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As alluded to earlier, orthopedic infections can be broadly divided into two categories. The first is spontaneous infection, where no orthopedic surgical intervention has occurred, and some combination of factors contributes to the infection. This encompasses pediatric and adult osteomyelitis, as well as spontaneous soft-tissue infections. The second broad category is that of postoperative or posttraumatic infections. These occur when the soft-tissue envelope has been breached either deliberately (postoperative infections) or traumatically. In modern trauma care, infection can often be attributed to both, as after surgical stabilization of open fractures.
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Pediatric Osteomyelitis
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Spontaneous osteomyelitis is a common entity in children. It may occur at any time from birth to adulthood, but generally possesses a decreasing incidence into adolescence, after which it is possible but becomes much rarer (see Clinical Corollary #1). The pathogenesis of pediatric osteomyelitis is thought to be due to the watershed nature of the metaphyseal vascularity, with a low-flow, centripetal system of vascularity. This allows normally encountered blood pathogens a microenvironment in which they may multiply isolated from most circulating lymphocytes, thereby evading initial immune surveillance. The most common pathogen is Staphylococcus aureus, followed by group A Streptococcus and Haemophilus influenzae. Patients suffering from sickle cell anemia have an unusual propensity for Salmonella infections.
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Upon multiplication, bacteria produce matrix metalloproteinases, which degrade the surrounding cancellous bone and allow abscess formation. The abscess further disrupts an already poor blood supply and shields bacteria from the immune response. This devascularization causes osteonecrosis and formation of a sequestrum, which is a radiographic hallmark of osteomyelitis. This sequestrum is seen as an area of hyperdense, necrotic bone surrounded by lysis on plain radiographs. The rate of progression depends on how robustly the host can respond to the infection. If the host is able to mount a response and surround the sequestrum, it will be encapsulated by a rim of living, immunocompetent bone called an involucrum. If, on the other hand, the infection spreads with enough vigor that the host bone cannot contain it, bacteria will continue to multiply. The abscess will enlarge and eventually destroy the surrounding cortex. This will cause a purulent response that will produce a very aggressive radiographic appearance, mimicking Ewing sarcoma (see Clinical Corollary #1). The purulent material will raise the surrounding periosteum, create a Codman triangle, and produce a permeative appearance in the subjacent cortex, and may even form a soft-tissue mass.
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Clinically, children with acute osteomyelitis typically appear ill. Many, if not most, will have a febrile response greater than 38.5°C. Nearly all will complain of localized pain and swelling and, in lower extremity cases, will present with an inability or unwillingness to ambulate. If the area of infection occurs beneath the adjacent joint capsule, an acute septic joint may occur with substantial pain, resistance to motion, and effusion. Radiographs may demonstrate the features described earlier and, in the case of joint sepsis, will have evidence of effusion. Laboratory analysis generally demonstrates leukocytosis with a left shift to greater than 70% neutrophils. Erythrocyte sedimentation rates (ESRs) will be elevated, as will C-reactive protein (CRP) levels. Laboratory results are especially important in the differential diagnosis of pediatric osteomyelitis because radiographs can easily be confused with pediatric sarcomas, especially Ewing sarcoma.
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Clinical Corollary #1
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Patient 1 is a healthy 15-year-old male student athlete who noted the onset of pain, swelling, and cramping in his left thigh 1 month before presentation. He denied any trauma. These symptoms gradually worsened to the point of his being unable to attend school. He also developed fevers, chills, night sweats, and malaise. Radiographs and a magnetic resonance imaging (MRI) scan were obtained by a community physician, and he was subsequently referred to a tertiary medical center.
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X-rays were essentially normal (Figures 7–1, 7–2, 7–3, 7–4, and 7–5), but MRI scan revealed extensive bone marrow infiltration and a large soft-tissue mass involving nearly the entire circumference of the femur (Figures 7–6, 7–7, 7–8, 7–9, and 7–10). The differential diagnosis at this point included bone neoplasm versus infection. The patient was sent for a computed tomography (CT) scan–guided biopsy. The CT scan suggested intramedullary abscess formation and showed air within the soft tissues (Figure 7–11). Laboratory evaluation showed a white blood cell count of 14.0 × 103 cells/mL with 79.4% neutrophils. ESR and CRP were 114 mm/h and 22.31 mg/dL, respectively, consistent with infection. Biopsy revealed acute inflammatory cells and bacteria, further substantiating the diagnosis.
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The patient was taken to the operating room where a lateral approach to the femur was made. Copious amounts of purulent material were encountered, and the soft tissues were extensively irrigated and debrided. A 4-cm × 2-cm ovoid hole was made in the lateral cortex of the femur, and flexible reamers were passed into the proximal and distal femur. Antibiotic beads containing 1 g of tobramycin and 3 g of vancomycin per 40 g of polymethylmethacrylate (PMMA) were placed in the intramedullary canal (Figures 7–12, 7–13, 7–14, and 7–15). Operative cultures from the purulent material, soft tissue, and bone reamings were all positive for methicillin-sensitive S. aureus, and the patient was placed on intravenous therapy with continuous-infusion oxacillin for 6 weeks under the supervision of a musculoskeletal infectious disease consultant.
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Subsequent to the completion of systemic antibiotic therapy, he was taken back to the operating room for removal of the antibiotic beads, irrigation, and repeat intraoperative cultures of the bone and soft tissues. These cultures were all negative. At the most recent follow-up, his knee motion was normal. The laboratory parameters had normalized with an ESR of 3 mm/h and a CRP of less than 0.1 mg/dL.
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Adult osteomyelitis is fortunately rare. As the growing child reaches skeletal maturity, the metaphyseal bone vascularity changes, and the pediatric venous sinusoids are eliminated. This produces improved blood flow, decreasing the prevalence of spontaneous osteomyelitis. Most cases of adult osteomyelitis are therefore a result of skin penetration, either deliberate or accidental. A few cases merit special mention.
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Aside from accidental or surgical trauma, most cases of adult osteomyelitis occur in individuals who are unable to maintain a normal soft-tissue envelope over subjacent bone. This occurs with disturbing frequency in paraplegics and diabetics, as the normal protective sensation over bony prominences (sacrum, femora, ischial tuberosities, calcanei, and metatarsals) is disrupted. This leads to pressure sores, which, if untreated, will progress to the bone. Once the bone is exposed to air, its vascularity is compromised and osteomyelitis occurs. This form of osteomyelitis is much more chronic than that seen in children, and the symptomatology is quite different. Because many of these individuals are insensate, pain is not a prominent finding. Also, the acute purulent response found in the pediatric case is rarely present, instead manifesting as open, draining sinuses. Infectious indices (ESR/CRP) may demonstrate increased values, but a leukocytosis with left shift is generally absent. Individuals with this condition may persist for years or even decades with osteomyelitis, having no symptoms until developing squamous cell carcinoma (Marjolin ulcer) within the sinus tract.
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The situation is quite different in patients who are immunocompromised. Patients who are suffering from human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS), who have undergone solid organ or bone marrow transplantation, or who are undergoing cytotoxic chemotherapy may develop acute osteomyelitis. The hallmark of this disease is pain without an obvious source, and this symptom may occur anywhere in the involved bone. This condition may also produce spontaneous joint sepsis, most commonly in the sternoclavicular and sacroiliac joints. Immunocompromised individuals with osteomyelitis will present with pain and fever but will lack leukocytosis, as the dysfunctional immunity producing the osteomyelitis precludes an adequate immune response. Infectious indices are rarely useful, as many of these individuals have other causes of inflammation that will confound these nonspecific test parameters. A very high index of suspicion is required to make this diagnosis, as plain radiographs will likely only demonstrate osteopenia and MRI scanning shows only bony edema on T2-weighted sequences. Generally no abscess forms within the bone. In this instance, prompt diagnosis can be critical because patients do not possess the immunologic reserve to fight a fulminant infection.
Collinet-Adler S, Castro CA, Ledonio CG, Bechtold JE, Tsukayama DT:
Acinetobacter baumannii is not associated with osteomyelitis in a rat model: a pilot study.
Clin Orthop Relat Res 2011;469:274.
[PubMed: 3008889]
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Clinical Corollary #2
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Patient 2 is a 33-year-old man with a chief complaint of steadily increasing left thigh pain for 1 month. He denied any trauma or constitutional symptoms. He had a negative medical and surgical history but had a social history of heavy drug abuse. He was initially seen at a community hospital where radiographs suggested a permeative lesion in the lateral cortex of the left femur (Figure 7–16). He was subsequently transferred to a tertiary medical center for further management.
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At the tertiary medical center, he was found to be afebrile with stable vital signs. Laboratory evaluation disclosed a white blood cell count of 12.4 × 109 cells/L with 70.5% neutrophils and a platelet count of 524 × 103 cells/mL. His ESR and CRP were both elevated at 66 mm/h and 1.96 mg/dL, respectively.
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CT scan and MRI scan were obtained. CT scan showed changes in the femur consistent with sequestrum formation, and MRI scan revealed intense soft-tissue edema around the lesion. A presumptive diagnosis of tumor versus infection was made (Figures 7–17, 7–18, 7–19, and 7–20).
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The patient was subsequently taken to the operating room where an open biopsy of the left femur and the surrounding tissues was performed. Pathology on frozen section was consistent with acute infection and the diagnosis of osteomyelitis with soft-tissue involvement was made. The muscle around the femur was thoroughly debrided, and the femur itself was likewise debrided with rongeurs, curettes, and a high-speed burr (Figure 7–21). Cultures from the musculature, periosteum, bone, and intermedullary canal were all obtained. After copious irrigation, a strand of antibiotic beads containing 1 g of tobramycin and 3 g of vancomycin per 40 g of PMMA was made and placed next to the femur (Figure 7–22). The wound was closed in layers. Postoperative radiographs showed obliteration of the abnormal bone (Figure 7–23).
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All operative cultures were positive for methicillin-resistant S. aureus (MRSA). The patient was placed on oral antibiotic therapy with linezolid for 6 weeks with plans to remove his antibiotic beads and perform a repeat irrigation and debridement after the completion of antibiotic therapy.
Hamzaoui A, Salem R, Koubaa M, et al:
Escherichia coli osteomyelitis of the ischium in an adult.
Orthop Traumatol Surg Res 2009;95:636.
[PubMed: 19944663]
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Adult Spontaneous Soft-Tissue Infections
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Soft-tissue infections are common. Admissions to medical services for cellulitis, a common skin infection, are frequent in most hospitals. These conditions may occur in the setting of medical comorbidities, such as venous stasis, diabetes, obesity, or immunocompromise. They are generally treated with antibiotics alone, and rarely is surgical intervention necessary.
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Deep, abscess-producing skin infections in adults are usually the result of skin penetration. This occurs either due to trauma, iatrogenic skin penetration, or intravenous drug use. These causes are sometimes obvious, as in the case of intravenous drug use, but may be difficult to ascertain, as in septic olecranon bursitis. Bursitis is often presumed to be due to trauma, as the extensor surface of the elbow is frequently traumatized. Surgical treatment of simple abscesses with irrigation and drainage as well as wound packing or vacuum-assisted closure generally yields satisfactory results. Occasionally, intravenous drug abusers can present with a mixed picture of both bone and soft-tissue infection (see Clinical Corollary #2).
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Severe, spontaneous, deep soft-tissue infections, those occurring below the fascia, are decidedly rarer, and tend to occur in individuals with some form of immunocompromise. While the often publicized “flesh-eating bacteria” seen in necrotizing fasciitis may infect immunocompetent hosts, those with an immune-compromised comorbidity are at much greater risk. These individuals are generally as follows: patients who are neutropenic secondary to cytotoxic chemotherapy, those suffering from HIV/AIDS, or those with other, frequently autoimmune, diseases that render the normal tissues susceptible to bacteria in the environment. In immunocompromised individuals, the typical signs of infection may be absent, and the patient may simply manifest a high fever (>38.5°C), tenderness, and erythema. Advanced imaging with MRI may demonstrate only edema within the affected area because the patient often does not have adequate immunity to form an abscess. These patients are at great risk, and surgical debridement coupled with broad-spectrum antibiotics may be lifesaving.
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Because of the vascular nature of muscle, pyomyositis in immunocompetent individuals is rare. Etiologically, pyomyositis is different than simple abscess formation; in pyomyositis, the bacteria occlude the small vascular inflow into the muscle, producing necrosis. This avascular bed is an ideal culture medium for bacteria, and liquefactive necrosis occurs. Treatment of pyomyositis is more extensive than many soft-tissue infections because all necrotic material must be thoroughly removed before the infection can be controlled. Serial debridement and adjunctive intravenous antibiotics are the mainstays of treatment, as initial debridement often fails to remove all necrotic material.
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Necrotizing fasciitis is the most dreaded deep soft-tissue infection. Classically caused by Clostridium perfringens, it can become a rapidly progressive, life-threatening event. Necrotizing fasciitis caused by other organisms may not present with as fulminant a course and may more closely mimic cellulitis or other soft-tissue infections. Necrotizing fasciitis is a clinical diagnosis: although MRI may demonstrate T2 enhancement of the fascia, this finding is extremely nonspecific, and the clinician acting on the clinical findings will yield a much more timely diagnosis. Clinically, the patients are quite ill, with fever, malaise, and localized pain. Signs of systemic sepsis may be present, with mental status changes, tachycardia, or even hypotension. Palpation of the affected area demonstrates a swollen, boggy texture to the skin and soft tissues. The skin may also be hypermobile, similar to after a fasciocutaneous injury. Bullous changes may also occur.
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Treatment of necrotizing fasciitis is time dependent. Time should not be wasted obtaining confirmatory diagnostic tests, as these are rarely specific enough to change the clinical diagnosis, and substantial delays may be limb or life threatening. Surgical treatment is extensive and requires debridement of all affected skin and fascia. In fulminant cases, soft-tissue reconstruction is generally required. Debridement to healthy, vascularized skin is mandatory, and debridement of the subjacent muscle may be required. The presence of myonecrosis may make amputation necessary, and the performance of a high amputation such as a hip disarticulation or forequarter amputation may be necessary as a lifesaving measure.