The term pelvic inflammatory disease (PID) comprises a spectrum of infections of the female upper reproductive tract. It is a common and serious disease initiated by ascending infection from the vagina and cervix. PID includes salpingitis, endometritis, myometritis, parametritis, oophoritis, and tubo-ovarian abscess and may extend to produce periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh–Curtis syndrome). PID is the most common serious infection in sexually active women age 16 to 25 years.¹

Long-term sequelae, including tubal factor infertility, implantation failure after in vitro fertilization, ectopic pregnancy, and chronic pain, may ultimately affect 11% of reproductive-aged women.² The most common cause of death is rupture of a tubo-ovarian abscess, and the mortality associated with rupture remains at 5% to 10%, even with current treatment methods.

ORGANISMS ASSOCIATED WITH PID

Neisseria gonorrhoeae and Chlamydia trachomatis can be isolated in many cases of PID, and therapy is directed primarily against these organisms. However, polymicrobial infection, including infection with anaerobic and aerobic vaginal flora, is evident from cultured material from the upper reproductive tract.³ Table 103-1 lists common pathogenic organisms associated with PID. N. gonorrhoeae and C. trachomatis are often instrumental in initial infection of the upper genital tract, whereas anaerobes, facultative anaerobes, and other bacteria are isolated increasingly as inflammation increases and abscesses form.

Bacterial vaginosis (BV) is frequently identified in women with PID, and the type of BV-associated microorganism (Gardnerella vaginalis, Mycoplasma hominis, Ureaplasma urealyticum, pigmented or nonpigmented anaerobic gram-negative rods) may make a difference in the likelihood of developing PID.^4,5

Infection with Trichomonas vaginalis is associated with a fourfold increase in the incidence of acute endometritis. Co-infection with herpes simplex virus 2 and C. trachomatis, N. gonorrhoeae, or bacteria causing vaginosis is also associated with acute endometritis. Infection with herpes simplex virus 2 causes fallopian tube inflammation and lower tract ulceration that may disrupt the endocervical canal mucous barrier.⁶ Human immunodeficiency virus 1 (HIV-1) infection is associated with an increased incidence of C. trachomatis infection, increased incidence of co-infection with Candida and human papillomavirus, and increased risk of progression to PID.⁷

PID may result from Mycobacterium tuberculosis infection in endemic areas.⁸ Schistosomes can cause genital infection, including a PID-like tubal infection, infertility, and chronic abortion, and a recent report links schistosomiasis to HIV transmission in Africa. Actinomyces species have been identified almost exclusively in patients with intrauterine devices (IUDs).⁹

ASCENDING INFECTION

Most cases of PID are presumed to originate with sexually transmitted infections (STIs) of the lower genital tract, followed by ascending infection of the upper tract. The original STI may be asymptomatic. The precise mechanisms by which upper genital tract infection and inflammation are initiated and propagated are not well known. Although the cervical mucus serves as a functional barrier to ascending infection much of the time, its efficacy may be decreased by hormonal changes during menstruation and ovulation and by retrograde menstruation. Intercourse may contribute to the ascent of infection due to rhythmic mechanical uterine contractions. Bacteria also may be carried by, or along with, sperm into the uterus and tubes. Uterine infection usually is limited to the endometrium but can be more invasive in a gravid or postpartum uterus. Tubal infection initially affects only the mucosa, but acute, complement-mediated transmural inflammation may develop rapidly and increase in intensity with repeated infection. Inflammation may extend to uninfected parametrial structures, including the appendix and bowel. Infection may spread by direct extension of purulent material from the fallopian tubes or via lymphatic spread beyond the pelvis to involve the hepatic capsule with acute perihepatitis (Fitz-Hugh–Curtis syndrome) and produce acute peritonitis.

RISK FACTORS FOR PID

Multiple risk factors are associated with development of PID (Table 103-2).^{4,10,11,12,13,14,15,16,17}

IUD use has been associated with an increased risk for PID. Although the majority of risk occurs within 21 days of insertion, the presence of an IUD is associated with complicated PID irrespective of the duration of use.^9,13,14,15 The risk of PID in IUD users is more related to the development of STI than the IUD,^18,19 and STI screening and treatment at the time of insertion can significantly decrease the likelihood that PID will develop.²⁰

Pregnancy decreases the risk of PID because the cervical os is protected by the mucous plug. However, PID can occur during the first trimester and is associated with substantial fetal loss and preterm delivery.

COMPLICATIONS OF PID

PID is associated with a number of serious clinical sequelae. Tubo-ovarian abscess is reported in up to one third of women hospitalized for PID. Infection and inflammation can lead to scarring and adhesions within tubal lumens. Ectopic pregnancy is more frequent in women who have had PID than in those who have never had an ectopic pregnancy. Tubal factor infertility is increased by 12% to 50% in women with a past diagnosis of PID, and the incidence increases with the number and severity of past PID episodes.²¹ Asymptomatic or silent PID appears to be associated with tubal factor infertility as well. Sequelae of PID include recurrence of PID, chronic pelvic pain, menstrual disturbances, and chronic dyspareunia. Recurrence of PID may occur because of inadequately treated infection, nontreatment of partner(s), or reinfection from another sexual contact. In follow-up to the Pelvic Inflammatory Disease Evaluation and Clinical Health trial, those with recurrence of PID were five times more likely to experience chronic pelvic pain.²² PID may also be associated with an increased risk of ovarian borderline tumors.²³

The clinical presentation of PID is variable. The most common presenting complaint is lower abdominal pain, most frequently described as bilateral and dull or crampy. Pain may be exacerbated by movement or by sexual activity. Other symptoms include abnormal vaginal discharge (75% of individuals), vaginal and postcoital bleeding (more than one third of patients), irritative voiding symptoms, fever, malaise, nausea, and vomiting.²⁴ Symptoms occur most commonly early in the menstrual cycle or at the end of the menses and are attributed to low progesterone levels and coincident thinning of the cervical mucosal barrier.

The physical examination is usually notable for lower abdominal tenderness, cervical motion tenderness, and uterine or adnexal tenderness. Involuntary guarding and rebound tenderness may be present and may indicate associated peritonitis. The positive predictive value of these findings varies depending on the prevalence of PID in a given clinical population. Adnexal tenderness appears to have a sensitivity of 95%.²⁵ Mucopurulent cervicitis is a common finding, and its absence should raise consideration of another diagnosis. In women who are suspected of having PID and for whom there is no likely alternative diagnosis for abdominal pain, the presence of fever, adnexal tenderness, and an elevated erythrocyte sedimentation rate are significant independent predictors of endometritis and correctly classify 65% of patients with laparoscopically proven PID (95% confidence interval, 61% to 99%).^25,26

Right upper quadrant tenderness, particularly with jaundice, may indicate perihepatic inflammation. Fitz-Hugh–Curtis syndrome is perihepatitis, demonstrated by right upper quadrant pain in a woman with a clinical diagnosis of PID and no other cause for this pain. It is an uncommon complication and responds to standard antibiotic treatment for PID.²⁷

The differential diagnosis of PID is broad and includes cervicitis, ectopic pregnancy, endometriosis, ovarian cyst, ovarian torsion, spontaneous abortion, septic abortion, cholecystitis, gastroenteritis, appendicitis, diverticulitis, pyelonephritis, and renal colic. Look for signs of other STIs, such as herpes simplex, syphilis, and human papillomavirus infection.

The diagnosis is based on history and clinical findings. No single piece of historical, physical, or laboratory information is sensitive and specific for the disease. Laboratory evaluation of any woman of childbearing age in the ED always should include a pregnancy test. Consider the possibility of ectopic pregnancy or septic abortion; the most common alternative diagnosis in missed ectopic pregnancy is PID. Concurrent pregnancy also influences patient treatment and disposition.

Current Centers for Disease Control and Prevention guidelines encourage initiation of empiric treatment in women at risk for PID who exhibit lower abdominal pain, adnexal tenderness, and cervical motion tenderness. Guidelines stratify diagnostic criteria into the three groups shown in Table 103-3.