Pelvic Inflammatory Disease

Epidemiology

Monitoring PID trends is critical to quantifying the public health burden in the US. In 2000, there were an estimated 770,000 US cases, with 20% occurring among sexually active girls <19 years. However, national surveillance data for monitoring PID rates has been limited over the years, partially attributed to a shift in care from inpatient to outpatient settings as well as the diagnostic challenges surrounding PID. Additionally, PID is not nationally notifiable, and surveillance data are typically lacking on the state and local levels. As such, public health officials have relied on other data sources, including administrative claims and self-reported data from surveys. Using these data sources, there has been a general decline in rates of PID between 2006 and 2016, though the burden of PID is still substantial. These declines have been attributed to improved detection and treatment of STDs such as increased chlamydia screening, use of more sensitive STD diagnostic tests, and availability of single-dose therapies for uncomplicated lower genital tract infections. ^{, ,}

Several risk factors have been associated with PID development, and many of them mirror those associated with the acquisition of STDs. Engaging in unprotected sex, multiple sex partners, age discrepancy of partners, early age of sexual debut, drug or alcohol abuse, and serially monogamous relationships of short duration can all contribute to elevated risk. ^, The developing adolescent may also be biologically more vulnerable due to the presence of a cervical transitional zone of columnar epithelium (i.e., ectropion) that is the mucosal target site of C. trachomatis and N. gonorrhoeae .

Contraceptives play an important role in modulating the risk of PID. When properly used, barrier methods decrease the risk of STD acquisition and subsequent development of PID. ^, Most studies that evaluate the role of oral contraceptives demonstrate a protective role, which may result from thickening of the cervical mucus, shorter duration of menses, and/or a decreased receptivity of the endometrium to infection. Intrauterine devices (IUDs) have had limited use among the adolescent population due to concerns about the increased risk of PID and STDs. There is a reported small increased risk of PID associated with modern IUDs occurring within the first 3 weeks following insertion. The risk of PID associated with IUD insertion can be reduced by screening for Chlamydia and gonorrhea prior to or on the day of insertion, followed by treatment as indicated. Women with evidence of cervical infection should defer IUD insertion until the infection is treated. ^,

A prior history of PID or STD is a recognized risk factor for PID. In some women, the increased risk observed reflects reinfection from untreated partners. Other hypotheses include relapse from inadequate therapy for the first infection or continued presence of other risk factors. Estimates that almost one-third of female adolescents diagnosed with PID return with a subsequent STD or PID within 6 months of their original treatment highlight that risk of reinfection is high in this group. Vaginal douching contributes to an alteration of the vaginal flora, but whether douching increases the risk for PID remains to be determined.

Etiologic Agents

C. trachomatis and N. gonorrhoeae are universally accepted as etiologic agents of PID. Chlamydia is the most reported STD in the US. Recent estimates suggest there were 2.4 million prevalent chlamydial infections among women aged 15–39 years in 2018, and 67% of them were among young women (aged 15–24 years). Data from prospective studies suggest that about 8%–10% of untreated chlamydial infections progress to clinically diagnosed PID. ^, Infection with C. trachomatis has been associated with tubal scarring, obstruction, and peritubal adhesions. Evidence demonstrates that C. trachomatis remains a significant pathogen associated with PID, especially in the context of subclinical or silent PID , a term used to describe women with lower genital tract infections and concurrent endometritis or salpingitis but with mild or no symptoms. Subclinical PID is estimated to account for ≥50 % of all PID cases. In earlier PID studies, N. gonorrhoeae was a commonly isolated pathogen. More recently, its role as a causal agent has diminished. However, when isolated and associated with PID, the clinical course of cases tends to be more acute and severe. Although recommended laboratory testing for patients suspected of having PID still centers on C. trachomatis and N. gonorrhoeae testing, other organisms have been implicated. Endogenous anaerobes associated with bacterial vaginosis (BV), a condition marked by the disruption of the normal vaginal microflora leading to an overgrowth of anaerobic and facultative bacteria, have been recovered from the upper genital tract in women with acute PID. Specific organisms include Gardnerella vaginalis , Ureaplasma spp., Mycoplasma hominis , Mobiluncus spp., Prevotella spp. and several other bacteria, including anaerobes. It has been suggested that BV facilitates the ascending spread of vaginal microorganisms and provides an inoculum of potentially pathogenic microorganisms. It is uncertain whether Mycoplasma genitalium is an important etiological agent of PID. ^, Little is known about the role of other mollicutes, including Ureaplasma urealyticum , in PID.

Pathophysiology

The spontaneous ascension of infectious microorganisms from the cervix through the endometrium to the fallopian tubes is the most common antecedent to PID. After infection-induced inflammation reaches the fallopian tube, a complex interaction of epithelial degeneration, edema, and other inflammatory responses occurs. This leads to tubal thickening and scarring of the fallopian tube ^, ( Fig. 52.1 ). The presence of other bacteria may be explained by priming of tissue by the STD organisms (i.e., monomicrobial phase) for opportunistic invasion by facultative and anaerobic bacteria from the lower genital tract (i.e., polymicrobial phase). Priming can result from alteration of local mucosal defenses or anatomic interference with mechanical host defenses that drain secretions from the upper genital tract mucosa. The extent of inflammation is also mediated by an adaptive T-lymphocyte response. There is a range of individual immune responses and other host defenses to upper genital tract infections, and not all women have the same likelihood of reproductive sequelae from PID.

Diagnosis

Early diagnosis and treatment of PID are important for the prevention of long-term reproductive sequelae. Owing to the serious reproductive morbidity, a low threshold for both diagnosis and treatment is recommended. The following minimum criteria have been proposed by the US CDC: pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if cervical motion, uterine, or adnexal tenderness are identified on pelvic examination. Additional supportive criteria are intended to help clinicians recognize when PID should be suspected and when additional information is needed to increase diagnostic certainty.

Despite published guidelines ( Box 52.1 ), the diagnosis of PID is challenging due to variations in clinical presentation, imprecise clinical criteria for diagnosis, and the absence of accurate laboratory tests. Studies have documented suboptimal healthcare personnel adherence to recommended guidelines for the diagnosis and management of PID. Furthermore, PID may be confused with other pelvic conditions that exhibit similar symptoms, or non-gynecologic conditions ( Table 52.1 and Box 52.2 ). Identifying PID in female adolescents can pose even more challenges because they may be reluctant to disclose sexual behaviors to a healthcare provider. Healthcare personnel should consider PID in the differential diagnosis and maintain a low threshold for treating PID in at-risk populations (sexually active females presenting with lower abdominal or pelvic pain), and empiric therapy should be initiated unless another cause is discovered.