Pelvic Inflammatory Disease

Pelvic inflammatory disease is inflammation of the internal female reproductive organs. Pelvic inflammatory disease (PID) is usually due to an infection. It is most common in young, sexually active women. PID is a common cause of lower abdominal pain in women. In some cases, however, there are no obvious symptoms, and affected women may be unaware that they have had the condition until they undergo an examination to assess their fertility.

Causes

Pelvic inflammatory disease may not have any obvious cause, but it usually occurs as a result of a sexually transmitted infection, such as a chlamydial infection. It may also occur after a miscarriage, abortion (see abortion, induced), or childbirth. Use of an IUD increases the risk of infection, particularly soon after insertion of the device.

Symptoms and complications

Common symptoms of PID include pain and tenderness in the lower abdomen, fever, and irregular menstrual periods.There may also be a profuse vaginal discharge consisting of blood and/or pus. Pain often occurs after menstruation and may be worse during sexual intercourse (see intercourse, painful). There may also be malaise, vomiting, or backache. PID may be acute or chronic.

Diagnosis and treatment 

A diagnosis is usually made by an internal pelvic examination and examination of swabs from the vagina or cervix to look for infectious organisms. Laparoscopy (examination of the abdominal cavity using a viewing instrument) can confirm the diagnosis. Antibiotic drugs are prescribed to clear the infection, and sometimes analgesic drugs (painkillers) may be given. If an IUD is the suspected cause of PID, the device may need to be removed.

Outlook

If PID is detected and treated early, the patient should recover fully. Some affected women, however, have repeated attacks with or without reinfection. A pelvic abscess may develop as a complication of the condition. PID may cause infertility or increase the risk of ectopic pregnancy; this is primarily due to scarring of the fallopian tubes, which prevents eggs from travelling down the tubes to the uterus.

Pelvic inflammatory disease in detail - technical

Essentials

Pelvic inflammatory disease (PID) is an infection of the fallopian tubes caused by a wide variety of bacteria, including Chlamydia trachomatis, Neisseria gonorrhoeae, and genital tract bacteria, most notably anaerobes.

Manifestations of PID range from mild pelvic pain and tenderness to severe peritonitis. Pelvic abscess formation is a serious infectious complication. However, only about 40% of patients with PID have a fever and even fewer have severe infectious manifestations. Thus, PID is often not diagnosed and it is commonly confused with other pelvic conditions, with a differential diagnosis that most notably includes ectopic pregnancy, appendicitis, and ovarian cyst.

Antibiotic therapy is aimed primarily at C. trachomatis, N. gonorrhoeae, and anaerobic bacteria, with prompt identification and treatment of PID recommended in an attempt to reduce the 10% rate of tubal infertility and the 10-fold increased rate of ectopic pregnancy following this infection.

Introduction

Pelvic inflammatory disease (PID) comprises a wide spectrum of female upper genital tract infections, including any combination of endometritis, salpingitis, tuboovarian abscess, and pelvic peritonitis. Salpingitis, or infection of the fallopian tubes, is the most important feature of PID. This is one of the most common and serious infections of the female genital tract because of its long-term effects including infertility, ectopic pregnancy, and chronic pelvic pain.

Aetiology

PID is caused by the canalicular spread of microorganisms along the mucosal surfaces from the cervix, and to a lesser extent from the vagina, into the upper genital tract. Cervical mucus provides a relative barrier to this spread, but virulent microbes can traverse the mucus, which, in any case, is lost during menses. Little is known of local defence mechanisms that might prevent this spread of microorganisms. Certain HLA types appear to be important in chlamydial PID. Factors that appear to influence the ascent of microbes from the cervix into the upper genital tract include surgical procedures such as dilatation and curettage, induced abortion, insertion of an intrauterine device (IUD), and hysterosalpingograms. Vaginal douching with medicated products disrupts the vaginal flora and appears to increase the incidence of PID. Contraceptives can influence the incidence of PID. Barrier contraception reduces the risk of PID by preventing the acquisition of Neisseria gonorrhoeae and chlamydia. Oral contraceptives also appear to decrease the incidence of PID, perhaps by reducing the inflammatory response to chlamydial infection. However, bacteria adhere to IUDs, so increasing the risk of PID.

Most initial episodes of PID are attributable to N. gonorrhoeae and Chlamydia trachomatis. While one or both bacteria can be isolated from the cervix in up to 75% of patients with acute PID, there is a wide variation in the prevalence of these bacteria. In populations where gonorrhoea is highly endemic, there is a 50 to 80% prevalence of N. gonorrhoeae in women with PID. A study of 1900 patients with PID, conducted across eight countries, found that the prevalence of N. gonorrhoeae varied from 5 to 80%, with a mean of 26%. C. trachomatis was isolated from 5 to 50% of these women (mean prevalence of 29%). In Europe, there was a 30 to 50% prevalence of C. trachomatis and a 5 to 15% prevalence of N. gonorrhoeae in women with PID. Between 10 and 20% of patients with PID harbour both bacteria. However, the use of DNA amplification techniques may reveal even higher numbers of infections with these bacteria.

Mycoplasma hominis and M. genitalium cause tubal infection in primates, and M. genetalium appears to play a role in human PID. Ureaplasma urealyticum has been isolated from the fallopian tubes but appears to play little role in PID.

Facultative and anaerobic bacteria common to the vagina are also isolated from the fallopian tubes of women with PID. In the initial episode of PID, these bacteria appear less frequent than N. gonorrhoeae and C. trachomatis, but they can become secondary invaders and are important among women with prolonged symptoms. Anaerobic bacteria are virtually always present in pelvic abscesses associated with initial or recurrent episodes of PID. These bacteria are important in recurrent PID, where N. gonorrhoeae and C. trachomatis are infrequent.

Clinical features 

Women with PID have a vast array of clinical symptoms, varying in intensity from negligible to severe. No symptom, clinical sign, or laboratory result is pathognomonic of PID. In women with mild or uncharacteristic manifestations, the diagnosis of PID is usually missed. Perhaps two-thirds of cases of PID go unrecognized, often because the symptoms are mild or suggestive of common, less serious conditions. The diagnostic threshold of PID must be sufficiently low to include women with mild PID, but as the threshold is lowered, diagnostic specificity decreases. However, it is better to overdiagnose than fail to treat mild PID. Most recognized cases of PID present with moderate symptoms and signs such as lower abdominal pain. Symptoms such as abnormal vaginal discharge or bleeding, dysuria, or vomiting do not distinguish women with PID from those whose fallopian tubes are apparently normal at laparoscopy. Among women with PID diagnosed by laparoscopy, only 40% have both a temperature over 38°C and peripheral blood leucocytosis. Women with severe symptoms and signs usually have peritonitis, often from N. gonorrhoeae infection, or they have an abscess. Such patients can be very ill. Laparoscopy should be considered both for those with florid peritonitis, to exclude other causes, such as appendicitis and a ruptured abscess, and for those with abscesses greater than 6 cm in diameter, to allow percutaneous drainage.

Perihepatitis (FitzHugh–Curtis syndrome) occurs in about 10% of women with PID. There is often moderate to severe pleuritic pain and tenderness, usually in the right-upper quadrant. These symptoms are often so severe that lower abdominal pain, suggesting PID, may not be noticed. Perihepatitis must therefore be distinguished from other causes of upper quadrant pain and tenderness by careful pelvic examination. Perihepatitis is associated with N. gonorrhoeae, C. trachomatis, and other aetiologies.

Diagnosis

Cervical samples should be obtained to identify N. gonorrhoeae and C. trachomatis by culture or DNA technology. Patients with severe manifestations should have peripheral white blood cell counts. Other laboratory tests are usually of little benefit. Ultrasonography is helpful to identify the presence, and particularly the size, of an abscess. Dilated or thickened tubes or fluid within tubes are found in 80 to 90% of women with severe to moderate PID, but in only two-thirds of those with mild PID. Most sonographers have little experience with these findings. Laparoscopy provides an accurate diagnosis and is particularly useful for excluding serious surgical conditions such as ectopic pregnancy, appendicitis, bleeding ruptured ovarian cyst, or a ruptured abscess. Laparoscopy is also useful for difficult cases, such as those unresponsive to antibiotics in which the only objective finding is pelvic tenderness.

Differential diagnosis

Among 814 women who underwent laparoscopy because of a clinical diagnosis of PID, 12% had intraabdominal conditions other than PID: ectopic pregnancy, appendicitis, ruptured ovarian cysts, and endometriosis. In older women, pyelonephritis, gastroenteritis, and diverticulitis can masquerade as PID. A patient with severe clinical signs or peritonitis should be admitted to hospital for ultrasound examination and/or exploratory laparoscopy. A pregnancy test is needed. If positive, an ectopic pregnancy or other pregnancy complications must be considered. If the pregnancy test is negative, and a wet mount of vaginal/cervical secretions reveals no neutrophils or bacterial vaginosis, an ultrasound scan is needed to diagnose gynaecological diseases other than PID or a gastrointestinal or urinary disorder. If the wet mount shows more neutrophils than vaginal epithelial cells, PID is probable, but other pelvic conditions are not completely excluded. Ultrasonography or an endometrial biopsy examined for plasma cells is useful to increase the accuracy of diagnosis.

Table 1 Inpatient and outpatient PID treatment regimens
Inpatient
Clindamycin 900 mg IV every 8 h + Gentamicin loading dose IV, or intramuscular IM (2 mg/kg of body weight) followed by a maintenance dose (1.5 mg/kg) every 8 h. The intravenous IV regimens should be continued for at least 48 h after substantial clinical improvement (but beware of gentamicin toxicity!), then followed by 100 mg doxycycline twice daily or 450 mg clindamycin 4 times daily (both orally) for a total of 14 days of therapy
Outpatient
Regimen A
Cefoxitin 2 g intramuscular IM + probenecid, 1 g orally in a single dose concurrently, or ceftriaxone 250 mg intramuscular IM or other parenteral third-generation cephalosporin (e.g. cefotaxime) ± Doxycycline 100 mg orally 2 times daily for 14 days
Regimen B
Ofloxacin 400 mg orally 2 times daily or levofloxacin 500 mg orally once daily for 14 days ± Metronidazole 500 mg orally 2 times daily for 14 days. This regimen should only be used when the risk of gonorrhea is low. (A culture for gonorrhoea is essential because of its resistance to fluroquinolones.)
Other
Amoxicillin/clavulanic acid with doxycycline, or azithromycin with metronidazole have provided short-term clinical cures    

IM, intramuscular; IV, intravenous.

Treatment

Treatment is aimed at eradicating N. gonorrhoeae and C. trachomatis, and, especially for those with moderate-to-severe disease, anaerobic bacteria (Table 1). Women with PID who are HIV-seropositive appear less likely to be infected with N. gonorrhoeae and C. trachomatis, but they are more likely to develop abscesses. These patients respond to treatment as promptly as those who are HIV-seronegative, unless they are severely immunosuppressed.

Complications

Despite prompt treatment, sequelae are common. Tubal infertility is the most common and disturbing complication. About 10% of women develop tubal infertility after a single episode of PID. Tubal infertility is increased by delaying the treatment of abdominal pain by more than 3 days in chlamydial PID, in women aged over 25 years at the time of PID, and particularly by the number of episodes of PID. Tubal infertility occurs in about 20% of women after two episodes and 40% after three episodes of PID. Tubal infertility occurs in about two-thirds of those with a pelvic abscess or severely damaged tubes observed laparoscopically. There is no correlation between clinical manifestations and the degree of tubal damage observed laparoscopically. Thus, women with mild symptoms but severe tubal damage may become infertile from a single episode of PID. About 7 to 10% of women who become pregnant following PID develop an ectopic pregnancy. Chronic pelvic pain of over 6 months’ duration occurs in about 15% of patients following PID.

Prevention

Attempts should be made to prevent PID. Ideally N. gonorrhoeae and C. trachomatis infection should be diagnosed and treated before PID can develop. Reduction of C. trachomatis infection has lowered the incidence of PID. This should be the aim of primary care providers, especially since C. trachomatis can now be diagnosed more readily using new sensitive DNA detection methods.

Further reading

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Centers for Disease Control and Prevention (2006). Sexually transmitted diseases treatment guidelines 2006. MMWR, 55, 51–8.

Cohen CR, et al. (1998). Effect of human immunodeficiency virus type 1 infection upon acute salpingitis: a laparoscopic study. J Infect Dis, 178, 1352–8.

Eschenbach DA, et al. (1975). Polymicrobial etiology of acute pelvic inflammatory disease. N Engl J Med, 293, 166–71.

Jacobsen L, Westrom L (1969). Objectivized diagnosis of pelvic inflammatory disease. Diagnostic and prognostic value of routine laparoscopy. Am J Obstet Gynecol, 105, 1088–98.

Molander P, et al. (2001). Transvaginal power Doppler findings in laparoscopically proven acute pelvic inflammatory disease. Ultrasound Obstet Gynecol, 17, 233–8.

Scholes D, et al. (1996). Prevention of pelvic inflammatory disease by screening for cervical chlamydial infection. N Engl J Med, 334, 1362–6.

Westrom L (1980). Incidence, prevalence, and trends of acute pelvic inflammatory disease and its consequences in industrialized countries. Am J Obstet Gynecol, 138, 880–92.

Westrom L, Eschenbach D (1999). Pelvic inflammatory disease. In: Holmes KK, et al. (eds.) Sexually Transmitted Diseases, pp. 783–809. McGraw-Hill, New York.