m and, more specifically, gallium citrate-67 and indium-111-labeled white blood cells, is helpful in localizing the area of involvement and in helping diagnose the condition.
Plain technetium, sequential technetium-gallium imaging, and indium-labeled leukocyte scintigraphy are the studies most commonly used. Indium 111-labeled leukocytes have been reported by a number of investigators as being more useful than other imaging in osteomyelitis complicated by fractures and nonunions (11,38,40,63) (see Chapter 132). Aspiration is used for the diagnosis, especially when there is no drainage or sinuses, and in some cases bone biopsy may be necessary.
Magnetic resonance imaging (MRI) has added a new dimension to the diagnosis, localization, and characterization of the extent of infection. MRI has been reported by Modic et al. to have a 94% accuracy in diagnosing spine infections (40). T1- and T2-weighted images are the initial screening techniques for diagnosing osteomyelitis. The MR finding in osteomyelitis on T1-weighted image sequences is a low signal intensity due to a dark marrow signal and an increased signal intensity due to a bright marrow signal on the T2-weighted image sequences (Fig. 133.2, Fig. 133.3).
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MRI has decreased the need for bone scanning and provides more useful information. Do sinograms whenever there is a sinus tract or open draining area from which the depth and extent of the infection can be determined (Fig. 133.4). Do abscessograms whenever an abscess is present and frank pus is aspirated. The abscessogram will help outline the extent of the abscess cavity (Fig. 133.5). MRI, computed tomographic scanning, and radiographic tomogram are all useful tools in evaluating osteomyelitis.
Figure 133.2. These are T1-weighted images of a 44-year-old woman with systemic lupus erythematosis and hematogenous osteomyelitis. There is decreased signal within the distal third of the tibia and a serpiginous area of low intensity consistent with osteonecrosis. A biopsy had been performed previously. At surgery, she had an abscess with sequestra.
Figure 133.3. These T2-weighted images of a 15-year-old boy show increased signal from the ankle to the mid tibia. There is increased signal in the adjacent soft tissues about the ankle and tibia. There is a minimal ankle effusion present. At surgery, the patient had an intramedullary abscess of the metaphysis and distal tibia.
Figure 133.4. Anterior (A) and posterior (B) roentgenograms of a sinogram in a 21-year-old man with chronic osteomyelitis that tracks into the intramedullary cavity.
Figure 133.5. Lateral radiograph (A) of a 15-year-old boy shows a subperiosteal abscess that was aspirated and injected with contrast material. Anteroposterior (B) and lateral (C) radiographs of a 9-year-old child show contrast material in the subperiosteal area and within the medullary cavity after pus had been aspirated. The contrast material demonstrates the extent of the abscess.
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PRINCIPLES OF TREATMENT OF INFECTED UNUNITED FRACTURES AND NONUNIONS
The principles of treatment are infection control, stabilization of the fracture, soft-tissue coverage, and bone graft of ununited fractures and large bone defects.
Infection control includes irrigation and debridement, culture and sensitivities, and antibiotic therapy. In chronic osteomyelitis, obtain aerobic, anaerobic, and fungal cultures. Recent studies have advocated taking of multiple deep cultures from purulent material, soft tissue, and bone (51,56). Marrie and Costerton postulated that different organisms may be growing in isolated microenvironments. Sampling differences and bacterial viability may influence the culture results (37).
Stabilization of the ununited fracture or nonunion is essential. Soft-tissue coverage may require the use of local muscle flaps and free vascularized muscle flaps for soft-tissue defects or an inadequate soft-tissue envelope after control of the osteomyelitis. Local muscle flaps and free vascularized muscle transfers also help by bringing in a new blood supply, which is important in host defense mechanisms, antibiotic delivery, and osseous and soft-tissue healing (46). For the tibia, use the gastrocnemius muscle for proximal-third defects, the soleus for middle-third, and for the distal-third, free vascularized muscle transfers.
For local muscle transfers, it is important to assess the muscle preoperatively and not to transfer damaged muscle. Also avoid using crushed or badly damaged muscle, as flap necrosis or flap complications may result. In these cases, use free vascularized tissue transfer. Do preoperative angiograms on patients whose vascular status has been altered from any cause.
SURGICAL CONSIDERATIONS
TOURNIQUETS
Apply a tourniquet whenever possible except in patients with sickle cell disease or significant peripheral vascular disease. The tourniquet improves hemostasis and thus facilitates identification of the infection process. In acute cases with swelling, cellulitis, or abscess formation, elevate the extremity for several minutes before inflating the tourniquet. In chronic osteomyelitis without significant cellulitis or abscess formation, use an elastic bandage to extravasate the extremity before inflating the tourniquet.
DEBRIDEMENT
Thorough debridement of all sequestra and necrotic and desiccated bone is essential. Do not remove viable infected bone, so as not to create large bony defects. It is not necessary to debride viable infected bone. Dyes and tetracycline labeling have been used as a means of identifying necrotic bone, but I have not found these techniques to be useful.
Clinically dried out, exposed, desiccated bone is darker than normal and should be debrided. Necrotic bone that has not been exposed may appear at surgery more yellowish than viable bone, which is whitish. The main finding is that viable bone bleeds, whereas necrotic bone does not.
Use of an osteotome to superficially shave the outer cortex of the questionable bone results in small areas of punctate bleeding. Some bone that may have been exposed to air may be viable; in these cases, the exposed outer cortex should be debrided with an osteotome down to good bleeding bone. Evacuate all pus and abscess, and remove all necrotic and infected soft tissue.
IRRIGATION
Use copious amounts of irrigating fluid, which cleanses the area of purulent exudate, loose soft tissue, and bony fragments, and decreases the bacterial count. I use 10 L of irrigating fluid for most infected wounds. I use 2 L of antibiotic solution containing 50,000 units of bacitracin and 1 million units of polymyxin per liter as the final irrigating solution. Other antibiotics can be used for topical irrigation as well.
WOUND MANAGEMENT
The decision to leave a wound open or to close it requires careful judgment. In the majority of acute infections, and in all cases in which there is associated abscess formation with cellulitis and swelling, the wound should be left open. In some cases of early postoperative infection, the wound may be closed over drainage tubes, as long as the wound is thoroughly clean and the infection is not anaerobic.
In cases of chronic osteomyelitis in which there is no significant cellulitis or abscess formation and in which the wound has been adequately debrided and converted to a clean wound, the wound may be closed over drainage tubes. In some cases in which bone or metal will be exposed if the wound is left open, a partial closure over the bone or metal may be desirable, as long as an adequate pathway has been provided for drainage. When there is any doubt, it is safest to leave the wound open. If the wound is closed, the wound site must be examined daily for any signs of infection; if such signs appear, the wound must be opened.
Many wounds heal nicely by secondary intention. In the case of large wounds or when delayed closure is preferable, do not attempt closure until two criteria are met. First, the wound should appear clinically healthy, with clean granulating tissue and without any purulent exudate or necrotic tissue. If infected necrotic tissues are present, redebride the wound until it appears healthy. Second, once
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the clinical appearance of the wound is clean, take quantitative tissue cultures and do Gram stains. Wounds with either a positive Gram stain or quantitative tissue cultures with a bacterial count greater than 10-5 organisms should never be closed. (A positive Gram stain implies a bacterial count of greater than 10-5 organisms.)
These wounds should be considered infected and reassessed for further surgical debridement and the appropriateness of the systemic antibiotic therapy. With experienced surgical teams, tissue cultures are not routinely performed. It has been our practice to do a thorough initial debridement followed by an en bloc excision of the wound at closure or muscle transfer.
In secondary closure of wounds, it is important to redebride the wound at the time of closure and to do en bloc resection of the granulating tissue for several reasons. First, although the bacterial count is low, these tissues should still be considered contaminated; debridement will further reduce the bacterial count and thereby diminish the chance of infection. Second, debridement allows for cleaner, healthier tissue to be approximated by wound closure or covered by muscle transfer.
DRAINS
When the wounds are closed, Silastic (Jackson-Pratt) or polyethylene (Hemovac) drains may be used. I prefer the Jackson-Pratt drains. Penrose drains, made of rubber, are the most reactive, and if left in for long periods can cause foreign-body granulomas. Do not use Penrose drains in orthopaedic infection management.
Remove the suction drain in 48–72 hours. The drain allows the removal of all hematoma and tissue fluid, and the collapse of the potential dead space. The drains should be removed under sterile conditions and the tip cut off and sent for culture and sensitivity tests.
The drain tends to attract whatever bacteria are present because it is a foreign body and because tissue fluids are removed through it. In general, a positive culture of the drain tip is a bad prognostic sign: It means that bacteria remain behind. Monitor the clinical course and wound site closely; if any clinical signs of wound infection reappear, it may be necessary to consider redebridement and reassessment of antibiotic therapy.
WOUND PACKING
The purpose of leaving a wound open is to allow drainage. Make certain, therefore, when packing wounds with gauze or other materials, that packing does not obstruct drainage. If it does, the purulent exudate will be retained in the wound, possibly causing tissue breakdown and necrosis with secondary cellulitis or even abscess formation. It is best to put wicks perpendicular to the open wound to allow free drainage. Wicks can be either povidone-iodine (Betadine)-soaked gauze, plain gauze, or fine-mesh gauze. The size varies with the size of the wound. The ends of the wicks should always protrude through the skin edges to allow easy access and removal and to prevent retention.
ANTIBIOTIC BEAD POUCH
Antibiotic-loaded beads were first introduced by Klaus Klemm for use in osteomyelitis (30,31). Henry, Seligson, and Ostermann introduced a physician-made antibiotic bead pouch for use in open fractures (25,43). This concept has been expanded, and I now use a physician-made antibiotic bead pouch during the interval between the initial debridement and the time of muscle transfer, a median of 4 days. Microbe-specific antibiotic(s) can be added to either Palacos or Simplex PMMA. I prefer Palacos: The antibiotic elution has been reported by some investigators to be better them Simplex. Although most antibiotics may be added to PMMA depending on the microbial sensitivity results, tobramycin and other aminoglycosides are the most commonly used antibiotics.
I use 2.4 g tobramycin to 40 g Palacos PMMA, an amount sufficient to make enough bead chains to fill large defects. I use a mold to make 6- or 7-mm beads strung on 24- or 26-mm wire. For those surgeons who make beads without a mold, the bead size should be small because increased surface area allows for better antibiotic elution. The beads are then covered by Tegaderm, Opsite, or an equivalent material. The advantages of the antibiotic bead pouch used in this fashion are high local antibiotic levels with low systemic toxicity and less chance for secondary contamination because the wound is covered. Also important is patient comfort, as dressing changes are not required, and there are decreased requirements for wound care.
SURGICAL TECHNIQUES
HEMATOGENOUS OSTEOMYELITIS
Hematogenous osteomyelitis is most often seen in infants, children, drug abusers, and immunosuppressed hosts. In 1894, Lexer injected laboratory animals with S. aureus organisms and then traumatized a bony area, causing infection to appear at that site (34). Hobo explained that the predilection for the metaphysis in acute osteomyelitis was due to the fact that the arteries in this location are end arteries, that there is slowing of the venous flow in the sinusoids, and that phagocytosis is defective in this area (27).
Trueta later expanded on Hobo’s work (65). Once the metaphyseal region is seeded and exudate or pus forms, the suppurative process may then travel under pressure
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through the Volkmann canals into the subperiosteal region, extend itself within the medullary cavity, or spread into the epiphysis (Fig. 133.6). It is not uncommon for the joint to be involved secondarily, especially a joint in which the metaphysis is intra-articular, such as the hip or shoulder. Often the abscess extends into the soft tissues as well (42,67).
Figure 133.6. Outline of the pathophysiology of hematogenous seeding. When under pressure, the exudate or abscess can extend through the Volkmann canals into the subperiosteal region, and from there into the intramedullary cavity or the epiphysis. (Modified from Hobo T. Zur Pathogenese der Akuten Haematogene Osteomyelitis, mit Berucksichtigung der Vitalfarbungslehre. Acta Sch Med Univ Imper Kioto 1921;4:1.)
In cases in which the disease is not diagnosed promptly or in which either inadequate or no treatment is given, the disease enters the subacute stage (Fig. 133.7). Because of the introduction of antibiotics and improved diagnostic and surgical techniques, the chronic stage and its sequelae are no longer seen as frequently as they used to be.
Figure 133.7. A: A frog-leg lateral view shows a lytic area in the metaphysis of a 7-year-old boy with a 6-month history of pain and a limp. B: Anteroposterior radiograph taken at the time of biopsy. The lesion was found to be a subacute osteomyelitis caused by a Staphylococcus aureus organism.
One question that arises in the treatment of acute hematogenous osteomyelitis is whether to treat all patients surgically. Unless clinical evidence of an abscess is present, I treat patients with systemic antibiotics and without surgery. However, the clinical situation must be repeatedly assessed during treatment. Many osteomyelitic processes are seen early in the disease process or represent a cellulitic process of the bone, and pus or the abscess phase may not occur.
Although some authors have not found it necessary to drill a window in cases of subperiosteal or soft-tissue-extended osteomyelitis, I routinely window the cortical bone for better debridement of the residual intramedullary abscess and necrotic bone and tissue (Fig. 133.8) (see Chapter 176).
Figure 133.8. A: Anteroposterior radiograph in a child shows destructive lytic changes in the metaphyseal region with periosteal reaction. B: Lateral film shows the extent of the cortical window made for debridement of the medullary abscess. C: Lateral film taken 7 months later shows healing of both the cortical window and the osteomyelitic process.
Cortical Windowing for an Acute Intramedullary Abscess of the Tibia
  • Using tourniquet control, make a longitudinal incision along the posterior border of the medial tibia and over the affected part of the tibia. If a subperiosteal abscess is present (more likely in a child than in an adult), incise the periosteum longitudinally over the abscess.
  • If no subperiosteal abscess is found, observe the status of the cortex. The infected area is often soft and may be pitted, with or without obvious cortical destruction.
  • Drill several holes through the cortex into the medullary
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    canal. Unless the intramedullary abscess has already decompressed itself into the subperiosteum or soft tissues, pus will exude through these holes.
  • Outline with a drill an elongated cortical window extending along the extent of the intramedullary abscess. The outlined elongated window should be centered in the posterior half of the anteroposterior diameter of the bone to allow for dependent drainage. The length of the window depends on the extent of the intramedullary abscess, and the width depends on the diameter of the bone. For children, use a 1- to 2-cm-wide window. After debridement of any obvious sequestrum and copious irrigation, insert a Betadine gauze into the wound and leave it open. A similar type of window of the femur is made for osteomyelitis of the femur.
OSTEOMYELITIS FOLLOWING OPEN FRACTURES
For acute osteomyelitis following an open fracture, it is important to assess the extent of the infection and to obtain a Gram stain, culture, and sensitivity test. Start appropriate systemic antibiotics, and take the patient to surgery for irrigation, debridement, and stabilization of the fracture if it is not already adequately stabilized (Fig. 133.9). The majority of fractures in the tibia can be stabilized with half-pin external fixation devices. Use a biplanar or delta frame for more stability if required.
Figure 133.9. A: A 28-year-old man with an infected open fracture. B: There is a clean granulating wound 12 days after the fracture had been irrigated, debrided, and stabilized with an external fixator and the patient given systemic antibiotic. At this time, biplanar fixation with half-pins rather than full-length pins would be performed.
Once the open fracture infection has been controlled and the fracture stabilized, perform cancellous autogenous bone grafting, particularly for fractures with bone deficiency and type III open fractures. Fracture healing, which facilitates infection control, is an important principle in the management of infected nonunited fractures and nonunions. Although many fractures heal in the presence of infection, infection interferes with the osteogenic process and may lead to nonunion by a number of mechanisms: The bacteria compete with osteogenic cells for oxygen and nutrients, activate enzymes deleterious to the osteogenic process, lower the pH, affect oxygen potential, interfere with the differentiation of osteogenic cells, and retard tissue maturation.
For both unstable infected open tibial fractures and type III infected open tibial fractures, I recommend early autogenous cancellous bone grafting through a posterolateral approach. Alternatively, if a muscle flap has been made anteriorly for soft-tissue coverage, an autogenous
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cancellous bone graft can be done anteriorly 6 weeks later, provided there is no evidence of recurrent infection.
Posterolateral Bone Grafting of the Tibia
Posterolateral bone grafting is particularly useful in achieving union of an infected nonunion or an infected fracture of the tibia. Freeland and Mutz have reported a 100% union rate in 26 patients with infected nonunions treated in this manner (14). I have achieved a union rate of approximately 91% in the treatment of 61 infected tibial nonunions (49).
The approach is used for the distal two thirds of the tibia. It was described by Harmon and is also used for tibia-pro-fibula grafting (23) (Also, see Chapter 3).
  • Place the patient in either a prone or a lateral decubitus position. Identify the posterior border of the fibula and the lateral border of the gastrocnemius muscle. Using tourniquet control, begin an incision of appropriate length along the lateral border of the gastrocnemius and posterior to the fibula.
  • Once you have cut through the subcutaneous structure, identify the peroneal muscles anteriorly and develop a plane between the peroneals and the posterior muscles
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    consisting of the gastrocnemius, the soleus, and the flexor hallucis longus muscles.
  • Now reflect the soleus and flexor hallucis longus posteriorly and medially to expose the posterior aspect of the fibula.
  • Elevate the origin of the tibialis posterior muscle from the posterior aspect of the interosseous membrane. Locate the posterolateral border of the tibia and, using sharp dissection, expose the posterior surface of the tibia by stripping the muscles subperiosteally off the tibia. In the distal one third of the tibia, approximately four to five fingerbreadths above the tip of the lateral malleolus, an interosseous arteriole branch from the peroneal artery perforates the interosseous membrane and travels anteriorly to anastomose with the anterior tibial artery. Take care to protect this vessel. The posterior tibial neurovascular bundles lie between the tibialis posterior and flexor hallucis longus muscles and are not visible. The muscular branches of the peroneal artery lie within the peroneal muscles.
  • Once the posterior aspect of the tibia is exposed (Fig. 133.10), prepare the tibia and the posterior aspect of the fibula for bone grafting by roughening up the cortex with either a burr or an osteotome. Be extremely careful not to disturb the fracture site so as to avoid contamination posteriorly.
    Figure 133.10. A: A cadaveric specimen outlining the fibula. A skin incision varying with the exposure desired is made just posterior to the fibula along the lateral border of the gastrocnemius and soleus muscles. B,C: The peroneal muscles are retracted anteriorly and the border of the fibula is exposed. The tibialis posterior and the flexor hallucis muscles are dissected from the interosseus membrane and the posterior tibia and retracted posteriorly. The posterior tibialis neurovascular bundle is protected by the tibialis posterior and flexor hallucis longus muscles, which it lies between. D: The posterior aspect of the fibula is now exposed, and the posterior border of the fibula and interosseous membranes are visible.
  • Lay cancellous bone grafts posteriorly several inches above and below the fracture site and between the tibia and fibula across the interosseous membrane. The objective is to achieve not only union of the fracture site, but also a tibial–fibular synostosis (Fig. 133.11). A 1.5–2 oz medicine glass filled with cancellous bone is generally sufficient to repair a nonunion without bone loss.
    Figure 133.11. Anteroposterior and lateral films show healing of the fracture following the posterolateral bone graft. Note the synostosis between the tibia and fibula.
  • At this point, release the tourniquet and achieve hemostasis. Insert a Silastic drain. Allow the peroneal muscles and posterior muscle mass to return to their anatomic positions. Do not close the deep fascia.
  • Close the subcutaneous tissues and skin with interrupted sutures.
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  • Remove the Silastic drains in approximately 48 hours and elevate the leg for 72 hours.
  • Start full weight bearing to tolerance 7 days postoperatively if the patient is immobilized in a cast.
  • If an external fixator is used for an unstable fracture, it can generally be removed at 6–8 weeks and a walking cast applied.
  • Union generally occurs in 4–7 months, median time being 6 months.
DEAD-SPACE MANAGEMENT
It is important that soft-tissue and bony defects be filled to reduce the chance of continued infection and loss of function. Advances in microvascular techniques have made possible the transfer of muscle, myocutaneous, osseous, and osteocutaneous flaps to the soft-tissue and bony defects. Fitzgerald et al. reported a 93% success rate in the treatment of chronic osteomyelitis with local muscle flaps combined with thorough debridement and specific antimicrobial therapy (12). Our results using this technique have also been encouraging (46).
In general, for soft-tissue defects involving the proximal third of the tibia, use the gastrocnemius muscle; for those involving the middle third, use the soleus muscle; and for those involving the distal third, use a free-tissue transfer.
In cases of bony defects, perform autogenous cancellous bone grafting six or more weeks later. The muscle flap can be elevated and cancellous bone grafting performed underneath, provided there are no signs of infection (Fig. 133.12).
Figure 133.12. Anteroposterior (A) and lateral (B) radiographs of the tibia and fibula in a 21-year-old man who had a previous posterior bone graft and now shows the presence of a large sequestrum. Lateral film (C) shows debridement of the infection and sequestra. Lateral film (D) taken 10 months after a local flap was performed and an autogenous cancellous bone graft was performed.
According to Weiland et al., the highest rate of recurrence of infection in free-tissue transfer in osteomyelitis is found in cases associated with a segmental bone defect (70). It has been our experience that the fibula is the key factor in treating osteomyelitis with segmental bone loss of the tibia. If there is a bony defect or segmental loss of both the fibula and tibia with chronic osteomyelitis, an amputation is advisable. If the fibula is intact or without a bony defect, reconstruction of the bony defect is more likely to be successful. For defects up to 6 cm, autogenous cancellous bone grafting can be done (Fig. 133.13).
Figure 133.13. A: Anteroposterior radiograph of a 34-year-old woman with approximately a 6 cm defect. B: Anteroposterior and lateral films taken 1 year following performance of an autogenous cancellous bone graft to fill dead space caused by bony defects.
In larger defects, use a free vascularized osseous graft. A tibia-pro-fibula synostosis using the previously described posterolateral approach can be done when a free vascularized osseous graft or autogenous cancellous bone grafting of the defect is not possible (Fig. 133.14). The fibula hypertrophies with time, allowing for functional weight bearing.
Figure 133.14. A: Anteroposterior and lateral radiographs of a 48-year-old man who developed clostridial myonecrosis after an open fracture of the tibia and treatment with a tibia-pro-fibula synostosis. The distal synostosis site was bone grafted first and is seen here 10 weeks postoperatively. B: Radiographs taken 4 years after the tibia-pro-fibula synostosis for the segmental defect. Note the synostosis proximally and distally, and the hypertrophy of the fibula. C: Healed wounds show no evidence of recurrence of infection. Notice the area of defect in the middle calf area.
Another procedure for dead-space management is the open cancellous bone grafting procedure described by Rhinelander (57) and by Papineau et al. (45). This procedure is useful when tissue transfer is not possible.
Open Cancellous Bone Grafting
Open cancellous bone grafting has been effective in the treatment of infected bone defects. Papineau et al. (45), Roy-Camille et al. (59,60), Rhinelander (57), Higgs (26), Knight and Wood (32), Coleman et al. (9), Bickel et al. (2), and Green and Dlabal (19) have all reported favorable results. However, because of the associated long hospitalization time, long healing time, high complication rate, meticulous care required, and resulting unstable scar skin, I use it only if local muscle transfers or free-vascular tissue transfers with secondary cancellous bone grafting cannot be done.
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There are three stages to this technique:
  • Thorough debridement of all infected tissues, repeated as necessary; stabilization of the fracture with an external skeletal fixator
  • Cancellous autogenous bone grafting into a defect lined with clean uninfected granulation tissue
  • Skin coverage either by secondary epithelialization or, in larger defects, by split-thickness skin grafting
  • Debride all infected soft tissue and sequestra, and debride all necrotic bone to bleeding osseous tissue. Perform stabilization using an external skeletal fixator.
  • When exposed surfaces are covered with clean granulation tissue, pack finely morcelized autogenous cancellous bone into the defect created by the bone debridement or previous bone loss. The diameter of the graft should be slightly larger than the diameter of the bone being replaced, since the graft will tend to contract. Rhinelander recommends that the maximum graft thickness be 1.5 cm from the nearest granulation surface (57).
  • Dress the wound with gauze and keep it moist with a physiologic irrigating solution such as Ringer’s lactate, either by intermittent soaking of the dressings or by a slow intravenous drip. The dressing, which should be changed daily, is to be soaked with physiologic solution until the wound is covered by epithelialization or, in some cases, by secondary split-thickness skin grafting (Fig. 133.15).
    Figure 133.15. A: Lateral radiograph of the tibia and fibula in a 37-year-old woman with loss of the tibia following an infection that developed after the patient sustained a type III open fracture. B: Anteroposterior photograph shows the soft-tissue and bone loss and exposed tibial shaft. C: Photograph taken at the time of autogenous cancellous bone grafting of the dead space. D,E: Anteroposterior and lateral radiographs, taken after the grafts had consolidated, show healing of the fracture. F: Lateral photograph, taken 3 years after the procedure, shows knee flexion and the appearance of the leg. The patient has been free of infection.
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OSTEOMYELITIS IN THE PRESENCE OF INTERNAL FIXATION FOR FRACTURE STABILIZATION
Osteomyelitis in conjunction with internal fixation for fracture stabilization poses a special problem for the surgeon. Should the metal be removed or left in? The answer to this question is guided by such factors as the stage of fracture healing, the amount of stability provided, the amount of time since surgery, and the location of the fracture.
Gristina and Costerton reported that in 76% of prosthesis-related infections, microorganisms grew in a biofilm or glycocalyx that adhered to the surfaces of the biomaterials present (21). They suggested that infections in the presence of orthopaedic implants may be more resistant than normal to host defense mechanisms and to antimicrobial therapy.
If osteomyelitis develops in the presence of metal with a healed fracture, remove the metal. If the fracture is not united and the metal is not providing stability, remove the metal and restabilize the fracture. In the immediate
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postoperative period (within the first 1–6 weeks), retain the internal fixation device if it is stable and is required.
If the internal fixation device is stabilizing a nonunited articular fracture, retain it (Fig. 133.16). In general, for late infected nonunion of tibial shaft fractures with internal fixation, I recommend removal of the internal fixation device and stabilization with an external fixator. For late nonunion infections of the femur with plate fixation, I recommend removal of the plate and eventual stabilization with an intramedullary rod.
Figure 133.16. A: Anteroposterior radiograph of the distal tibia and fibula showing a comminuted fracture of the tibia and plafond. B,C: Anteroposterior and lateral films taken following open reduction and internal fixation show fractures nonunited at the time of infection. D: Anterior photograph of the ankle shows exposed metal and ankle joint with a necrotic anterior tibialis tendon after an acute postoperative infection. E: There is no evidence of infection 9 months following removal of metal and a free-vascularized latissimus dorsi muscle transfer.
In femoral infections with intramedullary rods, an exchange rodding is preferred. If an extensive intramedullary
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abscess with cellulitis is present, it may be necessary to insert antibiotic beads into the medullary canal, treat the patient in traction for several days, and then redebride the femur and stabilize the fracture with an intramedullary locked nail. I prefer intramedullary nail stabilization over external fixation in most cases because of the propensity for pin loosening, infections, and binding down of muscles with external fixation.
At the time of debridement, it is important to remove the infected membrane from within the canal by reaming followed by copious pulsatile irrigation. In the case of infected intramedullary nails involving the femoral shaft (unless there is an extensive associated intramedullary abscess), the metal does not adversely affect eradication of the infection, provided the infection has been appropriately treated with surgical debridement and parenteral antibiotics followed by fracture healing with or without autogenous cancellous bone grafting (54).
OSTEOMYELITIS OF THE METATARSAL HEADS AND PHALANGES FOLLOWING PUNCTURE WOUNDS OF THE FOOT
Pseudomonas has been reported to be the most common organism causing infection following nail puncture wounds of the foot. The treatment that produces the best results consists of surgical drainage, debridement, and curettage of the puncture wound in the bone, and debridement of all necrotic bone, along with specific antibiotic therapy. The antibiotic of choice for Pseudomonas infections is generally tobramycin, in combination with either piperacillin or a third-generation cephalosporin, depending on the sensitivity reports. Continue systemic antibodies for approximately 3 weeks (Fig. 133.17, Fig. 133.18).
Figure 133.17. The plantar aspect of the foot of a 5-year-old child has swelling, erythema, and abscess formation following a nail puncture wound to proximal phalanx of the second toe.
Figure 133.18. Anteroposterior radiograph of a 6-year-old child shows osteomyelitic changes of the proximal metaphysis with involvement of the first metatarsal phalangeal joint.
In most cases, use a plantar approach. A dorsal incision can be used when there is joint involvement, provided that debridement of the plantar surface of the metatarsal head or proximal phalanx is accomplished.
Plantar or Hoffman Approach
  • Make a plantar transverse incision distal to the weight-bearing area of the metatarsal heads but proximal to the web space of the toes. Carry the incision down through the subcutaneous tissues and identify the flexor tendons, which should be retracted to expose the involved metatarsal head.
  • Incise the periosteum and elevate it to expose the proximal metatarsal; generally, the periosteum has been destroyed and this latter step is not necessary.
  • Identify the area of osteomyelitis, and curet and debride the lytic infected bone. If there has been extensive destruction of the metatarsal head, the head can be excised through this approach.
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Dorsal Incision
  • Make a longitudinal incision over the affected joint. Retract the extensor tendons. Identify the joint capsule and incise it longitudinally. Debride the joint of any necrotic tissue.
  • Next, free the soft tissue from the plantar surface of the metatarsal, debride any necrotic bone and tissue, and curet the puncture site.
  • Finally, irrigate the wound with copious amounts of irrigating fluid, and leave a small Betadine gauze or wick in the wound.
OSTEOMYELITIS OF THE METATARSAL
The metatarsals are most likely to be infected in diabetic patients or persons who have open fractures. Depending on the extent of the infection, local debridement of all soft tissue and bone may be satisfactory. In more extensive infections in which the entire metatarsal is necrotic, it may be necessary to remove it.
  • Make a longitudinal incision over the involved bone extending from just distal to the distal row of tarsal bones to the middle of the proximal phalanx of the involved toe.
  • Identify the extensor tendons and retract them.
  • Identify the involved metatarsal, incise the periosteum longitudinally, and strip it and all soft tissues from the bone.
  • Resect the entire shaft or part of the shaft as indicated. In children, avoid injury to the physis.
  • Irrigate the wound with copious amounts of irrigating fluid. Pack the wound loosely with a Betadine gauge or a fine-mesh gauze and leave a wick protruding from the wound. When the infection is more localized, use a smaller longitudinal incision over the involved metatarsal.
  • Apply a below-the-knee splint and dress the wound.
OSTEOMYELITIS OF THE CALCANEUS
Osteomyelitis of the calcaneus can be extremely difficult to eradicate and requires adequate, thorough debridement. In early involvement, extensive local debridement and curettage are usually sufficient. With extensive involvement of the calcaneus, resection of the diseased area is necessary to eradicate or control the infection. Osteomyelitis occurring either medially or laterally in the calcaneus usually follows pin-track infections, gunshot wounds, or open fractures.
Medial and lateral approaches to the calcaneus are useful in draining a localized abscess, curetting the infected bone tissue, doing a local resection, and windowing the bone cortex for an osteomyelitic abscess.
In osteomyelitis involving the plantar surface of the calcaneus, use the approach described by Gaenslen (15), with modifications. Gaenslen divided the calcaneus with an osteotome from posterior to anterior, thereby exposing the inside of the bone. He used this technique primarily to treat hematogenous osteomyelitis.
The technique has a very serious drawback, however, in that it creates a fracture, which could cause an infection to continue, leading to extensive bone loss. Therefore, avoid splitting the calcaneus when you plan to preserve it. Excision of the calcaneus through this approach, especially when there is a wound or fistula on the weight-bearing surface of the heel, works well.
  • With the patient prone, make a longitudinal incision centered in the midline of the heel. Start the incision just inferior to the insertion of the Achilles tendon on the tuberosity, and extend it plantarward approximately to the level of the base of the fifth metatarsal.
  • Incise the plantar aponeurosis in a plane between the abductor digiti quinti and flexor digitorum brevis muscles. Visualize the lateral plantar artery and nerve in the distal aspect of the wound and retract them medially.
  • Expose the quadratus plantar muscle and split both it and the long plantar ligament longitudinally. The plantar surface of the calcaneus is now exposed. For localized infection use a curet to remove sequestra, infected tissue, and sinuses. For more extensive involvement use an osteotome to resect the involved bone parallel to the plantar surface of the foot (Fig. 133.19). After debridement and copious irrigation, place a Betadine-soaked gauze dressing in the wound and leave the wound open.
    Figure 133.19. Lateral radiograph of a 42-year-old man demonstrates extensive destruction of the calcaneus by osteomyelitis. A marking pen outlines the area of bones to be resected.
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  • Postoperatively, change dressings daily. Permit weight bearing after the incision has healed.
OSTEOMYELITIS OF THE FIBULA
Depending on the extent of the infection, it is safe to excise the proximal three fourths of the fibula, provided the fibular collateral ligament and the biceps femoris tendons are inserted into the tibia when this area of bone is sacrificed. The distal one fourth should not be excised, because excision would lead to impaired function of the ankle, and deformity. If it is necessary to remove this part, a tibial–talar fusion will be necessary later.
  • Make a longitudinal incision, starting on the posterior border of the fibula from the head of the fibula and extending distalward as needed. This incision can be carried down the entire length of the fibula.
  • Identify the common peroneal nerve in the proximal part of the wound; it crosses under the peroneus longus just distal to its attachment to the lateral surface of the head of the fibula. Identify the fascial plane between the soleus muscle and the peroneal muscles anteriorly, and carry the dissection down to the fibula.
  • Retract the peroneal muscles anteriorly, and expose the fibula by incising the periosteum. Take care not to injure the branches of the deep peroneal nerve, which lie on the deep surfaces of the peroneal muscles at the neck of the fibula and proximal 5 cm of the fibula. Now expose the fibula, and debride or resect the infected area.
  • The distal one fourth of the fibula is subcutaneous and can be easily exposed by a longitudinal incision along the posterior border of the fibula.
  • A Betadine-soaked gauze strip can be loosely placed in the wound.
  • Apply a long posterior molded splint. Dress the wound daily.
OSTEOMYELITIS OF THE PATELLA
  • Expose the patella through a longitudinal skin incision that starts just proximal to the patella and extends distally to the inferior pole. Carry the incision down through the subcutaneous tissue and fascia to the periosteum.
  • Incise the periosteum and elevate it with a periosteal elevator. Curette and debride the involved area of bone.
  • In cases of extensive involvement of the patella, either part or all of the patella can be removed. In cases in which the knee joint is involved, irrigate the knee with 10 L of irrigating fluid. Close the joint capsule over Silastic drainage tubes, which are removed in 48–72 hours.
OSTEOMYELITIS OF THE FEMUR
The predisposing factors leading to osteomyelitis of the femur are very important in its management. For hematogenous osteomyelitis, windowing of the cortex as described in this chapter is the preferred method of treatment.
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Posterolateral Approach
  • Use either a lateral decubitus position or turn the patient slightly to elevate the involved extremity. This approach provides access to the entire femoral shaft.
  • Make an incision from the base of the greater trochanter distally to the lateral femoral condyle, depending on the desired length of exposure. Incise the superficial fascia and the fascia lata along the anterior border of the iliotibial band.
  • Expose the vastus lateralis muscle and retract it anteriorly. Continue along the anterior surface of the lateral intermuscular septum, which attaches to the linea aspera.
  • Expose the periosteum and incise it longitudinally. Then use a periosteal elevator to expose the bone. Debride the area of infected necrotic tissue and bone.
  • In cases of nonunion in which a plate is present and the infection is seen late, remove the plate and apply an external fixation device. Follow with an autogenous cancellous bone-grafting procedure when the infection is controlled.
  • In the middle third of the thigh, take care to identify and ligate the second perforating branch of the profunda femoris artery and vein, which travel transversely from the biceps femoris to the vastus lateralis. Avoid damaging the sciatic nerve and profunda femoris artery and vein by not dividing the long and short heads of the biceps femoris muscle.
OSTEOMYELITIS OF THE ILIUM
Infection involving the ilium can occur on the medial, or inner, cortex and on the lateral, or outer, cortex, or on both. Hematogenous seeding is more common in young persons. In adults, osteomyelitis usually occurs following open fractures, bone-grafting procedures, or, in debilitated patients confined to bed, secondary to pressure sores.
  • Make an incision along the crest of the ilium extending the length of the infected area. Extend the dissection through the subcutaneous tissues to the crest.
  • Incise the periosteum over the top of the crest and subperiosteally strip the muscles from the lateral cortex of the iliac wing. Identify the abscess, if one is present, and the extent of bone involvement. Drain the abscess and debride all necrotic bone. Window the cortex as necessary. Be careful of the lateral femoral cutaneous nerve, which normally lies just medial to the anterior superior iliac spine. Perform local resection of the ilium for extensive local involvement, especially in chronic osteomyelitis (Fig. 133.20).
    Figure 133.20. A: Anteroposterior view of the ilium and hip showing a sinogram tract down to the ilium. This 44-year-old woman developed chronic osteomyelitis of the ilium following an open fracture. She had undergone multiple previous procedures. B: Radiograph after local resection of the ilium.
OSTEOMYELITIS OF THE ISCHIUM AND PUBIS
Osteomyelitis involving the ischial tuberosity is usually encountered in paraplegics or patients who are bedridden
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and develop pressure sores with secondary infection, necrosis, and osteomyelitis. In these infections, it is necessary to debride all necrotic tissue, after which the infected ischial tuberosity can be resected with an osteotome and mallet. Irrigate the wound copiously and leave it open, with Betadine-soaked gauze inserted into it to allow for drainage. In paraplegic patients, soft-tissue transfers are often necessary following infection control.
Abscesses in the ischiorectal fossa or beneath the obturator externus or internus often develop with osteomyelitis of the pubis and ischium.
OSTEOMYELITIS OF THE RADIUS AND ULNA
The ulna and the radius are most likely to become infected after open reduction and plating of fractures.
  • Because the posterior surface of the ulna lies subcutaneously essentially throughout its length, expose the ulna by a skin incision carried down through the fascia and periosteum.
  • Approach the radius in its distal third by the anterior approach, as described by Henry (24). Expose the proximal fourth of the radius with an anterior Henry incision or an extended Thompson approach.
  • The middle two thirds of the radius can then be exposed by the Thompson approach (64) (see Chapter 1).
OSTEOMYELITIS OF THE HUMERUS
In adults, osteomyelitis of the humerus most commonly follows internal fixation of the humerus. Often, draining sinuses are present (Fig. 133.21).
Figure 133.21. A sinogram tract down to metal and bone. The patient had persistent drainage for 7 months following open plating of the humerus. Notice that the fracture is healed.
  • After assessing the extent of the infection, expose the humeral shaft through an anterolateral approach (see Chapter 1). Make a skin incision along the anterior border of the deltoid muscle, extending it distally along the lateral border of the biceps muscle to within several inches of the elbow joint. Identify the cephalic vein and ligate it.
  • Retract the deltoid laterally and the biceps medially to expose the proximal shaft. Distal to the deltoid insertion, identify the brachialis and split it longitudinally to the bone, retracting the lateral half laterally and the medial half medially. The radial nerve is protected by the lateral half of the brachialis muscle. In the distal third of the exposure, identify the radial nerve, which lies between the brachioradialis and brachialis muscles, and protect it. Avoid injury to the musculocutaneous nerve.
  • Debride all infected and necrotic bone and soft tissue. If the humerus is unstable, remove the internal fixation and stabalize with external fixation. Leave the wound open.
ILIZAROV PROCEDURE
In osteomyelitis, the Ilizarov procedure has been found to be useful for the treatment of extensive bone loss problems or for angulatory nonunions (44) (Fig. 133.22). A more
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extensive discussion of the Ilizarov technique is presented in Chapter 32.
Figure 133.22. Correction of deformity and subsequent healing process in a 29-year-old man with an infected nonunion of the tibia in marked varus, treated with the Ilizarov technique.
ACKNOWLEDGMENT
I want to thank Dr. Paul Holtom, Associate Professor of Clinical Medicine and Orthopaedic Surgery, section of Infectious Disease, University of Southern California School of Medicine, for his technical assistance in the antibiotic section of this chapter.
REFERENCES
Each reference is categorized according to the following scheme: *, classic article; #, review article; !, basic research article; and +, clinical outcome study.
+ 1. Bach MC, Cocchetto DM. Ceftazidime as Single-agent Therapy for Gram-negative Aerobic Bacillary Osteomyelitis. Antimicrob Agents Chemother 1987;31:1605.
+ 2. Bickel WH, Bateman JG, Johnson WE. Treatment of chronic osteomyelitis by means of saucerization and bone grafting. Surg Gynecol Obstet 1953;96:265.
+ 3. Bowerman SG, Green NE, Mencio GA. Decline of Bone and Joint Infections Attributable to Haemophilus influenzae Type b. Clin Orthop 1997;341:128.
* 4. Bucholz HW, Elson RA, Heinen K. Antibiotic-loaded Acrylic Cement: Current Concepts. Clin Orthop 1984;190:96.
* 5. Bucholz HW, Engelbrecht H. Uber die Depotwirkunk Einiger Antibiotica bei Vermischung mit dem Kunstharz Palacos. Chirurgie 1970;41:511.
# 6. Canale ST, ed. Campbell’s Operative Orthopaedics, 9th ed. St. Louis, MO: CV Mosby, 1998.
+ 7. Cierney G III. Chronic Osteomyelitis—Results of Treatment. In: Green WB, ed. Instr Course Lect 1989;39:495.
* 8. Cierney G III, Mader JT, Penninck JJ. A Clinical Staging System for Adult Osteomyelitis. Contemp Orthop 1985;10:17.
+ 9. Coleman HM, Bateman JE, Dale GM, Starr DE. Cancellous Bone Grafts for Infected Bone Defects. Surg Gynecol Obstet 1946;83:392.
+ 10. Dombrowski ET, Dunn AW. Treatment of Osteomyelitis by Debridement and Closed Wound Irrigation—Suction. Clin Orthop 1965;43:215.
+ 11. Esterhai JL, Goll SR, McCarthy KE, et al. Indium-111 Leukocyte Scintigraphic Detection of Subclinical Osteomyelitis Complicating Delayed and Nonunion of Long Bone Fractures: A Prospective Study. J Orthop Res 1987;5:1.
+ 12. Fitzgerald RH Jr, Ruttle PE, Arnold PG, et al. Local Muscle Flaps in the Treatment of Chronic Osteomyelitis. J Bone Joint Surg Am 1985;67:175.
! 13. Flick AB, Herbert JC, Goodell J, Kristiansen T. Noncommercial Fabrication of Antibiotic-impregnated Polymethylmethacrylate Beads. Clin Orthop 1987;223:282.
+ 14. Freeland AE, Mutz B. Posterior Bone Grafting for Infected Un-united Fractures of the Tibia. J Bone Joint Surg Am 1976;58:653.
+ 15. Gaenslen FJ. Split-heel Approach in Osteomyelitis of the Os Calcis. J Bone Joint Surg 193lw:759.
+ 16. Gentry LO. Treatment of Skin, Skin Structure, Bone, and Joint Infections with Ceftazidime. Am J Med 1985;79(suppl 2A):67.
+ 17. Gentry LO, Rodriguez GG. Oral Ciprofloxacin Compared with Parenteral Antibiotics in the Treatment of Osteomyelitis. Antimicrob Agents Chemother 1990;34:40.
+ 18. Gifford GB, Patzakis MJ, Ivler D, Swezey RL. Septic Arthritis due to Pseudomonas in Heroin Addicts. J Bone Joint Surg Am 1975;57:63l.
+ 19. Green SA, Dlabal TA. The Open Bone Graft for Septic Non-union. Clin Orthop 1983;180:117.
! 20. Greene N, Holtom PD, Warren CA, et al. In Vitro Elution of Tobramycin and Vancomycin Polymethylmethacrylate Beads and Spacers from Simplex and Palacos. Am J Orthop 1998;27:201.
+ 21. Gristina AG, Costerton JW. Bacterial Adherence to Bio-materials and Tissue. J Bone Joint Surg Am 1985;67:264.
+ 22. Gustilo RB, Simpson L, Nixon RA, Indeck W. Analysis of 511 Open Fractures. Clin Orthop 1969;66:148.
+ 23. Harmon PH. A Simplified Surgical Approach to the Posterior Tibia for Bone Grafting and Fibular Transference. J Bone Joint Surg 1945;27:496.
# 24. Henry AK. Exposures of Long Bones and Other Surgical Methods. Brisol, UK: John Wright & Sons, 1927.
+ 25. Henry SL, Ostermann PAW, Seligson D. The Antibiotic Bead Pouch Technique: The Management of Severe Compound Fractures. Clin Orthop 1993;295:54.
+ 26. Higgs SL. The Use of Cancellous Chips in Bone Grafting. J Bone Joint Surg 1946;28:1.
* 27. Hobo T. Zur Pathogeneses der Akuten Haematogene Osteomyelitis, mit Berucksichtigung der Viratfarbungslehre. Acta Sch Med Univ Imper Kioto 1921;4:1.
+ 28. Jacobs RF, McCarthy RE, Elser JM. Pseudomonas Osteochondritis Complicating Puncture Wounds of the Foot in Children. A 10-year Evaluation. J Infect Dis 1989;160:657.
+ 29. Kelly PJ, Wilkowske CJ, Washington JA II. Musculoskeletal Infections due to Serratia marcescens. Clin Orthop 1973;96:76.
* 30. Klemm K. Die Behandlung Chronischer Knocheninfektionen mit Gentamycin-PMMA-Kugeln. Unfallchirurgie 1977;1:20.
+ 31. Klemm K. Indikation und Techhik zur Einlage von Gentamicin- PMMA-Kurgeln bei Knochen- und Wechteilinfekten. Aktuelle Probl Chir Orthop 1979;12.
+ 32. Knight MP, Wood GO. Surgical Obliteration of Bone Cavities Following Traumatic Osteomyelitis. J Bone Joint Surg 1945;27:547.
! 33. Kuechle, D.K, Landon, G.C, Musher, D.M, Noble, P.C. Elution of Vancomycin, Daptomycin, and Amikacin from Acrylic Bone Cement. Clin Orthop 1991;364:302.
P.3559

+ 34. Lexer E. Zur Experimentellen Erzeugung Osteomyelitischer Herdde. Langenbechs Arch Klin Chir 1894;48:181.
+ 35. Lister J. On the Antiseptic Principle in the Practice of Surgery. Br Med J 1867;2:246.
+ 36. Marks KE, Nelson CL, Lautenschlager EP. Antibiotic-impregnated Acrylic Bone Cement. J Bone Joint Surg Am 1976;58:358.
! 37. Marrie TJ, Costerton JW. Mode of Growth of Bacterial Pathogens in Chronic Polymicrobial Human Osteomyelitis. J Clin Microbiol 1985;22:924.
! 38. Merkel K, Brown M, Dewanjee M, Fitzgerald R. Comparison of Indium-labelled-leukocyte Imaging with Sequential Technetium-gallium Scanning in the Diagnosis of Low-grade Musculoskeletal Sepsis. J Bone Joint Surg Am 1985;67:465.
+ 39. Miskew DBW, Lorenz MA, Pearson RL, Pankovich AM. Pseudomonas aeruginosa Bone and Joint Infection in Drug Abusers. J Bone Joint Surg Am 1983;65:829.
! 40. Modic MT, Pflanze W, Freiglin DH, Belhobek G. Magnetic Resonance Imaging of Musculoskeletal Infections. Radiol Clin North Am 1986;24:247.
+ 41. Murray WR. Use of Antibiotic-containing Bone Cement. Clin Orthop 1984;190:89.
+ 42. Nade S. Acute Hematogenous Osteomyelitis in Infancy and Childhood. J Bone Joint Surg Br 1983;65:109.
+ 43. Ostermann PAW, Seligson D, Henry S. Local Antibiotic Therapy for Severe Open Fractures: A Review of 1085 Consecutive Cases. J Bone Joint Surg Br 1995;77:93.
+ 44. Paley D, Catagni M, Arganani F, et al.. Ilizarov Treatment of Tibial Nonunions with Bone Loss. Clin Orthop 1989;241:146.
+ 45. Papineau LJ, Alfageme A, Delcourt JP, Pilon BL. Chronic Osteomyelitis of Long Bones—Resection and Bone Grafting with Delayed Skin Closure. J Bone Joint Surg Br 1976;52:138.
+ 46. Patzakis MJ, Abdollahi K, Sherman R, et al. Treatment of Chronic Osteomyelitis with Muscle Flaps. Orthop Clin North Am 1993;24:505.
+ 47. Patzakis MJ, Dorr DL, Iver D, et al. The Early Management of Open Joint Injuries. J Bone Joint Surg Am 1974;57:1065.
* 48. Patzakis MJ, Harvey JP Jr, Ivler D. The Role of Antibiotics in the Management of Open Fractures. J Bone Joint Surg Am 1974;56:532.
+ 49. Patzakis MJ, Watkins R, Harvey JP Jr. Posterolateral Bone Grafting for Infected Non-unions of the Tibia. In: Moore TM, ed. American Academy of Orthopaedic Surgeons Symposium on Trauma to the Leg and Its Sequelae. St. Louis, MO: CV Mosby, 1981:235.
+ 50. Patzakis MJ, Wilkins J, Brien WW, Carter VS. Wound Site as a Predictor of Complications Following Deep Nail Punctures to the Foot. West J Med 1989;150:545.
+ 51. Patzakis MJ, Wilkins J, Kumar J, et al. Comparison of the Results of Bacterial Cultures from Multiple Sites in Chronic Osteomyelitis of Long Bones. J Bone Joint Surg Am 1994;76:664.
+ 52. Patzakis MJ, Wilkins J, Moore TM. Considerations in Reducing the Infection Rate in Open Tibial Fractures. Clin Orthop 1983;178:36.
+ 53. Patzakis MJ, Wilkins J, Moore TM. Use of Antibiotics in Open Tibial Fractures. Clin Orthop 1983;178:31.
+ 54. Patzakis MJ, Wilkins J, Wiss D. Infection Following Intra-medullary Nailing of Long Bones. Clin Orthop 1986;212:182.
# 55. Perez-Stable EJ, Hopewell PC. Current Tuberculosis Treatment Regimens: Choosing the Right One for Your Patient. Clin Chest Med 1989;10:323.
+ 56. Perry CR, Pearson RL, Miller GA. Accuracy of Cultures of Material from Swabbing of the Superficial Aspect of the Wound and Needle Biopsy in the Preoperative Assessment of Osteomyelitis. J Bone Joint Surg Am 1991;73:745.
+ 57. Rhinelander FW. Minimal Internal Fixation of Tibial Fractures. Clin Orthop 1975;107:188.
+ 58. Rissing JP. Antimicrobial Therapy for Chronic Osteomyelitis in Adults: Role of the Quinolones. Clin Infect Dis 1997;25:1327.
+ 59. Roy-Camille R, Reignier B, Saillant G, Berteaux D. Resultants de l’Operation de Papineau. Rev Chir Orthop 1976;62:347.
+ 60. Roy-Camille R, Reignier B, Saillant G, Berteaux D. Technique et Histoire Naturelle de l’Intervention de Papineau. Rev Chir Orthop 1976;62:337.
+ 61. Sapico FL, Montgomerie JZ. Vertebral Osteomyelitis in Intravenous Drug Abusers: Report of Three Cases and Review of the Literature. Rev Infect Dis 1980;2:196.
+ 62. Schmidt J, Hackenbroch MH, Kumm D, Taravati V. Is Instillation Drainage for the Treatment of Infected Joints, Bones and Soft Tissues Still up to Date? Arch Orthop Trauma Surg 1996;115:149.
+ 63. Seabold JE, Nepola JV, Conrad GR, et al. Detection of Osteomyelitis at Fracture Nonunion Sites. Comparison of Two Scintigraphic Methods. Am J Roentgenol 1989;152:1021.
* 64. Thompson JE. Anatomical Methods of Approach in Operations on the Long Bones of the Extremities. Ann Surg 1918;68:309.
* 65. Trueta J. The Three Types of Acute Hematogenous Osteomyelitis: A Clinical and Vascular Study. J Bone Joint Surg Br 1959;41:671.
! 66. Wahlig H, Dingledein E. Antibiotics and Bone Cements. Experimental and Clinical Long-term Observations. Acta Orthop Scand 1980;51:49.
* 67. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: A Review of Clinical Features, Therapeutic Considerations and Unusual Aspects. N Engl J Med 1970;282:198, 316.
! 68. Wallenkamp G. Small PMMA Beads Improve Gentamicin Release. Acta Orthop Scand 1989;60:668.
! 69. Wallenkamp GHIM, Vree TB, Van Rens TJG. Gentamicin-PMMA Beads. Pharmokinetics and Nephrotoxicological Study. Clin Orthop 1986;205:171.
+ 70. Weiland AJ, Moore JR, Daniel RK. The Efficacy of Free Tissue Transfer in the Treatment of Osteomyelitis. J Bone Joint Surg Am 1984;66:181.