Lymphadenopathy of regional lymph nodes caused by the presence of silicone carried from tributary organs.

Silicone consists of polymers of dimethylsiloxane. When repeating units are polymerized, a whole range of synthetic substances with chains of varying length is created; short chains produce liquid silicone, longer chains form gels, and cross-linking of chains results in silicone rubber or elastomer (1). Because silicone is not biodegradable and elicits little or no reaction from human tissues, it is widely utilized in the manufacture of implants for reconstructive, cosmetic, and orthopedic surgery (2,3). The most frequent applications of silicone are in mammoplasty and joint prostheses (Fig. 51.1). Originally, in cosmetic breast augmentation and breast reconstruction after mastectomy, liquid silicone (dimethicone) was injected directly into the breast. This technique was abandoned because the silicone tended to migrate as a result of gravity and absorption, so that disfiguring complications developed (4). In experiments performed in mice, low-molecular-weight silicones from breast implants that were injected subcutaneously disseminated to virtually all tissues and organs (5). The regional lymph nodes in particular receive silicone carried from tributary organs, and silicone lymphadenopathy was first reported in 1978 (3,6,7,8,9). Once outside the implant, silicone is able to migrate to distant sites via lymphatic channels and blood vessels. Silicone from breast implants has been reported in the upper extremity, groin, liver, synovium, and pleura (9,10,11,12). To prevent this from happening, silicone was mixed with various fatty acids, with the intention of inducing fibrosis around the injected fluid. However, fatty substances induce foreign-body giant cell reactions and scarring. Another substance used in the past to coat breast implants was polyurethane foam, which is deposited as triangular solid particles among reacting foreign-body giant cells (9,12,13). Best tolerated are the presently used silicone bags containing silicone gels or saline solutions. However, these may occasionally rupture, leak, or simply release microscopic particles through “bleeding” from the surface of the implant. Such particles, when carried to regional lymph nodes, may induce silicone lymphadenopathy even in the absence of frank implant rupture (3,8,9,14,15).

Enlarged axillary lymph nodes may be clinically indistinguishable from metastatic breast cancer (Fig. 51.2). On occasion, even internal mammary lymph nodes, which are relatively inaccessible to biopsy, may be affected by silicone migration (16). Therefore, the axilla of a patient with a silicone gel implant must be monitored routinely, particularly after a mammary tumor has been excised, and lymph node biopsy performed when necessary (17). Evidently, the presence of a silicone or another foreign-body lymphadenopathy does not preclude the coexistence of neoplasia in the same lymph nodes. Lymphoma in axillary nodes with silicone lymphadenopathy has been reported, as has metastatic prostatic adenocarcinoma in pelvic lymph nodes with foreign body histiocytosis as a reaction to total joint arthroplasty (18,19,20). When corrective silicone prostheses are placed in the small joints of fingers, hands, and feet deformed by rheumatoid arthritis, silicone is ultimately carried to the regional lymph nodes. Silicone lymphadenopathy has been reported in patients with metacarpophalangeal, metatarsophalangeal, and temporomandibular joint implants (21,22,23,24,25). The incidence of silicone lymphadenopathy in patients with joint prostheses has been estimated to be as low as 1.8% (22) and as high as 13% (23). In general, unilateral lymphadenopathies in persons with mammary or joint prostheses, even when they develop years after implantation of the device, must be evaluated (21,24).