Pelvic inflammatory disease

Pelvic inflammatory disease (PID) presents as a spectrum of inflammatory disorders within the upper genital tract of women and includes any combination of endometritis, salpingitis, tubo-ovarian abscess and pelvic peritonitis.[1] Despite development of improved broad-spectrum oral antibiotics for mucopurulent cervicitis, PID remains a major public health problem. Although chlamydial and gonorrheal cervicitis are reportable diseases in most states, PID is not. Accordingly, estimates of the incidence of PID underestimate the impact of this common infection.

It is estimated that one in 10 U.S. women has PID during her reproductive years.[2] Each year, at least 1 million U.S. women are diagnosed with PID and more than 200,000 are hospitalized, at an estimated total cost of more than $5 billion. It has been projected that the cost for treating PID will more than double by the year 2000.[3] At least one-fourth of women with PID have serious sequelae, such as infertility, ectopic pregnancy or chronic pelvic pain, and are at risk for major abdominal surgeries such as tubo-ovarian abscess drainage or lysis of pelvic adhesions.

Teenagers comprise one-fifth of the total cases of PID, and the rate of adolescents affected continues to rise.[4] Although most adolescents presenting with PID do not have a life-threatening condition, repeated PID may become "fertility-threatening." Evidence indicates that 10 to 25 percent of women become infertile after one episode of severe PID.[5] PID clearly threatens the fecundity of millions of young women, contributing to the tremendous cost and morbidity among women with this common disease. Clinicians caring for women must be prepared to meet this challenging epidemic.

Epidemiology

Assessing a woman's risk for PID facilitates correct diagnosis and helps identify women who need risk-reduction counseling. There is considerable overlap between the risk for acquiring a sexually transmitted disease (STD) and the risk for acquiring PID. Table 1 summarizes data from published reports correlating the risk for developing STDs and PID.[2,6-14]

[TABULAR DATA 1 OMITTED]

Personal behaviors and sexual practices emerge as highly significant risk factors for PID. PID is rare in women who are not sexually active. Multiple sex partners, frequent sexual intercourse and the acquisition of new sexual partners within the previous 30 days emerge as significant risk factors.[6] Contraceptive practices influence the risk for development of PID as well. Barrier methods, including condoms, diaphragms and vaginal spermicides, are associated with a decreased risk of STDs, PID and infertility, if they are used properly.[8] Concern has emerged about the possibility of an increased rate of cervical infection caused by Chlamydia trachomatis in women using oral contraceptives.[9] Yet combination oral contraceptive pills appear to offer some protection against the development of PID in women who contract chlamydial cervical infection.[15] It is not known whether progesterone injections or the Norplant method of contraception demonstrate a similar risk pattern.

The exact status of the intrauterine contraceptive device (IUD) as a risk factor for PID and sequelae such as infertility is being rethought. Older studies, some including data from users of the Dalkon shield, demonstrated an increased risk of PID and tubal infertility among IUD users.[16-18] Recent reviews indicate that, among users of the current copper and progestational "T" IUDs available in the United States, most cases of PID are related to the insertion process. A major risk for PID correlates with the risk for acquiring new STDs. Women without significant risk factors for STDs are less likely to develop PID if they experience skilled insertion of IUDs.[9,19]

The health-seeking behavior of women and their sex partner(s) remain important risk factors for PID. Prompt recognition by the physician, patient compliance with the treatment regimen and treatment of the sexual partner(s) decrease the risk of recurrent PID and its sequelae. A delay of only one or two days in seeking treatment can increase the likelihood of hospitalization by nearly 10 percent.[20] It has been demonstrated that institution of treatment within three days of the onset of symptoms resulted in a threefold reduction in the risk of subsequent infertility and ectopic pregnancy.[21]

Microbiology and Pathophysiology

PID results from an ascending infection of bacteria that have colonized the endocervix. PID is usually polymicrobial and includes both aerobic and nonaerobic bacteria.[22] Sexually transmissible organisms most frequently implicated in PID include Neisseria gonorrhoeae, Chlamydia trachomatis and genital Mycoplasma. In approximately one-third of women with gonococcal or chlamydial cervicitis, the infection progresses to PID if left untreated. The role of the genital Mycoplasma organisms Mycoplasma hominis and Ureaplasma urealyticum as pathogens in PID is less clear, yet they can be isolated in women with acute PID. Specific anaerobic bacteria implicated in PID include Peptococcus species, Peptostreptococcus species and Bacteroides species. Facultative aerobes involved with PID include Escherichia coli, group B streptococcus, Gardnerella vaginalis and Haemophilus influenzae.[23] Several investigations have shown an association between bacterial vaginosis and the development of acute PID.[24]

The exact pathogenesis of PID has yet to be determined.[25] A variety of anaerobic and facultative aerobic bacteria that comprise the normal vaginal flora in healthy women contribute to the pathogenesis of PID. Cervical cultures and cultures taken from the endometrium, salpinges and abdominal spaces correlate poorly. While gonococcal and chlamydial organisms can be isolated from the upper genital tract in less than one-third of laparoscopically confirmed cases, the endogenous cervicovaginal flora organisms have been isolated from the upper genital tract in nearly 85 percent of these women. Anaerobic bacteria are nearly always identified within intratubal, ovarian and pelvic abscesses, yet Chlamydia and gonococcus are uncommonly found, even when cervical gonorrhea or Chlamydia was implicated as the initial causative organism for Clearly, the interplay between the host, STD organisms and PID remains complex and incompletely understood.

Diagnosis

Using laparoscopy as the diagnostic standard, it has been demonstrated that PID is correctly diagnosed on the basis of clinical and laboratory indicators in only 65 percent of cases.[28] Since no historical, physical or laboratory findings conclusively make the diagnosis of PID, the ultimate diagnosis relies on clinical judgment coupled with empiric therapeutic intervention and careful follow-up.[29]

Table 2 lists the differential diagnosis for PID. Given this long and diverse differential diagnosis, it is understandable that historical, clinical and laboratory findings fall short of providing a specific diagnosis. In a series of 176 consecutive hospital admissions with a clinical diagnosis of PID,[30] 76 percent were confirmed by laparoscopy to be PID. The remaining 27 percent (non-PID cases). included a normal pelvis in 10 percent, hemorrhagic/ruptured corpus luteum in 8 percent, endometriosis in 3.4 percent, and appendicitis and adhesive disease, 1.1 percent each.

The Author

GARY R. NEWKIRK, M.D. is director of the Family Medicine Spokane (Wash. Residency and clinical professor in the Department of Family Medicine at the University of Washington School of Medicine, Seattle. He graduated from the University of California, San Diego, School of Medicine, La Jolla, and completed a residency in family medicine at the Yakima (Wash.) Valley Memorial Hospital. Address correspondence to Gary R. Newkirk, M.D., Family Medicine Spokane Residency, S. 510 Cowley, Spokane, WA 99202.

The "Gynecologic Care" section was developed and edited by Barbara Apgar, M.D., an associate editor of American Family Physician.

COPYRIGHT 1996 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group