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 (1155-1157). Sexually transmitted organisms, especially N. gonorrhoeae and C. trachomatis, often are implicated. Recent studies report that the proportion of PID cases attributable to N. gonorrhoeae or C. trachomatis is decreasing; of women who received a diagnosis of acute PID, approximately 50% have a positive test for either of those organisms (1158-1160). Micro-organisms that comprise the vaginal flora, such as strict and facultative anaerobes (1160) and G. vaginalis, H. influenzae, enteric gram-negative rods, and Streptococcus agalactiae, have been associated with PID (1161). In addition, cytomegalovirus (CMV), T. vaginalis, M. hominis, and U. urealyticum might be associated with certain PID cases (1072). Data also indicate that M. genitalium might have a role in PID pathogenesis (765,928) and might be associated with milder symptoms (919,923,928), although one study failed to demonstrate a substantial increase in PID after detection of M. genitalium in the lower genital tract (925).
Screening and treating sexually active women for chlamydia and gonorrhea reduces their risk for PID (1162,1163). Although BV is associated with PID, whether PID incidence can be reduced by identifying and treating women with BV is unclear (1161). Whether screening young women for M. genitalium is associated with a reduction in PID is unknown.
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Diagnostic Considerations
Acute PID is difficult to diagnose because of the considerable variation in symptoms and signs associated with this condition. Women with PID often have subtle or nonspecific symptoms or are asymptomatic. Delay in diagnosis and treatment probably contributes to inflammatory sequelae in the upper genital tract. Laparoscopy can be used to obtain a more accurate diagnosis of salpingitis and a more complete bacteriologic diagnosis. However, this diagnostic tool frequently is not readily available, and its use is not easily justifiable when symptoms are mild or vague. Moreover, laparoscopy will not detect endometritis and might not detect subtle inflammation of the fallopian tubes. Consequently, a PID diagnosis usually is based on imprecise clinical findings (1164-1166).
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Data indicate that a clinical diagnosis of symptomatic PID has a positive predictive value for salpingitis of 65%-90%, compared with laparoscopy (1167-1170). The positive predictive value of a clinical diagnosis of acute PID depends on the epidemiologic characteristics of the population, with higher positive predictive values among sexually active young women (particularly adolescents), women attending STD clinics, and those who live in communities with high rates of gonorrhea or chlamydia. Regardless of positive predictive value, no single historical, physical, or laboratory finding is both sensitive and specific for the diagnosis of acute 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 and reduces the number of women with PID who are identified.
Episodes of PID often go unrecognized. Although certain cases are asymptomatic, others are not diagnosed because the patient or the health care provider do not recognize the implications of mild or nonspecific symptoms or signs (e.g., abnormal bleeding, dyspareunia, and vaginal discharge). Even women with mild or asymptomatic PID might be at risk for infertility (1157). Because of the difficulty of diagnosis and the potential for damage to the reproductive health of women, health care providers should maintain a low threshold for the clinical diagnosis of PID (1158). The recommendations for diagnosing PID are intended to assist health care providers to recognize when PID should be suspected and when additional information should be obtained to increase diagnostic certainty. Diagnosis and management of other causes of lower abdominal pain (e.g., ectopic pregnancy, acute appendicitis, ovarian cyst, ovarian torsion, or functional pain) are unlikely to be impaired by initiating antimicrobial therapy for PID. Presumptive treatment for PID should be initiated for sexually active young women and other women at risk for STIs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following three minimum clinical criteria are present on pelvic examination: cervical motion tenderness, uterine tenderness, or adnexal tenderness.
More specific criteria for diagnosing PID include endometrial biopsy with histopathologic evidence of endometritis; transvaginal sonography or magnetic resonance imaging techniques demonstrating thickened, fluid-filled tubes with or without free pelvic fluid or tubo-ovarian complex, or Doppler studies indicating pelvic infection (e.g., tubal hyperemia); and laparoscopic findings consistent with PID. A diagnostic evaluation that includes some of these more extensive procedures might be warranted in certain cases. Endometrial biopsy is warranted for women undergoing laparoscopy who do not have visual evidence of salpingitis because endometritis is the only sign of PID for certain women.
Requiring that all three minimum criteria be present before the initiation of empiric treatment can result in insufficient sensitivity for a PID diagnosis. After deciding whether to initiate empiric treatment, clinicians should also consider the risk profile for STIs. More elaborate diagnostic evaluation frequently is needed because incorrect diagnosis and management of PID might cause unnecessary morbidity. For example, the presence of signs of lower genital tract inflammation (predominance of leukocytes in vaginal secretions, cervical discharge, or cervical friability), in addition to one of the three minimum criteria, increases the specificity of the diagnosis. One or more of the following additional criteria can be used to enhance the specificity of the minimum clinical criteria and support a PID diagnosis:
- Oral temperature >38.3°C (>101°F)
- Abnormal cervical mucopurulent discharge or cervical friability
- Presence of abundant numbers of WBCs on saline microscopy of vaginal fluid
- Elevated erythrocyte sedimentation rate
- Elevated C-reactive protein
- Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis
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The majority of women with PID have either mucopurulent cervical discharge or evidence of WBCs on a microscopic evaluation of a saline preparation of vaginal fluid (i.e., wet prep). If the cervical discharge appears normal and no WBCs are observed on the wet prep of vaginal fluid, a PID diagnosis is unlikely, and alternative causes of pain should be considered. A wet prep of vaginal fluid also can detect the presence of concomitant infections (e.g., BV or trichomoniasis).
Treatment
PID treatment regimens should provide empiric, broad-spectrum coverage of likely pathogens. Multiple parenteral and oral antimicrobial regimens have been effective in achieving clinical and microbiologic cure in randomized clinical trials with short-term follow-up (1171-1173). However, only a limited number of studies have assessed and compared these regimens with regard to infection elimination in the endometrium and fallopian tubes or determined the incidence of long-term complications (e.g., tubal infertility and ectopic pregnancy) after antimicrobial regimens (1159,1164,1174). The optimal treatment regimen and long-term outcome of early treatment of women with subclinical PID are unknown. All regimens used to treat PID should also be effective against N. gonorrhoeae and C. trachomatis because negative endocervical screening for these organisms does not rule out upper genital tract infection. Anaerobic bacteria have been isolated from the upper genital tract of women who have PID, and data from in vitro studies have revealed that some anaerobes (e.g., Bacteroides fragilis) can cause tubal and epithelial destruction. BV is often present among women who have PID (22,1160,1161,1175). Addition of metronidazole to IM or oral PID regimens more effectively eradicates anaerobic organisms from the upper genital tract (1160). Until treatment regimens that do not cover anaerobic microbes have been demonstrated to prevent long-term sequelae (e.g., infertility and ectopic pregnancy) as successfully as the regimens that are effective against these microbes, using regimens with anaerobic activity should be considered. Treatment should be initiated as soon as the presumptive diagnosis has been made because prevention of long-term sequelae is dependent on early administration of recommended antimicrobials. For women with PID of mild or moderate clinical severity, parenteral and oral regimens appear to have similar efficacy. The decision of whether hospitalization is necessary should be based on provider judgment and whether the woman meets any of the following criteria:
- Surgical emergencies (e.g., appendicitis) cannot be excluded
- Tubo-ovarian abscess
- Pregnancy
- Severe illness, nausea and vomiting, or oral temperature >38.5°C (101°F)
- Unable to follow or tolerate an outpatient oral regimen
- No clinical response to oral antimicrobial therapy
No evidence is available to indicate that adolescents have improved outcomes from hospitalization for treatment of PID, and the clinical response to outpatient treatment is similar among younger and older women. The decision to hospitalize adolescents with acute PID should be based on the same criteria used for older women.
Parenteral Treatment
Randomized trials have demonstrated the efficacy of parenteral regimens (1160,1171,1172,1176). Clinical experience should guide decisions regarding transition to oral therapy, which usually can be initiated within 24-48 hours of clinical improvement. For women with tubo-ovarian abscesses, >24 hours of inpatient observation is recommended.
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