CDC Guidelines for Pelvic Inflammatory Disease
PID comprises a spectrum of inflammatory disorders of the upper female genital tract, including any combination of endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis. Sexually transmitted organisms, especially Neisseria gonorrhoeae and Chlamydia trachomatis, are implicated in most cases; however, microorganisms that can be part of the vaginal flora (e.g., anaerobes, Gardnerella vaginalis, Haemophilus influenzae, enteric gram-negative rods, and Streptococcus agalactiae) also can cause PID. In addition, Mycoplasma hominis and Ureaplasma urealyticum might be etiologic agents of PID.
Diagnostic Considerations
Acute PID is difficult to diagnose because of the wide variation in the symptoms and signs. Many women with PID have subtle or mild symptoms that do not readily indicate PID. Consequently, delay in diagnosis and effective treatment probably contributes to inflammatory sequelae in the upper reproductive tract. Laparoscopy can be used to obtain a more accurate diagnosis of salpingitis and a more complete bacteriologic diagnosis. However, this diagnostic tool often is not readily available for acute cases, and its use is not easy to justify when symptoms are mild or vague. Moreover, laparoscopy will not detect endometritis and may not detect subtle inflammation of the fallopian tubes. Consequently, a diagnosis of PID usually is based on clinical findings. The clinical diagnosis of acute PID also is imprecise. Data indicate that a clinical diagnosis of symptomatic PID has a PPV for salpingitis of 65%-90% in comparison with laparoscopy. The PPV of a clinical diagnosis of acute PID differs depending on epidemiologic characteristics and the clinical setting, with higher PPV among sexually active young (especially teenaged) women and among patients attending STD clinics or from settings in which rates of gonorrhea or chlamydia are high. In all settings, however, no single historical, physical, or laboratory finding is both sensitive and specific for the diagnosis of acute PID (i.e., can be used both to detect all cases of PID and to exclude all women without PID). Combinations of diagnostic findings that improve either sensitivity (i.e., detect more women who have PID) or specificity (i.e., exclude more women who do not have PID) do so only at the expense of the other. For example, requiring two or more findings excludes more women who do not have PID but also reduces the number of women with PID who are identified.
Many episodes of PID go unrecognized. Although some cases are asymptomatic, others are undiagnosed because the patient or the health-care provider fails to recognize the implications of mild or nonspecific symptoms or signs (e.g., abnormal bleeding, dyspareunia, or vaginal discharge [atypical PID]). Because of the difficulty of diagnosis and the potential for damage to the reproductive health of women even by apparently mild or atypical PID, health-care providers should maintain a low threshold for the diagnosis of PID. Even so, the long-term outcome of early treatment of women with asymptomatic or atypical PID is unknown. The following recommendations for diagnosing PID are intended to help health-care providers recognize when PID should be suspected and when they need to obtain additional information to increase diagnostic certainty. These recommendations are based partially on the fact that diagnosis and management of other common causes of lower abdominal pain (e.g., ectopic pregnancy, acute appendicitis, and functional pain) are unlikely to be impaired by initiating empiric antimicrobial therapy for PID.
Empiric treatment of PID should be initiated in sexually active young women and others at risk for STDs if all the following minimum criteria are present and no other cause(s) for the illness can be identified:
· lower abdominal tenderness;
· adnexal tenderness; and
· cervical motion tenderness.
More elaborate diagnostic evaluation often is needed because incorrect diagnosis and management might cause unnecessary morbidity. These additional criteria may be used to enhance the specificity of the minimum criteria listed previously. Additional criteria that support a diagnosis of PID include the following:
· oral temperature greater than 101°F (greater than 38.3°C);
· abnormal cervical or vaginal discharge;
· elevated erythrocyte sedimentation rate;
· elevated C-reactive protein; and
· laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis.
The definitive criteria for diagnosing PID, which are warranted in selected cases, include the following:
histopathologic evidence of endometritis on endometrial biopsy;
· transvaginal sonography or other imaging techniques showing thickened fluid-filled tubes with or without free pelvic fluid or tubo-ovarian complex; and
· laparoscopic abnormalities consistent with PID.
Although treatment can be initiated before bacteriologic diagnosis of C. trachomatis or N. gonorrhoeae infection, such a diagnosis emphasizes the need to treat sex partners.
Treatment
PID treatment regimens must provide empiric, broad-spectrum coverage of likely pathogens. Antimicrobial coverage should include N. gonorrhoeae, C. trachomatis, anaerobes, gram-negative facultative bacteria, and streptococci. Although several antimicrobial regimens have been effective in achieving a clinical and microbiologic cure in randomized clinical trials with short-term follow-up, few investigations have a) assessed and compared these regimens with regard to elimination of infection in the endometrium and fallopian tubes or b) determined the incidence of long-term complications (e.g., tubal infertility and ectopic pregnancy).
All regimens should be effective against N. gonorrhoeae and C. trachomatis, because negative endocervical screening does not preclude upper-reproductive tract infection. Although the need to eradicate anaerobes from women who have PID has not been determined definitively, the evidence suggests that this may be important. Anaerobic bacteria have been isolated from the upper-reproductive tract of women who have PID, and data from in vitro studies have revealed that anaerobes such as Bacteroides fragilis can cause tubal and epithelial destruction. In addition, BV also is diagnosed in many women who have PID. Until treatment regimens that do not adequately cover these microbes have been shown to prevent sequelae as well as the regimens that are effective against these microbes, the recommended regimens should have anaerobic coverage. Treatment should be initiated as soon as the presumptive diagnosis has been made, because prevention of long-term sequelae has been linked directly with immediate administration of appropriate antibiotics. When selecting a treatment regimen, health-care providers should consider availability, cost, patient acceptance, and antimicrobial susceptibility.
In the past, many experts recommended that all patients who had PID be hospitalized so that bed rest and supervised treatment with parenteral antibiotics could be initiated. However, hospitalization is no longer synonymous with parenteral therapy. No currently available data compare the efficacy of parenteral with oral therapy or inpatient with outpatient treatment settings. Until the results from ongoing trials comparing parenteral inpatient therapy with oral outpatient therapy for women who have mild PID are available, such decisions must be based on observational data and consensus opinion. The decision of whether hospitalization is necessary should be based on the discretion of the health-care provider.
The following criteria for hospitalization are based on observational data and theoretical concerns:
· surgical emergencies such as appendicitis cannot be excluded;
· the patient is pregnant;
· the patient does not respond clinically to oral antimicrobial therapy;
· the patient is unable to follow or tolerate an outpatient oral regimen;
· the patient has severe illness, nausea and vomiting, or high fever;
· the patient has a tubo-ovarian abscess; or
· the patient is immunodeficient (i.e., has HIV infection with low CD4 counts, is taking immunosuppressive therapy, or has another disease suppressing the immune system).
Most clinicians favor at least 24 hours of direct inpatient observation for patients who have tubo-ovarian abscesses, after which time home parenteral therapy should be adequate.
There are no efficacy data comparing parenteral with oral regimens. Experts have extensive experience with both of the following regimens. Also, there are multiple randomized trials demonstrating the efficacy of each regimen. Although most trials have used parenteral treatment for at least 48 hours after the patient demonstrates substantial clinical improvement, this is an arbitrary designation. Clinical experience should guide decisions regarding transition to oral therapy, which may be accomplished within 24 hours of clinical improvement.
Source: Centers for Disease Control and Prevention. 1998 Guidelines for Treatment of Sexually Transmitted Diseases. The material in this report was prepared for publication by: National Center for HIV, STD and TB Prevention, Division of Sexually Transmitted Diseases Prevention. The complete January 1998 guidelines for PID can be accessed at http://www.cdc.gov/nchstp/dstd/STD98T11.HTM
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