1 Comment




Pelvic inflammatory disease (PID) refers to infection of the structures of the upper genital tract, such as the uterus (endometritis), fallopian tubes (salpingitis), and adnexal structures (ovarian abscess); pelvic peritonitis may be present. PID is the most frequently occurring serious infection among sexually active women between the ages of 15 and 24. It is estimated that more than 1 million episodes of PID occur yearly in the United States, resulting in more than 200,000 hospitalizations, more than 100,000 surgical procedures, and about 2.5 million outpatient visits. In recent years, the average cost of hospitalization for PID has increased nearly 150%, and the number of women hospitalized has decreased 25%. Approximately one woman in 50 between the ages of 15 and 24 acquires PID yearly. Most cases (85%) are community-acquired and relate to sexual activity, although the disease can be a complication of a gynecologic surgical procedure, such as a dilation and curettage or induced abortion. PID can develop after the insertion of an intrauterine contraceptive device (IUD), which may cause a cervical infection to spread to the uterus and fallopian tubes.
PID is an ascending infection in which organisms in the vagina and lower cervix spread to the normally sterile endometrial cavity and to the fallopian tubes and adnexal structures. The infecting organisms can be exogenous agents, such as sexually transmitted pathogens, or endogenous agents, such as the normal flora of the vagina or bowel. Acute PID can be either gonococcal or nongonococcal salpingitis, based on the results of endocervical or other cultures, such as that of the peritoneal fluid. When the gonococcus is not isolated, the patient has nongonococcal PID. The frequency of these two diseases varies with the population studied. A high proportion of cases of salpingitis seen at a city hospital are caused by the gonococcus, and a low proportion of gonococcal salpingitis is seen in private practice. The causes of nongonococcal PID include Chlamydia trachomatis, Mycoplasma hominis, or a mixture of the aerobic and anaerobic organisms that comprise the normal flora of the lower genital tract.
The frequency of cases caused by the different organisms varies between studies and geographic location. In Sweden, gonococcal disease is infrequent, and Chlamydia infection occurs more often. In North America, both Neisseria gonorrhoeae and Chlamydia are important causes of PID. In some patients, both organisms can be isolated. An endocervical culture yields the gonococcus in 10% to 85% of patients with acute salpingitis. Correlation of an endocervical culture for gonococci with specimens from peritoneal fluid, tubal exudate, or both is variable, with a range of 6% to 70%. In most studies, gonococci are recovered from the peritoneal fluid or fallopian tubes in about 10% to 20% of patients. Whether gonococci are responsible for cases of acute salpingitis when only a cervical culture reveals the organism is unknown. It is hypothesized that gonococci isolated from the endocervix may allow other organisms to ascend to infect the tubes. Chlamydia is isolated from both the cervix and fallopian tubes more often than any other organism. M. hominis and Ureaplasma urealyticum have been isolated from the peritoneal cavity in patients with PID. Gram-negative aerobic bacilli such as Escherichia coli and various anaerobes such as peptostreptococci and Bacteroides species may also be responsible for cases of PID. Actinomyces israelii rarely causes salpingitis in persons who use an IUD. PID caused by anaerobes is usually associated with instrumental trauma of the genital tract rather than sexual intercourse, tends to be more severe, and is often responsible for recurrent rather than first attacks of salpingitis. To date, viruses, except for mumps virus, which can cause oophoritis, have not been implicated as a cause of PID. Many cases of PID are of unknown cause.
Several factors predispose persons to the development of PID. Women who use an IUD have an increased risk compared with those who use other methods of contraception. Most of this risk occurs in the early months after insertion of an IUD and may not be related to sexually transmitted diseases. Women who have multiple sexual partners are also at a higher risk for PID. A single episode of PID increases the risk for a second infection. Thus, 20% of women after one episode of PID have recurrent salpingitis, often within 1 year. Both oral contraceptive agents and condoms appear to protect against PID. Clinical abortion also predisposes to PID, and this complication occurs with a frequency of 0.5%.
PID results from the spread of both exogenous, sexually transmitted organisms and endogenous bacteria in an ascending route to the fallopian tubes. The role of cervical factors (e.g., mucous plug), sexual activity (e.g., frequency and number of partners), sperm, age, and various organisms (e.g., Trichomonas) is unknown.
The clinical presentation does not distinguish gonococcal from nongonococcal PID; however, certain clues give a hint to the etiologic agent. The patient with gonococcal PID is usually young, febrile, and from a lower socioeconomic group. This is her first episode of PID, and the onset is at the time of or shortly after menses. The patient with chlamydial PID is also young, but she is often afebrile, and the onset is not related to menses. Anaerobic PID, usually seen in an older patient, is often not the first infection and may be associated with an IUD. The patient is sometimes severely ill.
The first problem facing the clinician is to establish the diagnosis and exclude other diseases that may closely mimic this condition, such as acute appendicitis, endo-metriosis, various types of ovarian cysts or tumors, ectopic pregnancy, urinary tract infection or calculi, and gastrointestinal disease. In one report, the clinical diagnosis of acute salpingitis was confirmed by laparoscopy in only 65% of patients. Of the remaining women, 23% had normal pelvic findings, and in 12% other diagnoses were established.
The diagnosis should be considered in any sexually active woman who presents with lower abdominal pain. Important observations are bilateral lower abdominal pain of less than 3 weeks’ duration, purulent vaginal discharge or an endocervical culture of a sexually transmitted pathogen, such as N. gonorrhoeae, and tenderness on bimanual pelvic examination. This combination of findings is present in most patients with confirmed PID. The classic findings of pelvic pain, abnormal vaginal discharge, tender adnexa, fever, leukocytosis, and an elevated sedimentation rate are present in only 20% of the patients. Fever (above 38°C) alone is reported in only one third of patients. Salpingitis is usually bilateral, but an 8% incidence of unilateral disease is reported. The presentation spectrum of salpingitis can vary from infection with minimal symptoms to an acute, life-threatening illness.
Right upper quadrant pain suggests the possibility of a concomitant perihepatitis caused by either gonococci or Chlamydia. A palpable adnexal swelling can be detected in half of patients with acute salpingitis. Routine laboratory studies such as the erythrocyte sedimentation rate and peripheral WBC count fail to distinguish salpingitis from a lower genital tract infection. The gold standard used to confirm the diagnosis of salpingitis is laparoscopy. A pelvic ultrasound examination can provide guidance in the diagnosis of abscesses, but normal study findings do not exclude the possibility of salpingitis. Serologic tests to detect gonococcal or chlamydial antibodies are not helpful in diagnosis.
When the diagnosis is uncertain, hospitalization is appropriate. Other indications for hospitalization are pregnancy, suspicion of a pelvic abscess, an adolescent patient, severe illness, inability to take oral antimicrobials, failure to respond to outpatient therapy after 72 hours, presence of an IUD, immunodeficient patient, and upper peritoneal signs.
Recommendations to treat PID empirically have been formulated by the Centers for Disease Control. Effective outpatient treatment regimens consist of an initial IM dose of 2 g of cefoxitin, 2 g of cefotetan, or 250 mg of ceftriaxone. Each regimen, except that for ceftriaxone, also includes 1 g of probenecid taken orally. This is followed by a course of 100 mg of doxycycline, taken orally twice a day, for 14 days. Tetracycline may be substituted for doxycycline in 500-mg doses taken orally four times a day for 14 days. The cephalosporins are effective against penicillinase-producing N. gonorrhoeae.
Several regimens can be used for hospitalized patients. One effective regimen consists of 2 g of cefoxitin, administered intravenously every 6 hours, or 2 g of cefotetan, given intravenously every 12 hours, plus 100 mg of doxycycline, administered intravenously or orally twice daily. On improvement, patients can be given 100 mg of doxycycline orally twice a day to complete a 14-day course. Alternative regimens for the hospitalized patient consist of clindamycin plus gentamicin, ampicillin-sulbactam plus doxycycline, or ofloxacin plus metronidazole.
Doxycycline or tetracycline should be avoided in pregnancy. If a pregnant woman has PID, an unusual circumstance, cefoxitin or ceftriaxone plus erythromycin or azithromycin should be used. Management of the pregnant woman who is allergic to penicillin is difficult, but spectinomycin plus erythromycin or azithromycin can be used.
Further studies are needed to define optimal treatment regimens. One report showed that cephalosporins, such as cefoxitin alone, resulted in an excellent clinical response but failed to eradicate. Chlamydia. Single-drug therapy is inadequate for PID despite an adequate clinical response. Combination therapy directed against Chlamydia and the gonococcus is essential for clinical as well as microbiologic cure.
If an IUD is in place, removal should be considered, although controlled studies on this aspect of management have not been performed. All male sexual partners of patients with PID should be tested and treated empirically for N. gonorrhoeae and C. trachomatis, as a high proportion (58%) of these men will have urethral infection, which is often asymptomatic. Screening of women at risk for chlamydial infection can markedly decrease the frequency of PID. (N.M.G.)
Aral SO, Mosher WD, Cates W Jr. Self-reported pelvic inflammatory disease in the United States, 1988. JAMA 1991;266:2570.
A discussion of risk factors associated with PID: age, race, vaginal douching, age at first intercourse, sexually transmitted disease history, and number of lifetime sexual partners.
Arredondo JL, et al. Oral clindamycin and ciprofloxacin versus intramuscular ceftriaxone and oral doxycycline in the treatment of mild-to-moderate pelvic inflammatory disease in outpatients. Clin Infect Dis 1997;24:170–178.
Clindamycin plus ciprofloxacin was an effective oral regimen for PID.
Barbosa C, et al. Pelvic inflammatory disease and human immunodeficiency virus infection. Obstet Gynecol 1997;89:65–70.
HIV-positive patients who had PID had longer hospital stays and persistent fever compared with HIV-negative patients who had PID.
Boardman LA, et al. Endovaginal sonography for the diagnosis of upper genital tract infection. Obstet Gynecol 1997;90:54–57.
A negative vaginal ultrasound examination does not exclude a diagnosis of PID.
Bowie WR, Jones H. Acute pelvic inflammatory disease in outpatients: association with Chlamydia trachomatis and Neisseria gonorrhoeae. Ann Intern Med 1981;95:685.
Chlamydia was isolated from 22% of patients and N. gonorrhoeae from 10%.
Centers for Disease Control. Pelvic inflammatory disease: guidelines for prevention and management. MMWR Morb Mortal Wkly Rep 1991;40(RR5):1.
Comprehensive review of diagnosis and management.
Centers for Disease Control and Prevention. 1998 Guidelines for treatment of sexually transmitted diseases. MMWR Morb Mortal Wkly Rep 1998;47(RR1):79–86.
Guidelines for management.
Eschenbach DA, et al. Polymicrobial etiology of acute pelvic inflammatory disease. N Engl J Med 1975;293:166.
Discusses the two forms of PID: gonococcal and nongonococcal. Anaerobes and aerobic species are important in the latter.
Falk V. Treatment of acute nontuberculous salpingitis with antibiotics alone and in combination with glucocorticoids. Acta Obstet Gynecol Scand 1965;44(Suppl 6):3.
Corticosteroids were of no value.
Hemsell DL, et al. Comparison of three regimens recommended by the Centers for Disease Control and Prevention for the treatment of women hospitalized with acute pelvic inflammatory disease. Clin Infect Dis 1994;19:720–727.
Three regimens (cefotetan-doxycycline, cefoxitin-doxycycline, clindamycin-gentamicin) were equally effective for hospitalized women with PID.
Jacobson L, Westrom L. Objectivized diagnosis of acute PID. Diagnostic and prognostic value of routine laparoscopy. Am J Obstet Gynecol 1969;105:1088.
Tumor, acute appendicitis, and ectopic pregnancy can mimic acute PID.
Kahn JG, et al. Diagnosing pelvic inflammatory disease: a comprehensive analysis and considerations for developing a new model. JAMA 1991;266:2594.
Comprehensive review of diagnostic studies. There is no ideal test for diagnosis of PID.
Mardh PA. An overview of infectious agents of salpingitis, their biology, and recent advances in methods of detection. Am J Obstet Gynecol 1980;138:933.
A review of infectious causes of salpingitis.
McCormack WM. Pelvic inflammatory disease. N Engl J Med 1994;330:115–119.
Review. Clinical presentation is often silent or with atypical features. Infertility occurs in about 25% of patients.
Muller-Schoop JW, et al. Chlamydia trachomatis as a possible cause of peritonitis and perihepatitis in young women. Br Med J 1978;1:1022.
Chlamydia infection may mimic the Fitz-Hugh–Curtis syndrome.
Peterson HB, Galaid EI, Cates W Jr. Pelvic inflammatory disease. Med Clin North Am 1990;74:1603.
Rice PA, Schachter J. Pathogenesis of pelvic inflammatory disease. JAMA 1991; 266:2587.
A discussion of the research questions related to pathogenesis of PID.
Rolfs RT, Galaid EI, Zaidi AA. Pelvic inflammatory disease: trends in hospitalizations and office visits, 1979 through 1988. Am J Obstet Gynecol 1992;166:983.
Hospitalization rates decreased by 36% and were highest for women ages 15 to 29 years.
Safrin S, et al. Long-term sequelae of acute pelvic inflammatory disease. Am J Obstet Gynecol 1992;166:1300.
In a retrospective study of PID, 24% of patients had pelvic pain for at least 6 months, 43% had a subsequent episode of PID, and 40% were infertile.
Scholes D, et al. Prevention of pelvic inflammatory disease by screening for cervical chlamydial infection. N Engl J Med 1996;334:1362–1366.
Screening for cervical infection with Chlamydia led to a 56% reduction in the incidence of PID.
Sellors J, et al. The accuracy of clinical findings and laparoscopy in pelvic inflammatory disease. Am J Obstet Gynecol 1991;164:113.
Laparoscopy had a sensitivity of 50% for salpingitis. When findings are negative, the physician should perform endometrial and fimbrial minibiopsy to diagnose PID.
Soper DE. Pelvic inflammatory disease. Infect Dis Clin North Am 1994;8:821–840.
Review. Patients with atypical PID may lack abdominal pain.
Swayne LC, Love MB, Karasick SR. Pelvic inflammatory disease: sonographic pathologic correlation. Radiology 1984;151:751.
Abnormal findings could be classified as endometritis, focal mass, or total pelvic distortion.
Sweet RL, Schachter J, Robbie MO. Failure of b-lactam antibiotics to eradicate Chlamydia trachomatis in the endometrium despite apparent clinical cure of acute salpingitis. JAMA 1983;250:2641.
Treatment of acute salpingitis should include an antimicrobial that eradicates Chlamydia, such as doxycycline.
Thompson SE, et al. The microbiology and therapy of acute pelvic inflammatory disease in hospitalized patients. Am J Obstet Gynecol 1980;136:179.
N. gonorrhoeae was isolated from the cervix in 80% of patients and from the peritoneal cavity in 33%.
Walters MD, Gibbs RS. A randomized comparison of gentamicin-clindamycin and cefoxitin-doxycycline in the treatment of acute pelvic inflammatory disease. Obstet Gynecol 1990;75:867.
The comparison shows similar clinical and microbiologic cure rates in acute PID with both agents.
Washington AE, et al. Assessing risk for pelvic inflammatory disease and its sequelae. JAMA 1991;266:2581.
A discussion of risk markers, such as socioeconomic status, and risk factors, such as contraceptive practices.
Wendel GD Jr, et al. A randomized trial of ofloxacin versus cefoxitin and doxycycline in the outpatient treatment of acute salpingitis. Am J Obstet Gynecol 1991;164:1390.
Oral ofloxacin given for 10 days was equal in efficacy to cefoxitin plus doxycycline.
Zhang J, Thomas AG, Leybovich E. Vaginal douching and adverse health effects: a meta-analysis. Am J Public Health 1997;87:1207–1211.
Frequent vaginal douching is associated with PID.



  1. Your means of explaining all in this paragraph is truly nice, every one be able to simply be aware of it, Thanks a lot.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

%d bloggers like this: