Metallosis is the result of soft tissue, synovium, and bone infiltration by metal debris that is shed from the prosthesis. Typically, this is caused by mechanically induced abrasion between metal and polyethylene components [56]. The resulting inflammatory reaction can lead to recurrent knee pain and effusion and potentially cause severe osteolysis, implant loosening, and arthroplasty failure. There are multiple causes of metallosis, with the most common being with metal-backed polyethylene patellar components where high stress forces on the small surface lead to increased creep and particle formation [57, 58]. Other reported causes include abrasive two-body wear from modified implants as well as joint instability leading to continuous focal impingement [56, 59].

Diagnostic workup for metallosis includes an analysis of inflammatory markers to rule out an underlying infection. Joint aspiration should have negative cultures, with a low leukocyte count and PMN percentage, but may be black-tinged with visible metallic particles (Fig. 25.4) [60]. Radiographs may show several distinct findings from the deposition of the metal debris in the soft tissue (Figs. 25.5 and 25.6). The “bubble sign” is a distinct curvilinear radiodensity resulting from metal outlining the joint capsule. The “cloud sign” is more fluffy and amorphous and represents general metal deposition. The “metal-line sign” is a thin rim of linear increased density normally seen in the suprapatellar region [61]. During revision surgery, the joint synovium may have visible metal deposits (Fig. 25.7), and soft tissue histology may show infiltration by giant cells, histiocytes, and black metal particles (Fig. 25.8) [56, 60–62].

Like metallosis, metal hypersensitivity is the result of a physiologic reaction to metal debris from the prosthesis. However, it manifests as a type IV delayed hypersensitivity allergy with lymphocyte activation and cytokine release mediated by the immune system [63]. Metal hypersensitivity can lead to knee pain, effusion, stiffness, and more uniquely also to localized or diffuse dermatitis, eczema, and hair loss [64, 65]. The underlying cause of metal hypersensitivity has not been well established, and a history of cutaneous metal allergy is not strongly correlated with an increased rate of revision arthroplasty; however, some authors advocate preoperative testing for patients with a history of cutaneous metal allergy [63, 66, 67].

Metal hypersensitivity will result in negative infectious markers and an aseptic joint aspiration. Radiographs may not necessarily show any significant osseous or soft tissue changes, unless osteolysis is severe and thus visible on radiographic imaging (Figs. 25.9 and 25.10). The two most commonly used diagnostic tests for metal hypersensitivity are skin patch testing and lymphocyte transformation testing. However, both of these tests have shortcomings: skin patch testing is subjective and may not correlate to deep reactivity around artificial implants, while lymphocyte transformation testing is not readily available and may not correlate with patch test results [68]. Because there is not a definitive diagnostic test available, metal hypersensitivity is currently a diagnosis of exclusion.

In cases of severe metallosis or hypersensitivity, treatment may include revision total knee arthroplasty and complete synovectomy. During revision, one indication of hypersensitivity is significant synovial hypertrophy (Figs. 25.11 and 25.12). A thorough and extensive debridement should be performed, especially for metallosis, to remove any particles that could lead to abrasive third-body wear and continued synovitis. Revision components composed of oxidized zirconium, ceramic, or titanium that limit the amount of cobalt-chrome should preferentially be used, both to limit the rate of metal wear and to lower the amount of metal ion allergens [61, 64, 69]. Continued clinical follow-up for these patients is required to ensure that the revision TKA components do not deteriorate or cause an allergic response.

Gout attacks can occur after total knee arthroplasty and cause acute pain and effusion similar to that seen in a native knee. It is important to distinguish between gout arthropathy and infection, especially because gout can present with constitutional symptoms such as fevers, chills, and generalized malaise [70, 71]. Gout arthritis results from abnormal purine metabolism with increased uric acid production and monosodium urate crystal deposition in the synovium and soft tissue. This pathologic process can still occur after total knee arthroplasty and cause significant problems.

Diagnosis of gout involves analyzing multiple markers; however, not all are specific and sensitive to gout. For instance, CRP and ESR levels may be abnormally high and not be helpful in ruling out infection [70, 72]. Elevated serum uric acid levels only suggest, and do not confirm, a gout attack [72]. Joint aspiration may yield leukocyte counts from 2000 to 20,000, which is well within or higher than the range seen in periprosthetic joint infections [73, 74]. Fluid analysis under microscopy normally shows negatively birefringent urate crystals, and this likely is the most important criteria for the diagnosis of gout arthropathy [70, 71]. However, there are cases of gout attacks without crystals seen in the joint aspiration [74].

Pseudogout is another type of crystalline arthropathy resulting from calcium pyrophosphate dihydrate deposition that can manifest after total knee arthroplasty, both in the acute postoperative period and many years after a successful TKA [75–78]. As with gout, pseudogout may present with symptoms of fever, swelling, and joint pain similar to that seen with periprosthetic joint infections [78]. CRP and ESR levels may be elevated, and joint aspiration may yield an elevated white blood cell (WBC) count [75, 77, 78]. Fluid analysis normally shows positively birefringent calcium crystals which aid in the diagnosis [77, 78].

With both types of crystalline arthropathy, accurate diagnosis is essential, mainly to exclude periprosthetic joint infection as the source of the symptoms. Joint aspiration with fluid analysis showing crystals normally is diagnostic and can help limit the rate of unnecessary invasive treatment [73]. Treatment of crystalline arthropathy after total knee arthroplasty can be managed medically until symptoms resolve; however, with extensive bone loss and implant loosening, a revision TKA surgery may still be required [70].

Rheumatoid arthritis is an autoimmune disorder resulting in an inflammatory cascade that can affect knee joint synovium, capsule, ligaments, and bone. Medical treatment utilizing disease-modifying antirheumatic drugs has been adopted as the mainstay of treatment and tremendously decreased the need for early surgery, but those with severe, uncontrolled disease may still require total joint arthroplasty [79]. After surgery, patients can present with recurrent rheumatoid synovitis and present with knee pain, effusion, and stiffness.

Ruling out a periprosthetic infection is critically important when evaluating the swollen knee in the rheumatoid patient. Multiple studies have shown an increased rate of infection after total knee arthroplasty for treatment of rheumatoid arthritic patients as compared to osteoarthritis patients [80–83]. This may be due to several factors including soft tissue and wound concerns due to chronic synovitis as well as attenuation of the immune system from medications such as corticosteroids [84]. Interestingly, the use of biologic and nonbiologic medications is not as well established, with some studies showing only limited correlation with infection after orthopaedic procedures and others suggesting an increased rate of periprosthetic joint infections [81, 85–87]. Serum analysis may show an elevated ESR and CRP, and joint aspiration can have elevated leukocyte counts from 5000 to 25,000 [88]. However, as opposed to infection, joint fluid aspiration will not be grossly purulent, and joint fluid cultures will be negative [88].

Other inflammatory arthropathies, such as ankylosing spondylitis and psoriatic arthritis, can present in a comparable fashion to that of rheumatoid arthritis [89]. In general, diagnosis is similar with an emphasis on ruling out periprosthetic joint infection. Patients who are on disease-modifying drugs or have soft tissue concerns must be carefully examined [89]. Revision knee arthroplasty for any patient with an inflammatory arthropathy is difficult, and a higher rate of complications must be anticipated [90].

Spontaneous, atraumatic hemarthrosis after total knee arthroplasty is uncommon with a reported incidence from 0.5 to 1.6% [91, 92]. The cause of hemarthrosis is still debated, with several authors suggesting entrapped synovium and soft tissue between articulating surfaces leading to recurrent bleeding [91, 93]. Other factors that have been identified include pseudoaneurysms, pigmented and nonpigmented villonodular synovitis, hemophilia, and chronic anticoagulation [94–98]. Diagnosis of hemarthrosis includes inflammatory markers and aspiration to rule out periprosthetic joint infection, blood profile and coagulation panel to evaluate the clotting cascade, and angiography or ultrasound to evaluate the vasculature. Anticoagulation medications should be stopped and conservative treatment with immobilization started. Operative treatments include embolization and arthroscopic or open synovectomy [99].

There are multiple causes of recurrent aseptic synovitis after total knee arthroplasty. Diagnostic options for evaluation include radiographs, laboratory studies, and joint aspiration. Imaging may show polyethylene wear, metal wear, and bone osteolysis but also may be normal. Laboratory blood studies should include WBC, ESR, and CRP, as well as other specific markers such as uric acid and metal ion levels. Joint aspiration with a leukocyte count, polymorphonuclear cell percentage, and cultures should always be performed. In addition, aspirate analysis may reveal crystals, metallic debris, or hematoma. Critically, a high degree of suspicion must be held for periprosthetic joint infection as the cause of synovitis, especially because low-grade infections may closely resemble many of the aseptic pathologies. Treatment options for aseptic synovitis will differ based on the underlying etiology. Medical management is the mainstay for some causes, such as crystalline and inflammatory arthropathy, while severe polyethylene wear or implant metallosis will likely require revision arthroplasty. Aseptic synovitis is a common and potentially detrimental condition after total knee arthroplasty and must be closely evaluated and treated by the orthopaedic surgeon.