Pelvic Inflammatory Disease Workup
- Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM; Chief Editor: Michel E Rivlin, MD more...
A number of procedures can be performed to improve the diagnosis of pelvic inflammatory disease (PID) and its complications. These procedures are not necessary, nor are they indicated, in the management of every case of PID. However, because of the difficulty of definitive clinical diagnosis and the number of surgical and gynecologic emergencies that may have similar presentations, the clinician should be aware of these modalities.
Procedures that may be appropriate for some patients, along with the corresponding findings specific for PID, are as follows:
Transvaginal ultrasonographic scanning or magnetic resonance imaging (MRI) showing thickened, fluid-filled tubes with or without free pelvic fluid or tubo-ovarian abscess (TOA)
Endometrial biopsy showing endometritis
Laparoscopy is the criterion standard for the diagnosis of PID, but the diagnosis of PID in emergency departments and clinics is often based on clinical criteria, with or without additional laboratory and imaging evidence. No single test is highly specific and sensitive for PID, but laboratory tests, imaging studies, and procedures may be used to increase the specificity of the diagnosis.
Additional criteria that improve diagnostic specificity include the following:
Oral temperature higher than 38.3° C (101° F)
Abnormal cervical or vaginal mucopurulent discharge
Abundant white blood cells (WBCs) on saline microscopy of vaginal secretions
Elevated erythrocyte sedimentation rate (ESR)
Elevated C-reactive protein (CRP) level
Laboratory evidence of cervical infection with N gonorrhoeae or C trachomatis (via culture or DNA probe)
In addition, obtaining a sample from the urethra in women with suspected PID can increase the diagnostic yield for gonorrhea and chlamydial infection. This step is recommended only if the more sensitive nucleic acid amplification test (NAAT) is unavailable.
Perform a pregnancy test. If the results are positive, the possibility of ectopic pregnancy must be addressed. Pregnancy also directly influences selection of an antibiotic regimen and consideration of the patient for admission.
On a complete blood count (CBC), fewer than 50% of women with acute PID have a WBC count higher than 10,000/µL. Because of its poor sensitivity and specificity, an elevated WBC count is not among the diagnostic criteria for PID formulated by the Centers for Disease Control and Prevention (CDC). Blood cultures are not helpful in the diagnosis of PID.
In fact, no single test is highly specific and sensitive for PID; however, a number of tests may be used to increase the specificity of the clinical diagnosis. Vaginal secretions that have been treated with saline and potassium hydroxide can be examined for leukorrhea (>10 WBC/high-power field; >1 WBC/epithelial cell), trichomoniasis, and clue cells.[16, 59] The presence of leukorrhea was found to be the most sensitive, laboratory indicator of upper tract infection, though not a specific one; the absence of leukorrhea is a negative predictor of PID.
Gonorrhea DNA probes and cultures are generally used to support the diagnosis and to provide epidemiologic data for public health departments. However, they are frequently negative in later stages of PID.
Chlamydial vulvovaginal or endocervical DNA probes and cultures are generally used to support the diagnosis and to provide epidemiologic data for public health departments, though recovery rates from the cervix vary widely (5-56%). Quantitative culture for Chlamydia identifies rapidly replicating bacteria that appear to be associated with active disease. However, DNA probe and culture results are often not available to the emergency physician at the time of initial evaluation.
One study suggested that women with high titers of immunoglobulin G (IgG) chlamydial antibodies, acute pelvic pain, and a clinical picture suggestive of PID were more likely to have salpingitis than adhesions alone. Those patients with high titers and chronic pelvic pain but with a clinical picture that did not suggest PID were more likely to have adhesions alone. In the investigators’ view, their limited data suggested that serologic testing might help establish the diagnosis.
Other tests that may be considered include the following:
Rapid protein reagin (RPR) test for syphilis (the incidence of which is again increasing in the United States)
Hepatitis virus and HIV
Urinalysis to help exclude urinary tract infections – Note, however, that a positive urinalysis does not exclude PID, because any inflammatory process in the contiguous pelvis can produce WBCs in the urine
Ultrasonographic scanning may be performed for cases of suspected PID in which clinical findings are nondiagnostic. Transvaginal ultrasonography is superior to transabdominal ultrasonography for diagnosing PID, as well as endometrial abnormalities and pelvic masses (see the images below). This modality is readily available and noninvasive and can be performed at the patient’s bedside.
There are no large randomized trials addressing the specificity and sensitivity of bedside ultrasonography for the diagnosis of PID. The literature demonstrates that the accuracy of this technique depends on the criteria used to indicate PID, the quality of the equipment, and the experience of the individual operator performing the test.
Transvaginal ultrasonography has poor sensitivity (81%) and specificity (78%) in mild or atypical PID. Helpful findings include thickened (>5 mm), fluid-filled fallopian tubes; thickened cilia; indistinct endometrial borders; ovaries with multiple small cysts; and moderate-to-large amounts of free pelvic fluid in acute, severe PID. Small amounts of free pelvic fluid have not been shown to be a discriminatory finding. These findings alone are not sufficiently specific to permit a definitive diagnosis of PID.
In the patient who appears toxic or has asymmetric pelvic findings, ultrasonographic scanning is an important diagnostic tool for the identification of a TOA. Pelvic abscesses may be seen as complex adnexal masses with multiple internal echoes. The modality has been shown to demonstrate as many as 70% of adnexal masses missed on physical examination.
Pelvic ultrasonographic scanning is also useful in evaluating the possibility of ectopic pregnancy in patients whose differential diagnosis includes both that condition and PID. The modality can also be helpful in evaluating other disorders in the differential diagnosis, including hemorrhagic ovarian cyst, ovarian torsion, endometrioma, and appendicitis. (At some adult academic medical centers, however, ultrasonography is considered adequate as a solo imaging modality to rule out appendicitis.)
Ultrasonographic results in patients with PID may be normal or nonspecific because salpingitis alone is not usually associated with imaging findings. Positive ultrasonographic findings in PID may include the following:
The uterus may be ill defined because of inflammation; however, inflammation of the uterus is an unusual finding
Endometritis may result in central-endometrial-cavity echo thickening and heterogeneity
Hydrosalpinx is depicted as a fluid-filled fallopian tube – If the fallopian tube walls are thickened and if debris is present within the tube, pyosalpinx should be considered in the differential diagnosis, but a pyosalpinx may be imaged as an echoless tube, whereas an imaged echo-filled tube may be from proteinaceous but noninfected fluid in a hydrosalpinx
Oophoritis results in enlarged ovaries with ill-defined margins that often appear adherent to the uterus; adjacent free fluid may be present in the adnexa or cul-de-sac
TOAs are depicted as complex adnexal masses with thickened walls and central fluid
Pelvic infection, with findings of tubal inflammation and hydrosalpinx detected by Doppler studies, is one of the most specific criteria in diagnosing PID 
Thickening of the endometrium is nonspecific for PID because this finding may also be seen with endometrial hyperplasia, polyps, or cancer. Knowledge of the patient’s clinical findings and other signs of infection can help in the differential diagnosis.
Hydrosalpinx and pyosalpinx can usually be readily distinguished from pelvic veins and bowel by visualizing the color flow within the patent blood vessels and peristalsis within the bowel.
Imaging findings in TOAs are usually nonspecific and must be distinguished from the following:
Abscesses from adjacent organs
Laparoscopy is the criterion standard for the diagnosis of PID. It is significantly more specific and sensitive than are clinical criteria alone. The minimum criteria for diagnosing PID laparoscopically include tubal wall edema, visible hyperemia of the tubal surface, and the presence of exudate on the tubal surfaces and fimbriae.
Pelvic masses consistent with TOA or ectopic pregnancy can be directly visualized. Hepatic abscess exudate or adhesions may be visible. Material can be obtained for definitive culture and histologic studies.
The main drawbacks of laparoscopy are that the procedure is expensive and invasive, exhibits interobserver variability, and requires an operating room and anesthesia. In addition, findings on laparoscopy do not necessarily correlate with the severity of illness, in that only the surfaces of structures are visible through the scope. In as many as 20% of cases, laparoscopy may not define PID fully.
Computed tomography (CT) may also be used as the initial diagnostic study for the investigation of nonspecific pelvic pain in a female, and PID may be found incidentally. Because of concerns about radiation exposure, ultrasonography is preferred to CT as the triaging tool in a female child or adolescent with right lower quadrant or pelvic pain.
In cases of PID in which no evidence of an abscess is found, CT scan findings are nonspecific. Inflammation obliterates the pelvic fat planes, with thickening of the fascial planes. Endometritis manifests as enlargement of the uterine cavity. If hydrosalpinx is present, a fluid-filled tubular structure may be seen in the adnexa.
Typically, a TOA is visualized as a mass; the mass may have regular margins and contain debris similar to that seen in endometriomas or hemorrhagic cysts. The margins may be thick and irregular. There may also be an associated low-attenuation area that may represent an adjacent or contained fluid-filled fallopian tube. Many adult centers prefer CT to ultrasonography when a diagnosis of appendicitis is in question.
Tubular, fluid-filled, nonvascular structures in the pelvis that are associated with an adnexal mass are suggestive of dilated fallopian tubes that correlate with cases of PID. A finding of an adjacent or surrounding complex mass confirms the diagnosis of TOA.
Magnetic Resonance Imaging
Although MRI has relatively high specificity (95%) and sensitivity (95%) in this setting, it is costly and is rarely indicated in cases of acute PID.
Hydrosalpinx is visualized on MRI as a tubular structure with low signal intensity on T1-weighted scans and high signal intensity on T2-weighted images. If the walls are thickened, pyosalpinx should be considered in the differential diagnosis. Oophoritis may be evidenced by enlarged, polycystic-appearing ovaries with ill-defined margins and adjacent fluid.
TOAs often appear as thick-walled masses with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Occasionally, TOAs may be isointense or hyperintense on T1-weighted images and may have heterogeneous signal intensity on T2-weighted images.
Culdocentesis can be performed rapidly in the emergency department. With the advent of transvaginal ultrasonographic scanning, culdocentesis is rarely performed today, but it remains valuable in settings where current technology is unavailable.
For the procedure, an 18-gauge spinal needle attached to a 20-mL syringe is inserted transvaginally into the cul-de-sac. Normally, this yields only 2-4 mL of clear to straw-colored free pelvic fluid; purulent fluid indicates an infectious or inflammatory process.
The potential positive findings of leukocytes and bacteria are nonspecific: They may indicate PID, or they may be a product of another infectious or inflammatory process in the pelvis (eg, appendicitis or diverticulitis), or they may result from contamination with vaginal contents. A yield of more than 2 mL of nonclotting blood is consistent with ectopic pregnancy.
Endometrial biopsy can be used to determine the histopathologic diagnosis of endometritis, a condition that is uniformly associated with salpingitis. Endometrial biopsy is approximately 90% specific and 90% sensitive. The procedure is performed with an endometrial suction pipette or curette and is well tolerated. Specimens for culture may also be obtained during the procedure, but these are frequently contaminated with vaginal flora.
Current CDC guidelines recommend endometrial biopsy in women undergoing laparoscopy who have no visible signs of salpingitis, on the grounds that endometritis may be the only sign of PID. Diagnostic use of endometrial biopsy in the emergency department is limited; significant operator training is required, and the results of the procedure are not immediately available to the clinician.
Endometrial biopsy findings usually confirm the presence of infection but rarely identify the causative organism. Chronic endometritis is more commonly seen than acute endometritis.
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].
Rivlin ME, Hunt JA. Ruptured tuboovarian abscess. Is hysterectomy necessary?. Obstet Gynecol. 1977 Nov. 50 (5):518-22. [Medline].
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].
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].
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].
Workowski KA, Berman S. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep. 2010 Dec 17. 59:1-110. [Medline]. [Full Text].
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].
Paavonen J. Chlamydia trachomatis infections of the female genital tract: state of the art. Ann Med. 2012 Feb. 44(1):18-28. [Medline].
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].
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.
[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].
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].
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].
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.
Mylonas I. Female genital Chlamydia trachomatis infection: where are we heading?. Arch Gynecol Obstet. 2012 May. 285(5):1271-85. [Medline].
Ross JD. Is Mycoplasma genitalium a cause of pelvic inflammatory disease?. Infect Dis Clin North Am. 2005 Jun. 19(2):407-13. [Medline].
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].
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].
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].
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.
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].
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].
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].
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].
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].
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].
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].
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].
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].
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].
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].
Shelton JD. Risk of clinical pelvic inflammatory disease attributable to an intrauterine device. Lancet. 2001 Feb 10. 357(9254):443. [Medline].
[Guideline] CDC, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. Aug 4 2006. 55(RR-11):1-94.
Kelly EK, Rudinsky SW. Intrauterine contraception: current evidence-based recommendations. J Midwifery Womens Health. 2007 Sep-Oct. 52(5):505-7. [Medline].
Meirik O. Intrauterine devices - upper and lower genital tract infections. Contraception. 2007. 06;75(6 Suppl/):S41-7.
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.
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].
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].
Levgur M, Duvivier R. Pelvic inflammatory disease after tubal sterilization: a review. Obstet Gynecol Surv. 2000 Jan. 55(1):41-50. [Medline].
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].
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].
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].
World Health Organization. Sexually transmitted infections. Available at http://www.who.int/mediacentre/factsheets/fs110/en/. Accessed: February 2, 2010.
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].
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].
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].
Banikarim C, Chacko MR. Pelvic inflammatory disease in adolescents. Adolesc Med Clin. 2004 Jun. 15 (2):273-85, viii. [Medline].
Zeger W, Holt K. Gynecologic infections. Emerg Med Clin North Am. 2003 Aug. 21 (3):631-48. [Medline].
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].
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].
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].
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].
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].
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].
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].
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].
Sanfilippo JS. The silent epidemic of Chlamydia: what are we missing here?. J Pediatr Adolesc Gynecol. 2008 Oct. 21(5):231-2. [Medline].
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].
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].
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].
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].
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].
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].
Horrow MM. Ultrasound of pelvic inflammatory disease. Ultrasound Q. 2004 Dec. 20(4):171-9. [Medline].
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].
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.
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].
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].
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].
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].
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].
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].
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].
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.
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].
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].
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].
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].
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.
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].
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].
Bradshaw CS, Chen MY, Fairley CK. Persistence of Mycoplasma genitalium following azithromycin therapy. PLoS One. 2008. 3(11):e3618. [Medline]. [Full Text].
[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.
[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].
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.