Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pelvic Inflammatory Disease Treatment & Management

  • Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM; Chief Editor: Michel E Rivlin, MD  more...
 
Updated: Sep 28, 2015
 

Approach Considerations

Treatment of pelvic inflammatory disease (PID) addresses the relief of acute symptoms, eradication of current infection, and minimization of the risk of long-term sequelae. These sequelae, including chronic pelvic pain, ectopic pregnancy, tubal factor infertility (TFI), and implantation failure with in vitro fertilization attempts, may occur in as many as 25% of patients.[67]

From a public health perspective, treatment is aimed at the expeditious eradication of infection in order to reduce the risk of transmission of infection to new sexual partners. In addition, identification and treatment of current and recent partners are indicated for further reduction of sexually transmitted infections (STIs).

Early diagnosis and treatment appear to be critical in the preservation of fertility. Current guidelines suggest that empirical treatment should be initiated in at-risk women who have lower abdominal pain, adnexal tenderness, and cervical motion tenderness. In view of the diagnostic difficulties and the potential for serious sequelae, the Centers for Disease Control and Prevention (CDC) advises that physicians maintain a low threshold for aggressive patient treatment, with overtreatment preferred to no or delayed treatment.[6]

Therapy with antibiotics alone is successful in 33-75% of cases. If surgical treatment is warranted, the current trend is toward conservation of reproductive potential with simple drainage, adhesiolysis, and copious irrigation or unilateral adnexectomy, if possible. Further surgical therapy is needed in 15-20% of cases so managed.

The CDC advises that there is insufficient evidence to recommend removal of intrauterine devices (IUDs) in women diagnosed with acute PID. However, close clinical follow-up is mandatory if the IUD is left in place.[64]

Current evidence suggests that adherence to clinical guidelines for PID diagnosis and management is less than optimal.[68, 69, 70] A systematic review of the literature revealed limited research on strategies to improve patient and practitioner adherence to guidelines. Interventions that make it easier to manage patients and provision of the entire treatment course to the patient at the time of evaluation improved compliance.[68]

Next

Consultations

Patients who do not improve in 72 hours should be reevaluated for possible laparoscopic or surgical intervention and for reconsideration of other possible diagnoses. Laparoscopy should be used if the diagnosis is in doubt. Laparoscopic pelvic lavage, abscess drainage, and adhesion lysis may be necessary.

Most TOAs (60-80%) resolve with antibiotic administration. If patients do not respond appropriately, laparoscopy may be useful for identifying loculations of pus requiring drainage. An enlarging pelvic mass may indicate bleeding secondary to vessel erosion or a ruptured abscess. Unresolved abscesses may be drained percutaneously via posterior colpotomy, under computed tomographic (CT) or ultrasonographic guidance, laparoscopically, or through laparotomy. For more information on treatment of TOA, see Fallopian Tube Disorders.

The advantages of laparoscopy include direct visualization of the pelvis and more accurate bacteriologic diagnosis if cultures are obtained. However, laparoscopy is not always available in acute PID; moreover, it is costly and requires general anesthesia.

Laparotomy is usually reserved for patients experiencing surgical emergencies (eg, abscesses that have ruptured or that have not responded to medical management and laparoscopic drainage) and for patients who are not candidates for laparoscopic management. Treatment is guided by intraoperative findings and the patient’s desire for fertility maintenance.

Surgical treatment may involve unilateral salpingo-oophorectomy or hysterectomy and bilateral salpingo-oophorectomy. Ideally, the operation is performed after the acute infection and inflammation have resolved. In patients with recurrent PID, dense pelvic adhesions may render surgery difficult.

Previous
Next

Prevention

Randomized, controlled trials suggest that preventing chlamydial infection reduces the incidence of PID.[71] In addition, anyone who has had sexual contact with a woman with PID in the 60 days preceding the onset of her symptoms should be treated empirically for C trachomatis and N gonorrhoeae. CDC guidelines recommend that even if a patient last had sexual intercourse more than 60 days before symptom onset or diagnosis, the most recent sex partner should be treated.[6]

Urethral gonococcal or chlamydial infection in the partner of an infected woman is highly likely and is frequently asymptomatic in men. Even in clinical settings where men do not receive treatment, arrangements for care or referral of male sex partners should be made.

Regardless of whether a woman’s sex partners were treated, women diagnosed with chlamydial or gonococcal infection should follow up with repeat testing within 3-6 months. These women have a high rate of reinfection within 6 months of treatment.[6] Adolescents are more likely to have recurrent PID than adults are and so may require a different approach to follow-up.[72]

Improved education, routine screening,[73] diagnosis, and empirical treatment of these infections should reduce the incidence and prevalence of these processes and the development of long-term sequelae. Education should concentrate on strategies to prevent PID and STIs, including reducing the number of sexual partners, avoiding unsafe sexual practices, and routinely using appropriate barrier protection. Adolescents, being at an increased risk for PID, should be advised to delay the onset of sexual intercourse until age 16 years or older.[52]

Women with PID should be counseled to abstain from sexual activity or use barrier protection strictly and appropriately until their symptoms and those of their partner[6] have fully abated and they have completed their entire treatment regimen.

The US Preventive Services Task Force (USPSTF) recommends screening for chlamydial infection in all sexually active nonpregnant women up to age 25 years and in nonpregnant women aged 25 years or older who are at increased risk (grade A recommendation), as well as in all pregnant women up to age 25 years and in pregnant women aged 25 years or older who are at increased risk (grade B recommendation). The USPSTF recommends against routine screening for women aged 25 years and older if they are not at increased risk (grade C recommendation).[74]

The USPSTF does not provide recommendations for Chlamydia screening in men; the available evidence is insufficient to allow accurate weighing of benefits and risks.[74] However, a 2008 demonstration project suggested that the combination of (a) partner notification and (b) screening of men with a relatively high prevalence of chlamydial infection and a larger number of partners would be more cost-effective than expanding screening to low-risk women would be.[75]

Some patients treated for STIs and PID fail to comply with medication regimens because of low medical literacy and a poor understanding of their diagnosis. These individuals frequently do not follow up or notify partners. Patients should be fully educated about these issues, as well as about the advisability of testing and treatment for other STIs, including HIV infection, hepatitis, and syphilis. In particular, the 2010 CDC guidelines state that HIV testing should be offered to all women diagnosed with acute PID.[6]

Previous
Next

Outpatient Versus Inpatient Treatment

Most patients with PID are managed as outpatients, and the available data do not clearly indicate that patients benefit from hospitalization. However, hospitalization should be considered for patients with the following conditions:

  • Uncertain diagnosis
  • Pelvic abscess on ultrasonographic scanning
  • Pregnancy
  • Inability to tolerate outpatient oral antibiotic regimen
  • Severe illness
  • Immunodeficiency (eg, patients with HIV infection who have a low CD4 count or patients who are using immunosuppressive medications)
  • Failure to improve clinically after 72 hours of outpatient therapy

Worldwide, more than 90% of HIV-positive individuals with PID are treated as outpatients.[76] A 2006 study in Nairobi, with investigators blinded to patient HIV status, demonstrated that HIV-infected women were more likely to have severe PID and that clinical improvement in PID took longer in HIV-infected women, irrespective of their CD4 count; however, no change in antibiotic regimen was necessary.[77]

Most patients show a clinical response within 48-72 hours after initiation of medical therapy. If a patient continues to have fever, chills, uterine tenderness, adnexal tenderness, and cervical motion tenderness, consider other possible causes and consider performing a diagnostic laparoscopy.

Hospital admission of HIV-infected patients and of adolescents should be reviewed on an individual basis. Admission decisions are based on the following factors:

  • Diagnostic certainty
  • Illness severity
  • Likelihood of compliance with an outpatient regimen
  • Whether or not the patient is pregnant
  • Coexisting immunosuppression or illness
  • Risk factors for significant anaerobic infection (eg, IUD use, a recent pelvic procedure, or the presence of a tubo-ovarian abscess [TOA])
  • The following consultations may be helpful:
  • Obstetrician/gynecologist
  • Surgeon (especially if appendicitis or another intra-abdominal process cannot be excluded)
  • Infectious disease consultant (especially in patients who are HIV-positive and may be on highly active antiretroviral treatment [HAART])
Previous
Next

Antibiotic Therapy

In the emergency department, clinic, or office setting, treatment should be expeditiously initiated and should include empirical broad-spectrum antibiotics to cover the full complement of common organisms. All regimens must be effective against C trachomatis and N gonorrhoeae, as well as against gram-negative facultative organisms, anaerobes, and streptococci.

To avoid inappropriate treatment, physicians should be aware of current guidelines and current national and local patterns of drug resistance in their patient populations.[78] The Royal College of Obstetricians and Gynaecologists (RCOG) recommends treating women with PID who are infected with HIV with the same antibiotic regimens used to treat women who are HIV-negative.[11]

A number of studies carried out between 1992 and 2006 demonstrated the effectiveness of various parenteral and oral regimens in eliminating acute symptoms and achieving microbiologic cure.[58] No differences in outcome were identified between inpatient and outpatient management in a large, randomized, multicenter clinical study that compared inpatient and outpatient oral and parenteral antibiotic regimens in the documented elimination of endometrial and tubal infection.[79]

Patients on an intravenous (IV) PID regimen can be transitioned to oral antibiotics 24 hours after clinical improvement. These should be continued for a total of 14 days. Oral therapy usually involves doxycycline; however, azithromycin can also be used.[80] In patients who have developed a TOA, oral therapy should include clindamycin or metronidazole.

All patients should be reevaluated in 72 hours for evidence of clinical improvement and compliance with their antibiotic regimen. Multiple studies have shown poor compliance with doxycycline therapy, and approximately 20-25% of patients have never filled their prescriptions.

Outpatient and inpatient regimens

The Centers for Disease Control and Prevention (CDC) has outlined antibiotic regimens for outpatient and inpatient treatment of PID.

For outpatient treatment, the CDC lists 2 currently accepted treatment regimens, labeled as A and B.[6] Regimen A consists of the following:

  • Ceftriaxone 250 mg intramuscularly (IM) once as a single dose plus
  • Doxycycline 100 mg orally twice daily for 14 days
  • Metronidazole 500 mg orally twice daily for 14 days can be added if there is evidence or suspicion of vaginitis or if the patient underwent gynecologic instrumentation in the preceding 2-3 weeks

Regimen B consists of the following:

  • Cefoxitin 2 g IM once as a single dose concurrently with probenecid 1 g orally in a single dose, or another single-dose parenteral third-generation cephalosporin (eg, ceftizoxime or cefotaxime) plus
  • Doxycycline 100 mg orally twice daily for 14 days
  • Metronidazole 500 mg orally twice daily for 14 days can be added if there is evidence or suspicion of vaginitis or if the patient underwent gynecologic instrumentation in the preceding 2-3 weeks

Inpatient treatment

For inpatient treatment of PID, the CDC also lists 2 currently accepted treatment regimens, again labeled as A and B.[6] Regimen A consists of the following:

  • Cefoxitin 2 g IV every 6 hours or cefotetan 2 g IV every 12 hours plus
  • Doxycycline 100 mg orally or IV every 12 hours

This regimen is continued for 24 hours after the patient remains clinically improved, after which doxycycline 100 mg is given orally twice daily for a total of 14 days. If a TOA is present, clindamycin or metronidazole is used with doxycycline for more effective anaerobic coverage.

Regimen B consists of the following:

  • Clindamycin 900 mg IV every 8 hours plus
  • Gentamicin IV in a loading dose of 2 mg/kg, followed by a maintenance dosage of 1.5 mg/kg q8h

IV therapy may be discontinued 24 hours after the patient improves clinically, and oral therapy with 100 mg doxycycline twice daily should be continued for a total of 14 days. If TOA is present, clindamycin or metronidazole may be used with doxycycline for more effective anaerobic coverage.

An alternative parenteral regimen is ampicillin-sulbactam 3 g IV every 6 hours in conjunction with doxycycline 100 mg orally or IV every 12 hours.

Additional information on antibiotic therapy

Oral doxycycline has the same bioavailability as the IV form and avoids the painful infusion and vein sclerosis associated with the latter. Gentamicin dosing may be every 24 hours. Other third-generation cephalosporins may be substituted for cefoxitin and ceftriaxone.

For individuals who are allergic to cephalosporins, spectinomycin is recommended in Europe and Canada; however, this agent is currently unavailable in the United States. A 2-g azithromycin dose may also be used in these patients, but it is not routinely recommended, because of concerns about rapid development of resistance to this antibiotic[81, 82] and about potential intolerance of this dose. For more information, see the CDC’s Antibiotic-Resistant Gonorrhea Web site and Gonococcal Infections.

In April 2007, the CDC ceased to recommend fluoroquinolone antibiotics for treatment of gonorrhea in the United States.[83] This change was based on analysis of data from the CDC’s Gonococcal Isolate Surveillance Project (GISP), which showed that the prevalence of fluoroquinolone-resistant gonorrhea cases in heterosexual men had reached 6.7%, an 11-fold increase from 0.6% in 2001. Fluoroquinolones may be a treatment option for disseminated gonococcal infection if antimicrobial susceptibility can be documented.

With fluoroquinolones no longer advocated, the drugs recommended for treatment of gonorrhea are limited to cephalosporins. However, gonococcal resistance to cephalosporins has also been increasing in the United States. GISP data showed that from 2000 to 2010, the percentage of isolates with elevated minimum inhibitory concentrations rose from 0.2% to 1.4% for cefixime and from 0.1% to 0.3% for ceftriaxone.

Consequently, the CDC no longer recommends the use of oral cephalosporins for gonococcal infections. For treatment of uncomplicated urogenital, anorectal, and pharyngeal gonorrhea, the CDC recommends a single IM dose of ceftriaxone 250 mg together with either a single oral dose of azithromycin 1 g or twice-daily oral administration of doxycycline 100 mg for 7 days.[84]

If ceftriaxone is not readily available, cefixime 400 mg can be given orally in combination with either azithromycin or doxycycline; if ceftriaxone cannot be given because of severe allergy, azithromycin 2 g can be given orally in a single dose. However, patients treated with one of these alternative regimens should return 1 week after treatment for a test of cure.[84]

Previous
 
 
Contributor Information and Disclosures
Author

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, Education Officer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Nicole W Karjane, MD Associate Professor, Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center

Nicole W Karjane, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Association of Professors of Gynecology and Obstetrics, North American Society for Pediatric and Adolescent Gynecology

Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD Former Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, Royal College of Surgeons of Edinburgh, Royal College of Obstetricians and Gynaecologists

Disclosure: Nothing to disclose.

Acknowledgements

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Wiesenfeld HC, Hillier SL, Meyn LA, Amortegui AJ, Sweet RL. Subclinical pelvic inflammatory disease and infertility. Obstet Gynecol. 2012 Jul. 120(1):37-43. [Medline].

  2. Rivlin ME, Hunt JA. Ruptured tuboovarian abscess. Is hysterectomy necessary?. Obstet Gynecol. 1977 Nov. 50 (5):518-22. [Medline].

  3. Laohaburanakit P, Treevijitsilp P, Tantawichian T, Bunyavejchevin S. Ruptured tuboovarian abscess in late pregnancy. A case report. J Reprod Med. 1999 Jun. 44 (6):551-5. [Medline].

  4. De Temmerman G, Villeirs GM, Verstraete KL. Ruptured tuboovarian abscess causing peritonitis in a postmenopausal woman. A difficult diagnosis on imaging. JBR-BTR. 2003 Mar-Apr. 86 (2):72-3. [Medline].

  5. Powers K, Lazarou G, Greston WM, Mikhail M. Rupture of a tuboovarian abscess into the anterior abdominal wall: a case report. J Reprod Med. 2007 Mar. 52 (3):235-7. [Medline].

  6. Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep. 2010 Dec 17. 59:1-110. [Medline]. [Full Text].

  7. Patton DL, Wolner-Hanssen P, Zeng W, Lampe M, Wong K, Stamm WE, et al. The role of spermatozoa in the pathogenesis of Chlamydia trachomatis salpingitis in a primate model. Sex Transm Dis. 1993 Jul-Aug. 20(4):214-9. [Medline].

  8. Paavonen J. Chlamydia trachomatis infections of the female genital tract: state of the art. Ann Med. 2012 Feb. 44(1):18-28. [Medline].

  9. Taylor BD, Darville T, Ferrell RE, Kammerer CM, Ness RB, Haggerty CL. Variants in toll-like receptor 1 and 4 genes are associated with Chlamydia trachomatis among women with pelvic inflammatory disease. J Infect Dis. 2012 Feb 15. 205(4):603-9. [Medline]. [Full Text].

  10. den Hartog JE, Ouburg S, Land JA, et al. Do host genetic traits in the bacterial sensing system play a role in the development of Chlamydia trachomatis-associated tubal pathology in subfertile women?. BMC Infect Dis. Jul 21 2006. 6:122.

  11. [Guideline] Royal College of Obstetricians and Gynaecologists (RCOG). Management of acute pelvic inflammatory disease. London (UK): Royal College of Obstetricians and Gynaecologists (RCOG).; 2008 Nov. [Full Text].

  12. Herzog SA, Althaus CL, Heijne JC, Oakeshott P, Kerry S, Hay P, et al. Timing of progression from Chlamydia trachomatis infection to pelvic inflammatory disease: a mathematical modelling study. BMC Infect Dis. 2012 Aug 11. 12:187. [Medline]. [Full Text].

  13. Hillis SD, Wasserheit JN. Screening for chlamydia--a key to the prevention of pelvic inflammatory disease. N Engl J Med. 1996 May 23. 334(21):1399-401. [Medline].

  14. Hook EW, Handsfield HH. Gonococcal infections in the adult. Holmes KK, Sparling PF, Stamm WE, et al. eds. Sexually Transmitted Diseases. 4th edition. New York: McGraw Hill, Inc; 2008. 627-645.

  15. Mylonas I. Female genital Chlamydia trachomatis infection: where are we heading?. Arch Gynecol Obstet. 2012 May. 285(5):1271-85. [Medline].

  16. Ross JD. Is Mycoplasma genitalium a cause of pelvic inflammatory disease?. Infect Dis Clin North Am. 2005 Jun. 19(2):407-13. [Medline].

  17. Bjartling C, Osser S, Persson K. Mycoplasma genitalium in cervicitis and pelvic inflammatory disease among women at a gynecologic outpatient service. Am J Obstet Gynecol. 2012 Jun. 206(6):476.e1-8. [Medline].

  18. Bravender T, Matson SC. Adolescents, IUDs, PID, and Enterococcus: a report of two cases. J Pediatr Adolesc Gynecol. 2012 Jun. 25(3):e73-4. [Medline].

  19. Avan BI, Fatmi Z, Rashid S. Comparison of clinical and laparascopic features of infertile women suffering from genital tuberculosis (TB) or pelvic inflammatory disease (PID) or endometriosis. J Pak Med Assoc. 2001 Nov. 51(11):393-9. [Medline].

  20. Cherpes TL, Wiesenfeld HC, Melan MA, Kent JA, et al. The associations between pelvic inflammatory disease, Trichomonas vaginalis infection, and positive herpes simplex virus type 2 serology. Sex Transm Dis. 2006. 33:747-52.

  21. Jarvis GA, Chang TL. Modulation of HIV transmission by Neisseria gonorrhoeae: molecular and immunological aspects. Curr HIV Res. 2012 Apr. 10(3):211-7. [Medline].

  22. Brunham RC, Kimani J, Bwayo J, Maitha G, Maclean I, Yang C, et al. The epidemiology of Chlamydia trachomatis within a sexually transmitted diseases core group. J Infect Dis. 1996 Apr. 173(4):950-6. [Medline].

  23. Bjartling C, Osser S, Johnsson A, Persson K. Clinical manifestations and epidemiology of the new genetic variant of Chlamydia trachomatis. Sex Transm Dis. 2009 Sep. 36(9):529-35. [Medline].

  24. Kinnunen A, Molander P, Morrison R, Lehtinen M, Karttunen R, Tiitinen A, et al. Chlamydial heat shock protein 60--specific T cells in inflamed salpingeal tissue. Fertil Steril. 2002 Jan. 77(1):162-6. [Medline].

  25. Makepeace BL, Watt PJ, Heckels JE, Christodoulides M. Interactions of Neisseria gonorrhoeae with mature human macrophage opacity proteins influence production of proinflammatory cytokines. Infect Immun. 2001 Mar. 69(3):1909-13. [Medline]. [Full Text].

  26. Champion JD, Piper J, Shain RN, Perdue ST, Newton ER. Minority women with sexually transmitted diseases: sexual abuse and risk for pelvic inflammatory disease. Res Nurs Health. 2001 Feb. 24(1):38-43. [Medline].

  27. Ness RB, Soper DE, Holley RL, Peipert J, Randall H, Sweet RL, et al. Douching and endometritis: results from the PID evaluation and clinical health (PEACH) study. Sex Transm Dis. 2001 Apr. 28(4):240-5. [Medline].

  28. Ness RB, Hillier SL, Kip KE, Richter HE, Soper DE, Stamm CA, et al. Douching, pelvic inflammatory disease, and incident gonococcal and chlamydial genital infection in a cohort of high-risk women. Am J Epidemiol. 2005 Jan 15. 161(2):186-95. [Medline].

  29. Koumans EH, Kendrick JS. Preventing adverse sequelae of bacterial vaginosis: a public health program and research agenda. Sex Transm Dis. 2001 May. 28(5):292-7. [Medline].

  30. Ness RB, Hillier SL, Kip KE, Soper DE, Stamm CA, McGregor JA, et al. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet Gynecol. 2004 Oct. 104(4):761-9. [Medline].

  31. Ness RB, Soper DE, Holley RL, Peipert J, Randall H, Sweet RL, et al. Hormonal and barrier contraception and risk of upper genital tract disease in the PID Evaluation and Clinical Health (PEACH) study. Am J Obstet Gynecol. 2001 Jul. 185(1):121-7. [Medline].

  32. Shelton JD. Risk of clinical pelvic inflammatory disease attributable to an intrauterine device. Lancet. 2001 Feb 10. 357(9254):443. [Medline].

  33. [Guideline] CDC, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. Aug 4 2006. 55(RR-11):1-94.

  34. Kelly EK, Rudinsky SW. Intrauterine contraception: current evidence-based recommendations. J Midwifery Womens Health. 2007 Sep-Oct. 52(5):505-7. [Medline].

  35. Meirik O. Intrauterine devices - upper and lower genital tract infections. Contraception. 2007. 06;75(6 Suppl/):S41-7.

  36. Centers for Disease Control and Prevention. Pelvic Inflammatory Disease – PID. CDC Fact Sheet. Available at http://www.cdc.gov/std/pid/stdfact-pid.htm. Accessed: December 9, 2012.

  37. Sufrin CB, Postlethwaite D, Armstrong MA, Merchant M, Wendt JM, Steinauer JE. Neisseria gonorrhea and Chlamydia trachomatis screening at intrauterine device insertion and pelvic inflammatory disease. Obstet Gynecol. 2012 Dec. 120(6):1314-21. [Medline].

  38. Viberga I, Odlind V, Lazdane G, Kroica J, Berglund L, Olofsson S. Microbiology profile in women with pelvic inflammatory disease in relation to IUD use. Infect Dis Obstet Gynecol. 2005 Dec. 13(4):183-90. [Medline]. [Full Text].

  39. Levgur M, Duvivier R. Pelvic inflammatory disease after tubal sterilization: a review. Obstet Gynecol Surv. 2000 Jan. 55(1):41-50. [Medline].

  40. Sutton MY, Sternberg M, Zaidi A, St Louis ME, Markowitz LE. Trends in pelvic inflammatory disease hospital discharges and ambulatory visits, United States, 1985-2001. Sex Transm Dis. 2005 Dec. 32(12):778-84. [Medline].

  41. Ness RB, Smith KJ, Chang CC, Schisterman EF, Bass DC. Prediction of pelvic inflammatory disease among young, single, sexually active women. Sex Transm Dis. 2006 Mar. 33(3):137-42. [Medline].

  42. Sorbye IK, Jerve F, Staff AC. Reduction in hospitalized women with pelvic inflammatory disease in Oslo over the past decade. Acta Obstet Gynecol Scand. 2005 Mar. 84(3):290-6. [Medline].

  43. World Health Organization. Sexually transmitted infections. Available at http://www.who.int/mediacentre/factsheets/fs110/en/. Accessed: February 2, 2010.

  44. Low N, Broutet N, Adu-Sarkodie Y, Barton P, Hossain M, Hawkes S. Global control of sexually transmitted infections. Lancet. 2006 Dec 2. 368(9551):2001-16. [Medline].

  45. Kamwendo F, Forslin L, Bodin L, Danielsson D. Programmes to reduce pelvic inflammatory disease--the Swedish experience. Lancet. 1998. 351 Suppl 3:25-8. [Medline].

  46. Kamwendo F, Forslin L, Bodin L, Danielsson D. Decreasing incidences of gonorrhea- and chlamydia-associated acute pelvic inflammatory disease. A 25-year study from an urban area of central Sweden. Sex Transm Dis. 1996 Sep-Oct. 23(5):384-91. [Medline].

  47. Banikarim C, Chacko MR. Pelvic inflammatory disease in adolescents. Adolesc Med Clin. 2004 Jun. 15 (2):273-85, viii. [Medline].

  48. Zeger W, Holt K. Gynecologic infections. Emerg Med Clin North Am. 2003 Aug. 21 (3):631-48. [Medline].

  49. Liou TH, Wu CW, Hao WR, Hsu MI, Liu JC, Lin HW. Risk of myocardial infarction in women with pelvic inflammatory disease. Int J Cardiol. 2012 Jan 20. [Medline].

  50. Chen PC, Tseng TC, Hsieh JY, Lin HW. Association between stroke and patients with pelvic inflammatory disease: a nationwide population-based study in Taiwan. Stroke. 2011 Jul. 42(7):2074-6. [Medline].

  51. Lin HW, Tu YY, Lin SY, Su WJ, Lin WL, Lin WZ, et al. Risk of ovarian cancer in women with pelvic inflammatory disease: a population-based study. Lancet Oncol. 2011 Sep. 12(9):900-4. [Medline].

  52. Simms I, Stephenson JM, Mallinson H, Peeling RW, Thomas K, Gokhale R, et al. Risk factors associated with pelvic inflammatory disease. Sex Transm Infect. 2006 Dec. 82(6):452-7. [Medline]. [Full Text].

  53. Toth M, Patton DL, Esquenazi B, Shevchuk M, Thaler H, Divon M. Association between Chlamydia trachomatis and abnormal uterine bleeding. Am J Reprod Immunol. 2007 May. 57(5):361-6. [Medline].

  54. Peipert JF, Ness RB, Blume J, Soper DE, Holley R, Randall H, et al. Clinical predictors of endometritis in women with symptoms and signs of pelvic inflammatory disease. Am J Obstet Gynecol. 2001 Apr. 184(5):856-63; discussion 863-4. [Medline].

  55. Molander P, Finne P, Sjoberg J, Sellors J, Paavonen J. Observer agreement with laparoscopic diagnosis of pelvic inflammatory disease using photographs. Obstet Gynecol. 2003 May. 101(5 Pt 1):875-80. [Medline].

  56. Risser WL, Risser JM, Benjamins LJ, Feldmann JM. Incidence of Fitz-Hugh-Curtis syndrome in adolescents who have pelvic inflammatory disease. J Pediatr Adolesc Gynecol. 2007 Jun. 20(3):179-80. [Medline].

  57. Sanfilippo JS. The silent epidemic of Chlamydia: what are we missing here?. J Pediatr Adolesc Gynecol. 2008 Oct. 21(5):231-2. [Medline].

  58. Haggerty CL, Ness RB. Newest approaches to treatment of pelvic inflammatory disease: a review of recent randomized clinical trials. Clin Infect Dis. 2007 Apr 1. 44(7):953-60. [Medline].

  59. Tukeva TA, Aronen HJ, Karjalainen PT, Molander P, Paavonen T, Paavonen J. MR imaging in pelvic inflammatory disease: comparison with laparoscopy and US. Radiology. 1999 Jan. 210(1):209-16. [Medline].

  60. Burnett AM, Anderson CP, Zwank MD. Laboratory-confirmed gonorrhea and/or chlamydia rates in clinically diagnosed pelvic inflammatory disease and cervicitis. Am J Emerg Med. 2012 Sep. 30(7):1114-7. [Medline].

  61. Schoeman SA, Stewart CM, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of best single sample for finding chlamydia in women with and without symptoms: a diagnostic test study. BMJ. 2012 Dec 12. 345:e8013. [Medline]. [Full Text].

  62. Taylor-Robinson D, Stacey CM, Jensen JS, Thomas BJ, Munday PE. Further observations, mainly serological, on a cohort of women with or without pelvic inflammatory disease. Int J STD AIDS. 2009 Oct. 20(10):712-8. [Medline].

  63. Thomassin-Naggara I, Darai E, Bazot M. Gynecological pelvic infection: what is the role of imaging?. Diagn Interv Imaging. 2012 Jun. 93(6):491-9. [Medline].

  64. Horrow MM. Ultrasound of pelvic inflammatory disease. Ultrasound Q. 2004 Dec. 20(4):171-9. [Medline].

  65. Goharkhay N, Verma U, Maggiorotto F. Comparison of CT- or ultrasound-guided drainage with concomitant intravenous antibiotics vs. intravenous antibiotics alone in the management of tubo-ovarian abscesses. Ultrasound Obstet Gynecol. 2007 Jan. 29(1):65-9. [Medline].

  66. Del Frate C, Girometti R, Pittino M, et al. Deep retroperitoneal pelvic endometriosis: MR imaging appearance with laparoscopic correlation. Radiographics. 2006. 26(6):1705-18.

  67. Romero R, Espinoza J, Mazor M. Can endometrial infection/inflammation explain implantation failure, spontaneous abortion, and preterm birth after in vitro fertilization?. Fertil Steril. 2004 Oct. 82(4):799-804. [Medline].

  68. Liu B, Donovan B, Hocking JS, Knox J, Silver B, Guy R. Improving adherence to guidelines for the diagnosis and management of pelvic inflammatory disease: a systematic review. Infect Dis Obstet Gynecol. 2012. 2012:325108. [Medline]. [Full Text].

  69. Simms I, Vickers MR, Stephenson J, Rogers PA, Nicoll A. National assessment of PID diagnosis, treatment and management in general practice: England and Wales. Int J STD AIDS. 2000 Jul. 11(7):440-4. [Medline].

  70. Shih TY, Gaydos CA, Rothman RE, Hsieh YH. Poor provider adherence to the Centers for Disease Control and Prevention treatment guidelines in US emergency department visits with a diagnosis of pelvic inflammatory disease. Sex Transm Dis. 2011 Apr. 38(4):299-305. [Medline].

  71. Scholes D, Stergachis A, Heidrich FE, Andrilla H, Holmes KK, Stamm WE. Prevention of pelvic inflammatory disease by screening for cervical chlamydial infection. N Engl J Med. 1996 May 23. 334(21):1362-6. [Medline].

  72. Trent M, Haggerty CL, Jennings JM, Lee S, Bass DC, Ness R. Adverse adolescent reproductive health outcomes after pelvic inflammatory disease. Arch Pediatr Adolesc Med. 2011 Jan. 165(1):49-54. [Medline].

  73. Anschuetz GL, Asbel L, Spain CV, et al. Association between enhanced screening for Chlamydia trachomatis and Neisseria gonorrhoeae and reductions in sequelae among women. J Adolesc Health. 2012 Jul. 51(1):80-5. [Medline].

  74. US Preventive Services Task Force. Available at . Screening for Chlamydial Infection. Available at http://www.ahrq.gov/clinic/uspstf/uspschlm.htm. Accessed: March 26, 2010.

  75. Gift TL, Gaydos CA, Kent CK, Marrazzo JM, Rietmeijer CA, Schillinger JA, et al. The program cost and cost-effectiveness of screening men for Chlamydia to prevent pelvic inflammatory disease in women. Sex Transm Dis. 2008 Nov. 35(11 Suppl):S66-75. [Medline].

  76. Irwin KL, Moorman AC, O'Sullivan MJ, Sperling R, Koestler ME, Soto I, et al. Influence of human immunodeficiency virus infection on pelvic inflammatory disease. Obstet Gynecol. 2000 Apr. 95(4):525-34. [Medline].

  77. Mugo NR, Kiehlbauch JA, Nguti R, Meier A, Gichuhi JW, Stamm WE, et al. Effect of human immunodeficiency virus-1 infection on treatment outcome of acute salpingitis. Obstet Gynecol. 2006 Apr. 107(4):807-12. [Medline].

  78. Trent M, Ellen JM, Walker A. Pelvic inflammatory disease in adolescents: care delivery in pediatric ambulatory settings. Pediatr Emerg Care. 2005 Jul. 21(7):431-6. [Medline].

  79. Ness RB, Soper DE, Holley RL, et al. for the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) Study Investigators. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: Results from the pelvic inflammatory disease evaluation and clinical health (PEACH) randomized trial. Am J Obstet Gynecol. 2001. 186:929-37.

  80. Savaris RF, Teixeira LM, Torres TG, Edelweiss MI, Moncada J, Schachter J. Comparing ceftriaxone plus azithromycin or doxycycline for pelvic inflammatory disease: a randomized controlled trial. Obstet Gynecol. 2007 Jul. 110(1):53-60. [Medline].

  81. Bevan CD, Ridgway GL, Rothermel CD. Efficacy and safety of azithromycin as monotherapy or combined with metronidazole compared with two standard multidrug regimens for the treatment of acute pelvic inflammatory disease. J Int Med Res. 2003 Jan-Feb. 31(1):45-54. [Medline].

  82. Bradshaw CS, Chen MY, Fairley CK. Persistence of Mycoplasma genitalium following azithromycin therapy. PLoS One. 2008. 3(11):e3618. [Medline]. [Full Text].

  83. [Guideline] CDC. Update to CDC's sexually transmitted diseases treatment guidelines, 2006. fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. Apr 13 2007. 56(14):332-6.

  84. [Guideline] Centers for Disease Control and Prevention (CDC). Update to CDC’s Sexually transmitted diseases treatment guidelines, 2010: oral cephalosporins no longer a recommended treatment for gonococcal infections. MMWR Morb Mortal Wkly Rep. 2012 Aug 10;61(31):. 590-4. [Medline]. [Full Text].

  85. Bakken IJ, Ghaderi S. Incidence of pelvic inflammatory disease in a large cohort of women tested for Chlamydia trachomatis: a historical follow-up study. BMC Infect Dis. Aug 14 2009. 9(1):130.

 
Previous
Next
 
"Violin-string" adhesions of chronic Fitz-Hugh-Curtis syndrome.
Transabdominal ultrasonogram shows anechoic tubular structures in adnexa; finding is compatible with hydrosalpinx.
Endovaginal ultrasonogram reveals tubular structure with debris in left adnexa; finding is compatible with pyosalpinx.
Ultrasonogram shows markedly heterogeneous and thickened endometrium; finding is compatible with endometritis.
Ultrasonogram reveals bilateral complex masses in patient who had pyometrium; finding is compatible with tubo-ovarian abscess.
Transabdominal ultrasonogram demonstrates echogenic region within endometrium with dirty shadowing; finding is compatible with air in endometrium and endometritis. Additionally, bilateral complex masses are present; finding is compatible with tubo-ovarian masses.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.