Radiographs in septic arthritis are often normal at presentation. Joint effusion, possibly leading to initial joint space widening, and/or soft tissue swelling may be detectable. Later findings include subchondral bony erosion/destruction that is present on both sides of the joint, uniform joint space narrowing secondary to cartilage damage, reactive bony sclerosis, and juxta-articular osteopenia. The regional osteopenia that develops in septic arthritis occurs as a result of the regional exuberant immune response with high levels of inflammatory cytokines and prostaglandins that act to inhibit regional bone formation and promote absorption. Coincident osteomyelitis is often present, leading to cortical destruction and reactive new bone formation of the periosteum termed “periosteal reaction” (see section entitled “Osteomyelitis”). There can be severe bony disorganization and destruction at this stage with secondary osteoarthritic change. Bony ankylosis can occur. Abscesses can form adjacent to the site of infection (see section “Abscess” below).

Ultrasound can demonstrate a joint effusion, which may not always be present, before it becomes visible on a radiograph. Septic joint effusion is usually complex in appearance with hyperechoic appearance secondary to pus, internal septations, and debris. Occasionally effusions are anechoic. The joint capsule is diffusely thickened. Hyperemia with increased flow on Doppler may be seen within the synovium and capsule. Depending on the joint and accessibility to detailed ultrasound evaluation, other changes may be visible including cartilage destruction demonstrated as loss of the normal convex hypoechoic cartilage contour which may be filled with hyperechoic synovium and complex fluid. Erosions, as focal cortical defects, and periosteal reaction with subperiosteal collection may also be visible. The adjacent soft tissues are also evaluated for associated collections. Assessment of osteomyelitis is limited and is best performed with MRI. Ultrasound can also confirm joint effusion and guide needle placement for joint aspiration.

While the diagnosis of septic arthritis should always be made based on appropriate synovial fluid sampling and culturing techniques, MRI can be a helpful adjunct to diagnosis. Multiple suggestive findings occurring in concert should raise suspicion. The adjacent bone can demonstrate erosions. Erosion is defined as a loss of the normal cortical contour of the bone, seen in two adjacent slices on MRI. The erosion shows loss of the normal cortical hypointensity and the normal trabecular hyperintensity on T1W images. Erosions are caused due to proliferative synovitis leading to pannus formation that invades into the adjacent bone, and thus post-gadolinium images show contrast enhancement within the pannus within the erosion. This pannus can also be seen as abnormal hyperintense signal within the erosion on T2W images due to the high water content in the inflamed tissue. Erosions typically occur first in the “bare area” – the marginal area of the joint near the area of attachment of the capsule that is minimally covered by cartilage and thus relatively unprotected. With continuing inflammation, however, erosions can involve any area of the articular surfaces, and severe bony destruction can occur. Adjacent bone marrow edema is also characteristic, which manifests as hypointensity on T1 and hyperintensity on T2. Synovial thickening and edema can be present, as well as a joint effusion. IV gadolinium can be used as a contrast agent and can differentiate synovium from joint effusion – in early post-gadolinium administration, synovium enhances, while joint effusion will not enhance. Soft tissue edema is present and occasionally soft tissue collections develop.

There are some unique features of tuberculous septic arthritis that can be seen on MRI. Forty percent develop synovial granulomas, which manifest as hypointense lesions on T2-weighted images. Areas of synovial proliferation (termed “pannus”) can be seen, and characteristically in tuberculous arthritis, there are both active (enhancing) and chronic (non-enhancing) pannus, which coexist. Intra-articular bodies, termed “rice bodies,” are related to ischemia of the synovium with subsequent shedding synovium and encasement by fibrin. They are classically seen in tuberculous arthritis but may also be present in entities such as rheumatoid arthritis and SLE. There can also be findings of microabscesses and evidence of osteomyelitis. Synovitis, effusions, and erosive changes are also seen as in other types of septic arthritis. Both central and peripheral erosions are seen.

Bone scan is not commonly used to aid in the diagnosis of septic arthritis as the findings are indistinguishable from other types of arthritis. Classically, there is joint hyperperfusion and hyperemia on early imaging, with increased activity at articular surfaces on delayed imaging. Occasionally a WBC scan is performed in cases where there is a differential diagnosis such as Charcot joint.

CT scanning is not commonly used in the setting of acute septic arthritis. Like plain radiographs, it can be normal in early stages or show only evidence of joint effusion or soft tissue swelling. It may be more sensitive to early findings of joint space widening due to effusion and later changes of erosions or periosteal reaction than radiographs, however. It could be considered when MRI is contraindicated but is generally considered inferior to MRI in septic arthritis.

Like septic arthritis, osteomyelitis can arise due to hematologic spread of infection, direct inoculation from trauma or surgery, or contiguous spread from adjacent structures, such as an infected joint. The vertebral body is the most commonly affected area in adults and the long bones in children. Risk factors for osteomyelitis include diabetes mellitus, particularly with vascular insufficiency, peripheral neuropathy, the presence of decubitus or other chronic ulcers, prosthetic joint material, and a history of trauma. The organisms typically involved depend on the site and mode of transmission. Osteomyelitis secondary to hematogenous seeding is most commonly due to a single bacterium. Staphylococcal species, particularly Staphylococcus aureus, and aerobic gram-negative bacteria are the most common causes, with streptococci and enterococci occurring less frequently. Osteomyelitis secondary to direct inoculation, such as in patients with chronic nonhealing ulcers, is more likely to be polymicrobial.

Osteomyelitis can present either acutely or chronically, and presentation can vary by chronicity and site. Hematogenous osteomyelitis affects the medullary area of bone initially, and the subsequent inflammatory reaction causes increased intramedullary pressure that can rupture through the bony cortex. This can compromise blood flow to the periosteal region, which can lead to necrotic areas that then become separated from the rest of the bone. These sequestrated necrotic areas are characteristic of chronic osteomyelitis and are referred to as “sequestra.” These can be helpful in the identification of osteomyelitis radiologically. Typically a layer of granulation tissue separates the sequestrum from the living bone, and the sequestrum can then become encased in reactive bone (termed “involucrum”). Sinus tracts through the cortical bone to the medulla can also be seen. Abscesses can form, in the subacute to chronic phase of osteomyelitis, particularly within the ends of tubular bones, and may be single or multiple, “Brodie’s abscess.” Due to developmental changes in blood supply and end vessels, the epiphysis is a common location of osteomyelitis in the infant and the metaphysis in the child. Spondylodiscitis is reviewed in detail in Chap.​ 15

Patients with acute osteomyelitis typically present with pain, warmth, and erythema of the affected site. Some sites, such as vertebral, hip, and sacroiliac, usually present with pain. Constitutional symptoms and signs such as fever and malaise may be present. In patients with ulcers, lack of improvement with appropriate wound care should raise the suspicion for underlying osteomyelitis. If an ulcer is larger than 2 × 2 cm in diameter or if bone is exposed, there is a high likelihood of underlying osteomyelitis. In these cases, treatment with antibiotics is often initiated empirically. A draining sinus tract and overlying tissue necrosis are also strong indicators.

Inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein are usually elevated in osteomyelitis but are nonspecific. Blood cultures are only positive in approximately 50 % of patients with acute hematogenous osteomyelitis but should still be performed in all patients. The gold standard for diagnosis of osteomyelitis is bone biopsy, and a positive result for osteomyelitis on bone biopsy has both histopathologic and microbial components. The biopsy should show inflammatory infiltrate within the bone leading to bony resorption and subsequent necrosis on histopathology, and an offending organism should be isolated on microbial cultures. However, bone biopsy may not be feasible in the setting of inaccessible anatomic areas or if there is concern regarding lack of healing in patients with compromised vascularity, and in this case empiric treatment is typically undertaken. Superficial wound cultures are only consistent with bone biopsy results in about 30 % of cases and thus should not be used for diagnosis routinely.

Treatment of osteomyelitis is dependent on several factors, including culture and sensitivity results, chronicity, and amount of devitalized bone and necrotic tissue present, and involves a combination of antibiotic therapy and surgical debridement. Initial antibiotic therapy is typically administered intravenously. Chronic osteomyelitis and/or osteomyelitis associated with cutaneous ulcers in patients with compromised regional vascularity can require more prolonged courses of antibiotics. There is little randomized controlled data in this area to guide therapy. Uncomplicated hematogenous osteomyelitis in children can be treated for as few as 4 days with IV therapy, with transition to oral antibiotics for a period of 4 weeks. Chronic osteomyelitis in adults is typically treated with 2–6 weeks of IV antibiotics initially, then oral antibiotics subsequently to complete a course of 4–8 weeks. More prolonged courses can be required in more complicated infections. Recurrence rates in adults are quoted as being around 30 % at 1 year and even higher (~50 %) for infections with Pseudomonas aeruginosa. Bony debridement is indicated when there is necrotic tissue, and prosthetic material at the site of infection may need to be removed. Adjunctive modalities for treatment of osteomyelitis include hyperbaric oxygen therapy and negative pressure wound therapy with vacuum-assisted devices.