Pelvic Inflammatory Disease and Tubo-ovarian Abscess

Abstract

Despite an increase in the number of effective broad-spectrum antibiotics, pelvic inflammatory disease (PID) and the complications arising from the disease continue to reach epidemic proportions into the 1990s. Acute salpingitis and PID account for more than 350,000 hospital admissions and 150,000 surgical procedures per year [1]. In addition, some report that nearly one-third of patients hospitalized for PID develop some degree of pelvic abscess [2]. Other sequels such as ectopic pregnancy, salpingitis isthmica nodosa, tubal infertility, chronic pelvic pain syndromes, and pelvic adhesions are other consequences of PID. Tubo-ovarian abscess (TOA) is the most serious manifestation of salpingitis because the intra-abdominal rupture of a TOA is potentially life-threatening, with mortality rates as high as 8.6 % [3]. Pelvic inflammatory disease and subsequent TOA may result whenever bacteria gain access to the upper female genital tract. Under normal circumstances, the Fallopian tubes and related pelvic structures are sterile. However, access of bacteria into the upper genital tract either via sexually transmitted diseases or through instrumentation of the uterus may inoculate the uterus with bacteria from the vagina, causing infection. It has been suggested that passive transport and vectors such as spermatozoa and Trichomonas assist in establishing the ascending infection from the polymicrobial vagina and cervix [4]. Once present in the upper genital tract in sufficient numbers and virulence, these bacteria initiate an inflammatory reaction (endometritis-salpingitis-peritonitis) that results in the signs and symptoms of PID. The rate of a TOA developing from typical PID is in the range of 1–4 % [5].