Osteomyelitis in Long Bones
المؤلف:
Longo, D., Fauci, A. S., Kasper, D. L., Hauser, S., Jameson, J. L., Loscalzo, J., Holland, S. M., & Langford, C. A.
المصدر:
Harrisons Principles of Internal Medicine (2025)
الجزء والصفحة:
22e , p1063-1064
2025-08-27
294
PATHOGENESIS
Osteomyelitis in long bones is a consequence of hematogenous seeding, exogenous contamination during trauma (open fracture), or perioperative contamination during surgery involving bone. Hematogenous infection in long bones typically occurs in children. In adults, the leading pathogenic source is exogenous fracture-related infection, mainly associated with internal fixation devices. For classification, the presence of a sequestrum and the status of the surrounding soft tissue are crucial for the decision as to whether a surgical intervention is required. Chronic osteomyelitis can be reactivated after a symptom free interval of >70 years. Such recurrences are most common among elderly patients who developed S. aureus osteomyelitis in the preantibiotic era.
EPIDEMIOLOGY
In adults, most cases of long-bone osteomyelitis are posttraumatic or postsurgical; less frequently, late recurrence arises from hematogenous infections during childhood. For postoperative or postsurgical osteomyelitis, the term “facture-related infection” was generated. The risk of infection depends on the type of fracture. After closed fracture, implant-associated infection occurs in fewer than 1% of patients. In contrast, after open fracture, the risk of osteomyelitis ranges from ~2% up to 30%, with the precise figure depending on the degree of tissue damage during trauma and the time between injury and admission to a specialized center.
MICROBIOLOGY
The spectrum of microorganisms causing hematogenous long-bone osteomyelitis does not differ from that in vertebral osteomyelitis. S. aureus is most commonly isolated in each type of osteomyelitis. In rare cases, mycobacteria or fungal agents such as Cryptococcus species, Sporothrix schenckii, Blastomyces dermatitidis, or Coccidioides species are found in patients who live or have traveled in endemic regions. Impaired cellular immunity (e.g., in HIV infection or after transplantation) predisposes to these etiologies. Coagulase-negative staphylococci are the second most common etiologic agents (after S. aureus) in implant-associated osteomyelitis. After open fracture, contiguous long-bone osteomyelitis is typically caused by gram-negative bacilli or a polymicrobial mixture of organisms.
CLINICAL MANIFESTATIONS
The leading symptoms in adults with primary or recurrent hematogenous long-bone osteomyelitis are pain and low-grade fever. Infection occasionally manifests as clinical sepsis and local signs of inflammation (erythema and swelling). After internal fixation, osteomyelitis can be classified as early (acute; <3 weeks), delayed (3–10 weeks), or late (chronic) infection. Early/acute long-bone osteomyelitis manifests as signs of surgical site infection, such as erythema and impaired wound healing. Acute implant-associated infection may also follow hematogenous seeding at any time after implantation of a device. Typical symptoms are new-onset pain and signs of sepsis. Delayed or late (chronic) infections are usually caused by low-virulence microorganisms or occur after ineffective treatment of early-onset infection. Patients may present with persisting pain, subtle local signs of inflammation, intermittent discharge of pus, or fluctuating erythema over the scar (Fig. 1). A special form of subacute osteomyelitis is Brodie’s abscess, which is characterized by pain (98%) and swelling (53%), mainly in the tibia or the femur. Fever and inflammatory markers are typical. The median delay from symptoms to diagnosis is 3 months. Thus, a young patient with unclear localized pain in the tibia or femur should be worked-up with an imaging modality (plain x-ray, MRI, or CT).
Fig1. A 42-year-old man who had sustained a malleolar fracture 6 weeks previously had persistent pain and slight inflammation after orthopedic repair. His infection was treated with oral antibiotics without debridement surgery. This insufficient management of an implant-associated Staphylococcus aureus infection was complicated by a sinus tract.
DIAGNOSIS
The diagnostic workup for acute hematogenous long-bone osteomyelitis is similar to that for vertebral osteomyelitis. Bone remodeling and thus marker uptake are increased for at least 1 year after surgery. Therefore, the three-phase bone scan is not useful during this interval. However, in late recurrences it allows rapid diagnosis at low cost. If the results are positive, CT is required to estimate the extent of inflamed tissue and detect bone necrosis (sequesters). Implant-associated infection should be suspected if CRP values do not return to the normal range or rise after an initial decrease. Clinical and laboratory suspicion should prompt surgical exploration and sampling.
In osteomyelitis of >1 year’s duration, single-photon emission CT plus conventional CT (SPECT/CT) is a good option, either with 99mTc methylene diphosphonate (99mTc-MDP)–labeled leukocytes or with labeled monoclonal antibodies to granulocytes. Surgical debridement is needed for diagnostic (biopsy culture, histology) and therapeutic reasons.
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