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Pelvic inflammatory disease (PID) is infection of the upper female genital tract: the cervix, uterus, fallopian tubes, and ovaries; abscesses may occur. Common symptoms and signs include lower abdominal pain, cervical discharge, and irregular vaginal bleeding. Long-term complications include infertility, chronic pelvic pain, and ectopic pregnancy. Diagnosis includes PCR of cervical specimens for Neisseria gonorrhoeae and chlamydiae, microscopic examination of cervical discharge (usually), and ultrasonography or laparoscopy (occasionally). Treatment is with antibiotics.
PID results from microorganisms ascending from the vagina and cervix into the endometrium and fallopian tubes. Infection of the cervix (cervicitis) causes mucopurulent discharge. Infection of the fallopian tubes (salpingitis) and uterus (endometritis) tend to occur together. If severe, infection can spread to the ovaries (oophoritis) and then the peritoneum (peritonitis). Salpingitis with endometritis and oophoritis, with or without peritonitis, is often called salpingitis even though other structures are involved.
Neisseria gonorrhoeae and Chlamydia trachomatis are common causes of PID; they are transmitted sexually. PID usually also involves other aerobic and anaerobic bacteria, including pathogens that cause bacterial vaginosis (see Vaginitis and Pelvic Inflammatory Disease (PID): Bacterial Vaginosis).
PID commonly occurs in women < 35. It is rare before menarche, after menopause, and during pregnancy. Risk factors include previous PID and presence of bacterial vaginosis or any sexually transmitted disease. Other risk factors, particularly for gonorrheal or chlamydial PID, include younger age, nonwhite race, low socioeconomic status, and multiple or new sex partners.
Symptoms and Signs
Lower abdominal pain, fever, cervical discharge, and abnormal uterine bleeding are common, particularly during or after menses.
Cervicitis
The cervix appears red and bleeds easily. Mucopurulent discharge is common; usually, it is yellow-green and can be seen exuding from the endocervical canal.
Acute salpingitis
Lower abdominal pain is usually present and bilateral but may be unilateral, even when both tubes are involved. Pain can also occur in the upper abdomen. Nausea and vomiting are common when pain is severe. Irregular bleeding and fever each occur in up to one third of patients. In the early stages, signs may be mild or absent. Later, cervical motion tenderness, guarding, and rebound tenderness are common. Occasionally, dyspareunia or dysuria occurs. Many women with inflammation that is severe enough to cause scarring have minimal or no symptoms.
PID due to N. gonorrhoeae is usually more acute and causes more severe symptoms than that due to C. trachomatis, which can be indolent.
Complications
Acute gonococcal or chlamydial salpingitis may lead to the Fitz-Hugh-Curtis syndrome (perihepatitis that causes upper right quadrant pain). Infection may become chronic, characterized by intermittent exacerbations and remissions.
A tubo-ovarian abscess (collection of pus in the adnexa) develops in about 15% of women with salpingitis. It can accompany acute or chronic infection and is more likely if treatment is late or incomplete. Pain, fever, and peritoneal signs are usually present and may be severe. The abscess may rupture, causing progressively severe symptoms and possibly septic shock. Hydrosalpinx (fimbrial obstruction and tubal distention with nonpurulent fluid) is usually asymptomatic but can cause pelvic pressure, chronic pelvic pain, or dyspareunia. Tubo-ovarian abscess, hydrosalpinx, or pyosalpinx (pus confined to one or both fallopian tubes) may produce a palpable adnexal mass and may lead to infertility.
Salpingitis may cause tubal scarring and adhesions, which commonly result in chronic pelvic pain, infertility, and increased risk of ectopic pregnancy. Salpingitis may also result in menstrual irregularities.
Diagnosis
PID is suspected when women of reproductive age, particularly those with risk factors, have lower abdominal pain or cervical or unexplained vaginal discharge. PID is considered when irregular vaginal bleeding, dyspareunia, or dysuria is unexplained. PID is more likely if lower abdominal, unilateral or bilateral adnexal, and cervical motion tenderness are present. A palpable adnexal mass suggests tubo-ovarian abscess. Because even minimally symptomatic infection may have severe sequelae, index of suspicion should be high.
If PID is suspected, PCR of cervical specimens for N. gonorrhoeae and C. trachomatis (which is nearly 100% sensitive and specific) and a pregnancy test are done. If PCR is unavailable, cultures are done. At the point of care, cervical discharge is usually examined to confirm purulence; a Gram stain or saline wet mount is used, but these tests are neither sensitive nor specific. If a patient cannot be adequately examined because of tenderness, ultrasonography is done as soon as possible. WBC count may be elevated but is not helpful diagnostically.
If the pregnancy test is positive, ectopic pregnancy, which can produce similar findings, should be considered. Other common causes of pelvic pain include endometriosis, adnexal torsion, ovarian cyst rupture, and appendicitis. Differentiating features of these disorders are discussed elsewhere (see Symptoms of Gynecologic Disorders: Pelvic Pain). Fitz-Hugh-Curtis syndrome may mimic acute cholecystitis but can usually be differentiated by evidence of salpingitis during pelvic examination or, if necessary, with ultrasonography.
If an adnexal or pelvic mass is suspected clinically or if patients do not respond to antibiotics within 48 to 72 h, ultrasonography is done as soon as possible to exclude tubo-ovarian abscess, pyosalpinx, and disorders unrelated to PID (eg, ectopic pregnancy, adnexal torsion). If the diagnosis is uncertain after ultrasonography, laparoscopy should be done; purulent peritoneal material obtained by laparoscopy is the diagnostic gold standard.
Treatment
Antibiotics are given empirically to cover N. gonorrhoeae and C. trachomatis and are modified based on laboratory test results. Patients with cervicitis or clinically mild to moderate PID do not require hospitalization. Outpatient treatment regimens (see Table 3: Vaginitis and Pelvic Inflammatory Disease (PID): Regimens for Treatment of Pelvic Inflammatory Disease* ) usually also aim to eradicate bacterial vaginosis (See Vaginitis and Pelvic Inflammatory Disease (PID): Bacterial Vaginosis), which often coexists. Sex partners of patients with N. gonorrhoeae or C. trachomatis infection should be treated.
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Table 3
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| Regimens for Treatment of Pelvic Inflammatory Disease* |
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Treatment
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Regimen
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Alternative Regimens
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Parenteral†
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Regimen A: Cefotetan 2 g IV q 12 h
Cefoxitin 2 g IV q 6 h
Doxycycline 100 mg po or IV q 12 h
Regimen B: Clindamycin 900 mg IV q 8 h
Gentamicin 2 mg/kg (loading dose) IV or IM, followed by a maintenance dose (1.5 mg/kg) q 8 h; possibly substitution of single daily dosing (eg, 4.5 mg/kg once/day)
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Ampicillin/sulbactam 3 g IV q 6 h
Doxycycline 100 mg po or IV q 12 h
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Oral‡
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Ceftriaxone 250 mg IM in a single dose
Doxycycline 100 mg po bid for 14 days
with or without
Metronidazole 500 mg po bid for 14 days
Cefoxitin 2 g IM in a single dose with probenecid 1 g po given concurrently in a single dose
plus
Doxycycline 100 mg po bid for 14 days
with or without
Metronidazole 500 mg po bid for 14 days
Another parenteral 3rd-generation cephalosporin (eg, ceftizoxime, cefotaxime)
plus
Doxycycline 100 mg po bid for 14 days
Metronidazole 500 mg po bid for 14 days
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§A fluoroquinolone (eg, levofloxacin 500 mg po once/day or ofloxacin 400 mg po bid for 14 days)
Metronidazole 500 mg po bid for 14 days||
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*Recommendations are from the Centers for Disease Control and Prevention: Updated recommended treatment regimens for gonococcal infections and associated conditions—United States, April 2007. Available at www.cdc.gov/std/treatment.
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†Clinical efficacy of parenteral and oral therapy for mild to moderately severe pelvic inflammatory disease (PID) appears similar. Clinical experience should guide the transition to oral therapy, which can usually be started within 24 h of clinical improvement.
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‡Oral therapy can be considered for mild to moderately severe acute PID because the clinical outcomes with oral and parenteral therapy are similar. If patients do not respond to oral therapy within 72 h, they should be reevaluated to confirm the diagnosis, and parenteral therapy should be given on an outpatient or inpatient basis.
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§This regimen may be considered if parenteral cephalosporin is not feasible and if community prevalence and individual risk of gonorrhea are low. Tests for gonorrhea must be done before therapy is started; if results are positive, the following is recommended:
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Positive nucleic acid amplification tests (NAATs): Parenteral cephalosporin
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Positive culture for gonorrhea: Treatment based on results of antimicrobial susceptibility
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Identification of quinolone-resistant Neisseria gonorrhoeae or antimicrobial susceptibility that cannot be assessed: Parenteral cephalosporin
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||Information about other outpatient regimens is limited; however, amoxicillin/clavulanate and doxycycline or azithromycin with metronidazole provide short-term clinical cure. There are no published data about the use of oral cephalosporins.
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Criteria for hospitalization in women with PID are usually the following:
In these cases, IV antibiotics (see Table 3: Vaginitis and Pelvic Inflammatory Disease (PID): Regimens for Treatment of Pelvic Inflammatory Disease*) are started as soon as cultures are obtained and are continued until patients have been afebrile for 24 h.
Tubo-ovarian abscess may require more prolonged IV antibiotics and hospitalization. Treatment with ultrasound- or CT-guided percutaneous or transvaginal drainage can be considered if response to antibiotics alone is incomplete. Laparoscopy or laparotomy is sometimes required for drainage. Suspicion of a ruptured tubo-ovarian abscess requires immediate laparotomy. In women of reproductive age, surgery should aim to preserve the pelvic organs (with the hope of preserving fertility).
Last full review/revision April 2007 by David E. Soper, MD
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