Pelvic Inflammatory Disease (PID)

Empiric treatment of Pelvic Inflammatory Disease

Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is an infection of the upper (internal) female reproductive organs. It usually begins as an infection of the cervix, which then spreads to the uterus and fallopian tubes.

The infection can spread beyond the reproductive organs into the tissues surrounding them. Chlamydia and gonorrhea are sexually transmitted infections (STIs) that commonly cause PID. Other infections that are not sexually transmitted can also cause PID.

Empiric Treatment

The patient with PID typically presents with abnormal bleeding, dyspareunia, vaginal discharge, lower abdominal pain, fever, and chills. Physical examination is often remarkable for fever, abnormal cervical or vaginal mucopurulent discharge, uterine or adnexal tenderness, and cervical motion tenderness. Laboratory examination may show an elevated peripheral white blood cell count, the presence of white blood cells in vaginal secretions, and elevated erythrocyte sedimentation rate and C-reactive protein measurements.

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The pathogenesis of PID involves a complex interaction between sexually transmitted bacteria and normal fl ora, particularly anaerobes. As such, it is a polymicrobial infection. The sexually transmitted bacteria that are most often implicated are Neisseria gonorrhoeae and Chlamydia trachomatis. Components of the vaginal flora frequently isolated from PID lesions include the anaerobic Bacteroides and Peptostreptococcus spp. as well as facultative bacteria such as Escherichia coli, Gardnerella vaginalis, Haemophilus infl uenzae, and group B streptococci. Currently, the extent to which each of these contributes to the progression of PID is unclear.

Empiric treatment of PID must take into account the spectrum of organisms that contribute to this infection as well as the severity of illness. All regimens should be effective against N. gonorrhoeae and C. trachomatis. Currently, the role of anaerobic bacteria in PID is controversial, but some experts feel that therapy should also be directed against these organisms. Individuals who have only mild-to-moderate disease should be treated as outpatients with oral antibiotics.

Recommended regimens include a single intramuscular dose of a cephalosporin (e.g., ceftriaxone, cefoxitin, probenecid, cefotaxime) along with a 14-day course of oral doxycycline with or without metronidazole. (Concurrent administration of probenecid with cefoxitin delays excretion of this antibiotic, prolonging therapeutic serum levels.)

Those who are severely ill should be admitted to the hospital and treated initially with intravenous agents. Common initial regimens include (1) a cephalosporin with anaerobic activity (e.g., cefotetan, cefoxitin) plus doxycycline or (2) clindamycin plus gentamicin. The latter regimen is efficacious because gentamicin is effective against the gram-negative N. gonorrhoeae and clindamycin has some activity against C. trachomatis

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as well as against many anaerobes.

Intravenous antibiotics can be discontinued 24 hours after patients show clinical improvement, and a total course of 14 days of therapy completed with oral doxycycline or oral clindamycin.

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