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Which tests are the most useful for diagnosing PID?
No single test has adequate sensitivity and specificity to reliably identify pelvic inflammatory disease (PID) and thus help to spare women serious sequelae, including infertility (strength of recommendation [SOR]: B, based on systematic reviews of cohort studies and individual cohort studies).
A large multisite US study found that using adnexal tenderness as a minimum clinical criterion raises the sensitivity of the Centers for Disease Control and Prevention (CDC) criteria from 83% to 95%.1 However, even the modified 2002 CDC criteria fail to identify women with subclinical PID who are at roughly equivalent risk for PID sequelae as those with acute symptomatic disease2 (SOR: B, based on individual cohort studies).
It’s prudent to treat when there is a clinical diagnosis of PID
Kismet T. Roberts, MD
University of Nebraska Medical Center; Offutt Air Force Base Family Medicine Residency
Women presenting with acute pelvic pain need thorough evaluation to rule out ectopic pregnancy, cystitis, pyelonephritis, appendicitis, and ovarian torsion. In my experience, a likely history of a sexually transmitted disease along with adnexal pain or cervical motion tenderness on examination is the most helpful in diagnosing PID.
An elevated white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP) may help support the diagnosis. PID often becomes a diagnosis of exclusion if human chorionic gonadotropin (hCG), urine evaluation, and pelvic ultrasound are negative.
While PID is sometimes a frustrating diagnosis to make and is often viewed as a “wastebasket” diagnosis, empiric treatment may be beneficial. While we would love to know whether treating pending culture results reduces the risk of sepsis and infertility, it seems prudent to treat when we have made a clinical diagnosis of PID.
Evidence summary
Our search for articles that examined patient- and primary care–oriented PID diagnostic tests resulted in 2 systematic reviews, no randomized controlled trials, 4 data analyses, and 5 cohort studies, all of which were fair- to good-quality.
Systematic reviews don’t show consistent results
One systematic review of 12 fair- to good-quality studies, based in Europe and the US, included urban populations treated in Ob/Gyn departments, emergency rooms, and sexually transmitted disease clinics. This review supports a thorough evaluation when more severe disease is suspected and the use of sensitive diagnostic tests for suspected mild disease—eg, CRP (74%–93% sensitivity) and ESR (64%–81% sensitivity for value >20 or 15 mm/h).3
Another systematic review of 19 fair-to good-quality cohort studies found a sensitivity of only 64% for laparoscopy, 50% to 87% for endometrial biopsy, and up to 80% for microbiological tests. Results were not consistent for the reported sensitivity of WBC, ESR, or CRP.4
Multivariate analyses of Swedish data come to different conclusions
We identified no randomized controlled trials that addressed the diagnosis of PID. Two multivariate analyses of the same Swedish data from the 1960s came to different conclusions.
The Lund analysis includes data collected between 1960 and 1969 at Lund University Hospital in Sweden on women with suspected PID, with about 625 cases included for these analyses. Simms et al5 found insufficient evidence from these data for any existing diagnostic criteria.
Looking at the same data, Hagdu et al proposed the use of a clinical criteria model including low abdominal pain and 2 or more of the following other criteria: vaginal discharge, temperature greater than 38°C, vomiting, irregular menses, urologic or proctitis symptoms, pelvic tenderness, adnexal mass or swelling, and ESR ≥15.6 This model had a reported sensitivity of 87%, specificity of 52.5%, and false-positive and false-negative rates of 21.2% and 33.3%, respectively.
Looking at adnexal tenderness aids sensitivity of other tests
Cross-sectional analysis of a multisite US randomized treatment trial supported using adnexal tenderness as a minimum clinical criterion to increase sensitivity.1 Further analysis of that trial suggests that some asymptomatic women are at equivalent risk of developing sequelae compared with symptomatic women diagnosed with PID. Those asymptomatic women who met diagnostic criteria with a positive endometrial biopsy were more likely to have pelvic tenderness than asymptomatic women who were not diagnosed.2
Symptoms >1 week and elevated WBC also helpful
Two small, fair-quality cohort studies (N=61 and 176, respectively) investigated the use of clinical diagnostic criteria for PID. The smaller study compared clinical criteria to several reference standards (laparoscopy, histology, microbiological markers, and transvaginal ultrasound) and found clinical criteria, specifically adnexal tenderness, most sensitive (87%), and laparoscopy most specific (100%).7
In the second study, the authors evaluated 176 consecutive admissions for clinically diagnosed PID, 76% of which were laparoscopically confirmed. Reviewing clinical indicators, they found that a combination of adnexal tenderness, symptoms for <1 week, and elevated WBC was the most sensitive set of predictors (sensitivity 86.6%, specificity 45.7%) with positive predictive value of 0.84 and negative predictive value of 0.52.8
Useful lab indicators: C-reactive protein, serum CA-125
Three small cohort studies (N=50–152) of fair-quality evaluated various laboratory indicators in the diagnosis of PID. Each used a different reference standard: clinical criteria, laparoscopy, and endometrial biopsy, respectively.
One study found CRP >10 to be 93% sensitive and 83% specific in a cohort of women admitted to the emergency department with an acute gynecological disorder.9 This population had a high baseline incidence of PID, pregnancy, and intrauterine device use.
A study of serum CA-125 levels showed a predictive value of 97% for values >16 U/mL in diagnosing salpingitis. This test might therefore be useful in confirming peritoneal involvement when PID is suspected clinically.10
Another study developed a model using vaginal WBC (the single most sensitive factor at 78%), serum WBC (the single most specific factor at 88%), CRP, and ESR. The model was 100% sensitive if the diagnosis only required 1 positive test, although the specificity was only 18%. The positive predictive value was 65%. If all 4 were positive, specificity was 95%, with 29% sensitivity, a positive predictive value of 90%, and a negative predictive value of 47%. Prevalence was 60% in the group studied.11
Recommendations from others
The CDC recommends empiric treatment of women with lower abdominal or pelvic pain who are at risk for sexually transmitted diseases with uterine, adnexal, or cervical motion tenderness and no other identifiable cause.12
Clinical Evidence found no RCTs that compared empiric treatment of suspected PID with waiting for microbiological test results for guidance.13
The Agency for Healthcare Research and Quality recommends requiring the presence of lower abdominal, adnexal and cervical tenderness, without alternative diagnosis, for the diagnosis of PID. Temperature >101°F, cervical or vaginal discharge, elevated ESR, and positive gonococcal or chlamydia cultures all increase specificity of diagnosis.14
The United Kingdom’s national guideline recommends maintaining a low threshold for empirical treatment, citing a lack of definitive diagnostic criteria and potential for sequelae, but does recommend testing for gonorrhea and chlamydia.15
1. Piepert JF, Ness RB, Blume J, et al. Clinical predictors of endometritis in women with symptoms and signs of pelvic inflammatory disease. Am J Obstet Gynecol 2001;184:856-864.
2. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005;32:400-405.
3. Kahn JG, Walker CK, Washington AE, et al. Diagnosing pelvic inflammatory disease: a comprehensive analysis and considerations for developing a new model. JAMA 1991;266:2594-2604.
4. Munday PE. Pelvic inflammatory disease: an evidence-based approach to diagnosis. J Infect 2000;40:31-41.
5. Simms I, Warburton F, Westrom L. Diagnosis of pelvic inflammatory disease: time for a rethink. Sex Transm Infect 2003;79:491-494.
6. Hagdu A, Westrom L, Brooks CA, et al. Predicting acute pelvic inflammatory disease: a multivariate analysis. Am J Obstet Gynecol 1986;155:954-960.
7. Gaitan H, Angel E, Diaz R, et al. Accuracy of five different diagnostic techniques in mild-to-moderate pelvic inflammatory disease. Infect Dis Obstet Gynecol 2002;10:171-180.
8. Morcos R, Frost N, Hnat M, et al. Laparoscopic versus clinical diagnosis of acute pelvic inflammatory disease. J Reprod Med 1993;38:53-56.
9. Hemila M, Henriksson L, Ylikorkala O. Serum CRP in the diagnosis and treatment of pelvic inflammatory disease. Arch Gynecol Obstet 1987;241:177-182.
10. Duk JM, Kauer FM, Fleuren GJ, et al. Serum CA 125 levels in patients with a provisional diagnosis of pelvic inflammatory disease. Acta Obstet Gynecol Scand 1989;68:637-641.
11. Peipert JF, Boardman L, Hogan JW, et al. Laboratory evaluation of acute upper genital tract infection. Obstet Gynecology 1996;87:730-736.
12. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):56-61.
13. Ross J. Pelvic infectious diseases. Clinical Evidence 2006. Web publication date December 1, 2005. Available at: www.clinicalevidence.com/ceweb/conditions/seh/1606/1606.jsp. Accessed on February 20, 2007.
14. Common Gynecologic Problems: A Guide to Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2002.
15. United Kingdom National Guideline for the Management of Pelvic Inflammatory Disease. London, England: British Association for Sexual Health and HIV; 2005.
No single test has adequate sensitivity and specificity to reliably identify pelvic inflammatory disease (PID) and thus help to spare women serious sequelae, including infertility (strength of recommendation [SOR]: B, based on systematic reviews of cohort studies and individual cohort studies).
A large multisite US study found that using adnexal tenderness as a minimum clinical criterion raises the sensitivity of the Centers for Disease Control and Prevention (CDC) criteria from 83% to 95%.1 However, even the modified 2002 CDC criteria fail to identify women with subclinical PID who are at roughly equivalent risk for PID sequelae as those with acute symptomatic disease2 (SOR: B, based on individual cohort studies).
It’s prudent to treat when there is a clinical diagnosis of PID
Kismet T. Roberts, MD
University of Nebraska Medical Center; Offutt Air Force Base Family Medicine Residency
Women presenting with acute pelvic pain need thorough evaluation to rule out ectopic pregnancy, cystitis, pyelonephritis, appendicitis, and ovarian torsion. In my experience, a likely history of a sexually transmitted disease along with adnexal pain or cervical motion tenderness on examination is the most helpful in diagnosing PID.
An elevated white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP) may help support the diagnosis. PID often becomes a diagnosis of exclusion if human chorionic gonadotropin (hCG), urine evaluation, and pelvic ultrasound are negative.
While PID is sometimes a frustrating diagnosis to make and is often viewed as a “wastebasket” diagnosis, empiric treatment may be beneficial. While we would love to know whether treating pending culture results reduces the risk of sepsis and infertility, it seems prudent to treat when we have made a clinical diagnosis of PID.
Evidence summary
Our search for articles that examined patient- and primary care–oriented PID diagnostic tests resulted in 2 systematic reviews, no randomized controlled trials, 4 data analyses, and 5 cohort studies, all of which were fair- to good-quality.
Systematic reviews don’t show consistent results
One systematic review of 12 fair- to good-quality studies, based in Europe and the US, included urban populations treated in Ob/Gyn departments, emergency rooms, and sexually transmitted disease clinics. This review supports a thorough evaluation when more severe disease is suspected and the use of sensitive diagnostic tests for suspected mild disease—eg, CRP (74%–93% sensitivity) and ESR (64%–81% sensitivity for value >20 or 15 mm/h).3
Another systematic review of 19 fair-to good-quality cohort studies found a sensitivity of only 64% for laparoscopy, 50% to 87% for endometrial biopsy, and up to 80% for microbiological tests. Results were not consistent for the reported sensitivity of WBC, ESR, or CRP.4
Multivariate analyses of Swedish data come to different conclusions
We identified no randomized controlled trials that addressed the diagnosis of PID. Two multivariate analyses of the same Swedish data from the 1960s came to different conclusions.
The Lund analysis includes data collected between 1960 and 1969 at Lund University Hospital in Sweden on women with suspected PID, with about 625 cases included for these analyses. Simms et al5 found insufficient evidence from these data for any existing diagnostic criteria.
Looking at the same data, Hagdu et al proposed the use of a clinical criteria model including low abdominal pain and 2 or more of the following other criteria: vaginal discharge, temperature greater than 38°C, vomiting, irregular menses, urologic or proctitis symptoms, pelvic tenderness, adnexal mass or swelling, and ESR ≥15.6 This model had a reported sensitivity of 87%, specificity of 52.5%, and false-positive and false-negative rates of 21.2% and 33.3%, respectively.
Looking at adnexal tenderness aids sensitivity of other tests
Cross-sectional analysis of a multisite US randomized treatment trial supported using adnexal tenderness as a minimum clinical criterion to increase sensitivity.1 Further analysis of that trial suggests that some asymptomatic women are at equivalent risk of developing sequelae compared with symptomatic women diagnosed with PID. Those asymptomatic women who met diagnostic criteria with a positive endometrial biopsy were more likely to have pelvic tenderness than asymptomatic women who were not diagnosed.2
Symptoms >1 week and elevated WBC also helpful
Two small, fair-quality cohort studies (N=61 and 176, respectively) investigated the use of clinical diagnostic criteria for PID. The smaller study compared clinical criteria to several reference standards (laparoscopy, histology, microbiological markers, and transvaginal ultrasound) and found clinical criteria, specifically adnexal tenderness, most sensitive (87%), and laparoscopy most specific (100%).7
In the second study, the authors evaluated 176 consecutive admissions for clinically diagnosed PID, 76% of which were laparoscopically confirmed. Reviewing clinical indicators, they found that a combination of adnexal tenderness, symptoms for <1 week, and elevated WBC was the most sensitive set of predictors (sensitivity 86.6%, specificity 45.7%) with positive predictive value of 0.84 and negative predictive value of 0.52.8
Useful lab indicators: C-reactive protein, serum CA-125
Three small cohort studies (N=50–152) of fair-quality evaluated various laboratory indicators in the diagnosis of PID. Each used a different reference standard: clinical criteria, laparoscopy, and endometrial biopsy, respectively.
One study found CRP >10 to be 93% sensitive and 83% specific in a cohort of women admitted to the emergency department with an acute gynecological disorder.9 This population had a high baseline incidence of PID, pregnancy, and intrauterine device use.
A study of serum CA-125 levels showed a predictive value of 97% for values >16 U/mL in diagnosing salpingitis. This test might therefore be useful in confirming peritoneal involvement when PID is suspected clinically.10
Another study developed a model using vaginal WBC (the single most sensitive factor at 78%), serum WBC (the single most specific factor at 88%), CRP, and ESR. The model was 100% sensitive if the diagnosis only required 1 positive test, although the specificity was only 18%. The positive predictive value was 65%. If all 4 were positive, specificity was 95%, with 29% sensitivity, a positive predictive value of 90%, and a negative predictive value of 47%. Prevalence was 60% in the group studied.11
Recommendations from others
The CDC recommends empiric treatment of women with lower abdominal or pelvic pain who are at risk for sexually transmitted diseases with uterine, adnexal, or cervical motion tenderness and no other identifiable cause.12
Clinical Evidence found no RCTs that compared empiric treatment of suspected PID with waiting for microbiological test results for guidance.13
The Agency for Healthcare Research and Quality recommends requiring the presence of lower abdominal, adnexal and cervical tenderness, without alternative diagnosis, for the diagnosis of PID. Temperature >101°F, cervical or vaginal discharge, elevated ESR, and positive gonococcal or chlamydia cultures all increase specificity of diagnosis.14
The United Kingdom’s national guideline recommends maintaining a low threshold for empirical treatment, citing a lack of definitive diagnostic criteria and potential for sequelae, but does recommend testing for gonorrhea and chlamydia.15
No single test has adequate sensitivity and specificity to reliably identify pelvic inflammatory disease (PID) and thus help to spare women serious sequelae, including infertility (strength of recommendation [SOR]: B, based on systematic reviews of cohort studies and individual cohort studies).
A large multisite US study found that using adnexal tenderness as a minimum clinical criterion raises the sensitivity of the Centers for Disease Control and Prevention (CDC) criteria from 83% to 95%.1 However, even the modified 2002 CDC criteria fail to identify women with subclinical PID who are at roughly equivalent risk for PID sequelae as those with acute symptomatic disease2 (SOR: B, based on individual cohort studies).
It’s prudent to treat when there is a clinical diagnosis of PID
Kismet T. Roberts, MD
University of Nebraska Medical Center; Offutt Air Force Base Family Medicine Residency
Women presenting with acute pelvic pain need thorough evaluation to rule out ectopic pregnancy, cystitis, pyelonephritis, appendicitis, and ovarian torsion. In my experience, a likely history of a sexually transmitted disease along with adnexal pain or cervical motion tenderness on examination is the most helpful in diagnosing PID.
An elevated white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP) may help support the diagnosis. PID often becomes a diagnosis of exclusion if human chorionic gonadotropin (hCG), urine evaluation, and pelvic ultrasound are negative.
While PID is sometimes a frustrating diagnosis to make and is often viewed as a “wastebasket” diagnosis, empiric treatment may be beneficial. While we would love to know whether treating pending culture results reduces the risk of sepsis and infertility, it seems prudent to treat when we have made a clinical diagnosis of PID.
Evidence summary
Our search for articles that examined patient- and primary care–oriented PID diagnostic tests resulted in 2 systematic reviews, no randomized controlled trials, 4 data analyses, and 5 cohort studies, all of which were fair- to good-quality.
Systematic reviews don’t show consistent results
One systematic review of 12 fair- to good-quality studies, based in Europe and the US, included urban populations treated in Ob/Gyn departments, emergency rooms, and sexually transmitted disease clinics. This review supports a thorough evaluation when more severe disease is suspected and the use of sensitive diagnostic tests for suspected mild disease—eg, CRP (74%–93% sensitivity) and ESR (64%–81% sensitivity for value >20 or 15 mm/h).3
Another systematic review of 19 fair-to good-quality cohort studies found a sensitivity of only 64% for laparoscopy, 50% to 87% for endometrial biopsy, and up to 80% for microbiological tests. Results were not consistent for the reported sensitivity of WBC, ESR, or CRP.4
Multivariate analyses of Swedish data come to different conclusions
We identified no randomized controlled trials that addressed the diagnosis of PID. Two multivariate analyses of the same Swedish data from the 1960s came to different conclusions.
The Lund analysis includes data collected between 1960 and 1969 at Lund University Hospital in Sweden on women with suspected PID, with about 625 cases included for these analyses. Simms et al5 found insufficient evidence from these data for any existing diagnostic criteria.
Looking at the same data, Hagdu et al proposed the use of a clinical criteria model including low abdominal pain and 2 or more of the following other criteria: vaginal discharge, temperature greater than 38°C, vomiting, irregular menses, urologic or proctitis symptoms, pelvic tenderness, adnexal mass or swelling, and ESR ≥15.6 This model had a reported sensitivity of 87%, specificity of 52.5%, and false-positive and false-negative rates of 21.2% and 33.3%, respectively.
Looking at adnexal tenderness aids sensitivity of other tests
Cross-sectional analysis of a multisite US randomized treatment trial supported using adnexal tenderness as a minimum clinical criterion to increase sensitivity.1 Further analysis of that trial suggests that some asymptomatic women are at equivalent risk of developing sequelae compared with symptomatic women diagnosed with PID. Those asymptomatic women who met diagnostic criteria with a positive endometrial biopsy were more likely to have pelvic tenderness than asymptomatic women who were not diagnosed.2
Symptoms >1 week and elevated WBC also helpful
Two small, fair-quality cohort studies (N=61 and 176, respectively) investigated the use of clinical diagnostic criteria for PID. The smaller study compared clinical criteria to several reference standards (laparoscopy, histology, microbiological markers, and transvaginal ultrasound) and found clinical criteria, specifically adnexal tenderness, most sensitive (87%), and laparoscopy most specific (100%).7
In the second study, the authors evaluated 176 consecutive admissions for clinically diagnosed PID, 76% of which were laparoscopically confirmed. Reviewing clinical indicators, they found that a combination of adnexal tenderness, symptoms for <1 week, and elevated WBC was the most sensitive set of predictors (sensitivity 86.6%, specificity 45.7%) with positive predictive value of 0.84 and negative predictive value of 0.52.8
Useful lab indicators: C-reactive protein, serum CA-125
Three small cohort studies (N=50–152) of fair-quality evaluated various laboratory indicators in the diagnosis of PID. Each used a different reference standard: clinical criteria, laparoscopy, and endometrial biopsy, respectively.
One study found CRP >10 to be 93% sensitive and 83% specific in a cohort of women admitted to the emergency department with an acute gynecological disorder.9 This population had a high baseline incidence of PID, pregnancy, and intrauterine device use.
A study of serum CA-125 levels showed a predictive value of 97% for values >16 U/mL in diagnosing salpingitis. This test might therefore be useful in confirming peritoneal involvement when PID is suspected clinically.10
Another study developed a model using vaginal WBC (the single most sensitive factor at 78%), serum WBC (the single most specific factor at 88%), CRP, and ESR. The model was 100% sensitive if the diagnosis only required 1 positive test, although the specificity was only 18%. The positive predictive value was 65%. If all 4 were positive, specificity was 95%, with 29% sensitivity, a positive predictive value of 90%, and a negative predictive value of 47%. Prevalence was 60% in the group studied.11
Recommendations from others
The CDC recommends empiric treatment of women with lower abdominal or pelvic pain who are at risk for sexually transmitted diseases with uterine, adnexal, or cervical motion tenderness and no other identifiable cause.12
Clinical Evidence found no RCTs that compared empiric treatment of suspected PID with waiting for microbiological test results for guidance.13
The Agency for Healthcare Research and Quality recommends requiring the presence of lower abdominal, adnexal and cervical tenderness, without alternative diagnosis, for the diagnosis of PID. Temperature >101°F, cervical or vaginal discharge, elevated ESR, and positive gonococcal or chlamydia cultures all increase specificity of diagnosis.14
The United Kingdom’s national guideline recommends maintaining a low threshold for empirical treatment, citing a lack of definitive diagnostic criteria and potential for sequelae, but does recommend testing for gonorrhea and chlamydia.15
1. Piepert JF, Ness RB, Blume J, et al. Clinical predictors of endometritis in women with symptoms and signs of pelvic inflammatory disease. Am J Obstet Gynecol 2001;184:856-864.
2. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005;32:400-405.
3. Kahn JG, Walker CK, Washington AE, et al. Diagnosing pelvic inflammatory disease: a comprehensive analysis and considerations for developing a new model. JAMA 1991;266:2594-2604.
4. Munday PE. Pelvic inflammatory disease: an evidence-based approach to diagnosis. J Infect 2000;40:31-41.
5. Simms I, Warburton F, Westrom L. Diagnosis of pelvic inflammatory disease: time for a rethink. Sex Transm Infect 2003;79:491-494.
6. Hagdu A, Westrom L, Brooks CA, et al. Predicting acute pelvic inflammatory disease: a multivariate analysis. Am J Obstet Gynecol 1986;155:954-960.
7. Gaitan H, Angel E, Diaz R, et al. Accuracy of five different diagnostic techniques in mild-to-moderate pelvic inflammatory disease. Infect Dis Obstet Gynecol 2002;10:171-180.
8. Morcos R, Frost N, Hnat M, et al. Laparoscopic versus clinical diagnosis of acute pelvic inflammatory disease. J Reprod Med 1993;38:53-56.
9. Hemila M, Henriksson L, Ylikorkala O. Serum CRP in the diagnosis and treatment of pelvic inflammatory disease. Arch Gynecol Obstet 1987;241:177-182.
10. Duk JM, Kauer FM, Fleuren GJ, et al. Serum CA 125 levels in patients with a provisional diagnosis of pelvic inflammatory disease. Acta Obstet Gynecol Scand 1989;68:637-641.
11. Peipert JF, Boardman L, Hogan JW, et al. Laboratory evaluation of acute upper genital tract infection. Obstet Gynecology 1996;87:730-736.
12. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):56-61.
13. Ross J. Pelvic infectious diseases. Clinical Evidence 2006. Web publication date December 1, 2005. Available at: www.clinicalevidence.com/ceweb/conditions/seh/1606/1606.jsp. Accessed on February 20, 2007.
14. Common Gynecologic Problems: A Guide to Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2002.
15. United Kingdom National Guideline for the Management of Pelvic Inflammatory Disease. London, England: British Association for Sexual Health and HIV; 2005.
1. Piepert JF, Ness RB, Blume J, et al. Clinical predictors of endometritis in women with symptoms and signs of pelvic inflammatory disease. Am J Obstet Gynecol 2001;184:856-864.
2. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005;32:400-405.
3. Kahn JG, Walker CK, Washington AE, et al. Diagnosing pelvic inflammatory disease: a comprehensive analysis and considerations for developing a new model. JAMA 1991;266:2594-2604.
4. Munday PE. Pelvic inflammatory disease: an evidence-based approach to diagnosis. J Infect 2000;40:31-41.
5. Simms I, Warburton F, Westrom L. Diagnosis of pelvic inflammatory disease: time for a rethink. Sex Transm Infect 2003;79:491-494.
6. Hagdu A, Westrom L, Brooks CA, et al. Predicting acute pelvic inflammatory disease: a multivariate analysis. Am J Obstet Gynecol 1986;155:954-960.
7. Gaitan H, Angel E, Diaz R, et al. Accuracy of five different diagnostic techniques in mild-to-moderate pelvic inflammatory disease. Infect Dis Obstet Gynecol 2002;10:171-180.
8. Morcos R, Frost N, Hnat M, et al. Laparoscopic versus clinical diagnosis of acute pelvic inflammatory disease. J Reprod Med 1993;38:53-56.
9. Hemila M, Henriksson L, Ylikorkala O. Serum CRP in the diagnosis and treatment of pelvic inflammatory disease. Arch Gynecol Obstet 1987;241:177-182.
10. Duk JM, Kauer FM, Fleuren GJ, et al. Serum CA 125 levels in patients with a provisional diagnosis of pelvic inflammatory disease. Acta Obstet Gynecol Scand 1989;68:637-641.
11. Peipert JF, Boardman L, Hogan JW, et al. Laboratory evaluation of acute upper genital tract infection. Obstet Gynecology 1996;87:730-736.
12. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):56-61.
13. Ross J. Pelvic infectious diseases. Clinical Evidence 2006. Web publication date December 1, 2005. Available at: www.clinicalevidence.com/ceweb/conditions/seh/1606/1606.jsp. Accessed on February 20, 2007.
14. Common Gynecologic Problems: A Guide to Diagnosis and Treatment. Boston, Mass: Brigham and Women’s Hospital; 2002.
15. United Kingdom National Guideline for the Management of Pelvic Inflammatory Disease. London, England: British Association for Sexual Health and HIV; 2005.
Evidence-based answers from the Family Physicians Inquiries Network
What are contraindications to IUDs?
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
Based on limited evidence, use of intrauterine devices (IUDs) is not contraindicated for women with HIV/AIDS (strength of recommendation [SOR]: C), multiple sexual partners (SOR: C), previous actinomyces colonization (SOR: C), most types of fibroids (SOR: C), or previous ectopic pregnancy (SOR: C).
The risk to IUD users of pelvic inflammatory disease (PID) is similar to women using no contraception (SOR: B). Nulliparous women may experience increased insertion discomfort and higher rates of expulsion (SOR: B). IUD use of <3.5 years is not associated with decreased fertility (SOR: B).
IUDs are an excellent choice when estrogens are contraindicated or adherence is an issue
Shashi Mittal, MD
Baylor Family Medicine Residency at Garland, Garland, Tex
One percent of contraceptive users in the United States choose an IUD, compared with 25% in Europe. This is partly due to misinformation. An older IUD, the Dalkon shield, had a braided polyfilament tail that was associated with a higher risk of PID. People in the US still associate IUDs with this risk.
However, modern IUDs have a monofilament tail, which has not been linked to higher rates of PID. IUDs are an excellent alternative when estrogens are contraindicated, for prevention of pregnancy up to 5 days after unprotected sex, during lactation, and when adherence to a contraceptive has been difficult.
Evidence summary
IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.
Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.1 IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.2 In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.3
In the US, approximately 1 in 1000 women develop PID after IUD insertion.3 Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).4 In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.5
Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).6 Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;7 however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.8
Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).9 There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.10,11
Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.
Recommendations from others
Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).
TABLE
Contraindications to IUD placement
| ACOG | WHO* | MANUFACTURER | |
|---|---|---|---|
| Uterine anomaly (including distension of uterine cavity) | L, C | L, C | L, C |
| History of PID | L, C (past 3 mo only) | L, C (current PID only for both) | L (if no subsequent pregnancy), C |
| Postpartum endometritis or septic abortion in the past 3 months | L, C | L, C (immediately post-septic abortion for both) | L, C |
| Untreated cervicitis/vaginitis, including bacterial vaginosis | L, C | L, C (not bacterial vaginosis) | L, C (including genital actinomycosis) |
| Multiple sexual partners | L, C (increased STI risk is a relative contraindication for both) | L, C | |
| Immunosuppression | L, C (AIDS is a contraindication for both, unless clinically well on antiretroviral therapy) | L, C | |
| * Includes conditions rated as level 3 (risks usually outweigh benefits) or 4 (represents an unacceptable health risk) by WHO | |||
| L, levonorgestrel (Mirena) IUD; C, Copper T 380 (Paragard) IUD; IUD, intrauterine device; ACOG, American College of Obstetricians and Gynecologists; WHO, World Health Organization; PID, pelvic inflammatory disease; STI, sexually transmitted infection | |||
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
1. Sinei SK, Morrison CS, Sekadde-Kigondu C, Allen M, Kokonya D. Complications of use of intrauterine devices among HIV-1-infected women. Lancet 1998;351:1238-1241.
2. Ryden G, Fahraeus L, Molin L, Ahman K. Do contraceptives influence the incidence of acute pelvic inflammatory disease in women with gonorrhoea? Contraception 1979;20:149-157.
3. Steen R, Shapiro K. Intrauterine contraceptive devices and risk of pelvic inflammatory disease: standard of care in high STI prevalence settings. Reprod Health Matters 2004;12:136-143.
4. Ferraz do Lago R, Simoes JA, Bahamondes L, et al. Follow-up of users of intrauterine devices with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105-109.
5. Mao K, Guillebaud J. Influence of removal of intrauterine contraceptive devices on colonisation of the cervix by actinomyces-like organisms. Contraception 1984;30:535-544.
6. Weiner E, Berg AA, Johansson I. Copper intrauterine contraceptive devices in adolescent nulliparae. Br J Obstet Gynaecol 1978;85:204.-
7. Hubacher D, Lara-Richaldi R, Taylor DJ, Guerra-Infante F, Guzman-Rodriguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561-567.
8. Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304-314.
9. Ikomi A, Mansell E, Spence-Jones C, Singer A. Treatment of menorrhagia with the levonorgestrel intrauterine system: Can we learn from our failures? J Obstet Gynaecol 1998;20:630-631.
10. Seibel MM, Hann L. Pregnancy and an IUD in separate horns of a bicornate uterus. JAMA 1982;247:753-754.
11. Caspi B, Shoham Z, Barash A, Lancet M. Sonographic demonstration of an intrauterine device perforating a uterine myoma. J Clin Ultrasound 1989;17:535-537.
Evidence-based answers from the Family Physicians Inquiries Network