Pelvic inflammatory disease after tubal sterilization: a review

Exceptions ot the common notion that tubal occlusion protects from recurrent pelvic inflammatory disease (PID) do exist. Since 1975, 71 cases of salpingitis and 38 tubo-ovarian abscesses (TOA) in sterilized women have been published. The majority of cases of salpingitis after previous tubal occlusion (SPOT) developed more than a year after either laparoscopic or laparotomy sterilization procedures. For tubo-ovarian abscess after previous tubal occlusion (TOAPOT), this time interval ranged from several weeks to almost two decades. Most cases of salpingitis showed inflammation of both tubal segments. When only one segment was involved, it was generally the proximal segment. The appearance of the TOAPOT at the time of surgery was typical to TOA. The symptoms of salpingitis were not different from symptoms in any other case of PID, and those associated with TOAPOT were typical of TOA. Laboratory findings included leucocytosis and growth of Neisseria gonorrohoea and Chlamydia trachomatis from the cervix, the infected tube, and the peritoneal fluid. Pus cultures obtained from cases of TOAPOT grew mixed or single organisms. Detailed histopathologic studies in tubal specimens after the failure of an occlusion procedure are available from cases with no infection. They have demonstrated distortion, loss of musculature, and loss of lumen configuration, all of which may have been the result of compromised blood supply to the tube. These findings may be extrapolated to cases of SPOT and TOAPOT, assuming similar changes may be present before the development of infection. The mechanisms by which infection may develop in previously occluded tubes are divided into three groups: The first group consists of situations where there is persistence of free passage between the proximal and distal portions of the tube. These include toboperitoneal fistula, spontaneous anastomosis at the occlusion site, recanalization of the occluded site, incomplete tubal occlusion due to a faulty surgical technique or rupture of the weakened tubal wall. The second group consists of infections initiated by the surgical procedure itself, such as introduction of pathogens at surgery, exacerbation of chronic PID, and ascending infection secondary to surgical manipulation. In the third group, the infection is initiated systemically by hematogeneous spread, lymphatic spread, or change in immunologic status.