eMedicine Specialties > Emergency Medicine > Obstetrics & Gynecology

Pelvic Inflammatory Disease

Iris Reyes, MD, Advisory Dean; Director of Quality Improvement, Associate Professor, Department of Emergency Medicine, University of Pennsylvania
Ritu Kumar, MD, Resident, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Stephanie Abbuhl, MD, Vice Chair, Associate Professor, Department of Emergency Medicine, University of Pennsylvania School of Medicine; Attending Physician in Emergency Services, Hospital of the University of Pennsylvania

Updated: Feb 4, 2009

Introduction

Background

Pelvic inflammatory disease (PID) is a spectrum of infections of the female genital tract that includes endometritis, salpingitis, tubo-ovarian abscess, and peritonitis.

Pathophysiology

Pelvic inflammatory disease is caused by organisms ascending to the upper female genital tract from the vagina and cervix. It most commonly is associated with Chlamydia trachomatis and Neisseria gonorrhoeae, but other organisms and, in many cases, multiple organisms, have been isolated.

Anaerobic bacteria, including those in the genera Peptococcus, Peptostreptococcus, and Bacteroides, appear to play an important role. The genital Mycoplasma and Ureaplasma organisms and the gut coliforms also have been isolated from the upper genital tract of women with pelvic inflammatory disease.

Frequency

United States

Pelvic inflammatory disease is the single most frequent serious infection encountered by women. The disease afflicts more than 1 million women each year and generates annual health care costs of approximately 4.2 billion dollars. It is responsible for nearly 250,000 hospitalizations per year.

Mortality/Morbidity

Several long-term sequelae have been clearly associated with pelvic inflammatory disease.

• Ectopic pregnancy rates are 12-15% higher in women who have had an episode of pelvic inflammatory disease.
• Tubal occlusion with infertility occurs at a rate of 12-50% in these patients, increasing with each episode of pelvic inflammatory disease.
• Chronic pelvic pain has been associated with pelvic inflammatory disease at an incidence as high as 18% after a single episode of the disease.

Sex

Pelvic inflammatory disease is a disease of the female upper genital tract.

Age

Sexually active women younger than 25 years are at greatest risk, although pelvic inflammatory disease can occur at any age.

Other risk factors include previous history of chlamydia or another sexually transmitted infection, prior episode of pelvic inflammatory disease, high number of sexual partners, inconsistent or no regular use of condoms, sexual intercourse at an early age, and women who exchange sex for money or drugs.

Screening recommendations
 
Based on published data, the US Preventive Services Task Force (USPSTF) recommends that all nonpregnant women younger than 24 years should be screened for chlamydia, regardless of their risk factors. Additionally, women older than 25 years should be screened if they are at increased risk (A level recommendation). Screening women older than 25 years who are not at increased risk carries a C level recommendation from the USPSTF. No data weigh the benefits and risks of screening men, and, thus, the USPSTF does not provide recommendations for chlamydia screening in men.

Clinical

History

• Most women with pelvic inflammatory disease typically report symptoms of bilateral lower abdominal pain.
• Vaginal discharge
• Low back pain
• Irregular vaginal bleeding
• Depending on the severity of the infection, patients with pelvic inflammatory disease may be minimally symptomatic or may present with toxic symptoms of fever, nausea, vomiting, and severe pain.
• Gonococcal pelvic inflammatory disease is thought to have an abrupt onset with more toxic symptoms than nongonococcal disease.
• Gonorrhea- and chlamydia-associated infections are more likely to cause symptoms toward the end of menses and in the first 10 days following the menstrual period.

Physical

Physical examination findings of pelvic inflammatory disease are described below.

• The lower abdomen is usually tender. This is a very sensitive but nonspecific finding.
• Pelvic examination
  • Mucopurulent cervical discharge
  • Cervical motion tenderness
  • Uterine tenderness
  • Adnexal tenderness (usually bilateral)
• An adnexal mass may be found in more extensive cases, suggesting a tubo-ovarian abscess, or peritonitis may be present, mimicking an acute surgical abdomen.
• The clinical diagnosis of pelvic inflammatory disease can be difficult and imprecise due to the nonspecific nature of the presenting signs and symptoms.
  • Diagnosis is also complicated because a subset of women with pelvic inflammatory disease appear to exhibit subtle symptoms that often are undiagnosed by a health care provider or are unappreciated by the patient.
  • Because of the serious potential complications of untreated pelvic inflammatory disease and the endemic prevalence of the infection, the Centers for Disease Control and Prevention (CDC) has adopted an approach to maximize diagnosis by using minimal criteria and by urging providers to maintain a low threshold for diagnosis and empiric treatment. Institute empiric treatment of pelvic inflammatory disease when a patient has all of the following minimal clinical criteria in the absence of an established cause other than pelvic inflammatory disease:
    • Lower abdominal tenderness on palpation
    • Adnexal tenderness
    • Cervical motion tenderness
• Data from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) trial shows that the presence of adnexal tenderness has a sensitivity of 95.5% for histologic endometritis. This trial supports the empiric treatment of all women at risk for pelvic inflammatory disease with adnexal tenderness and no other obvious cause. Based on data from the PEACH trial, the CDC recommends that all women at risk for pelvic inflammatory disease and who exhibit adnexal, uterine, or pelvic tenderness on bimanual examination, and no other explanation for these findings, be treated empirically for pelvic inflammatory disease.
• Additional criteria, especially in women with more severe clinical signs, can be used to increase the specificity of the diagnosis.
  • Oral temperature more than 38.3°C (101°F)
  • Abnormal cervical or vaginal discharge
  • Elevated erythrocyte sedimentation rate (ESR)
  • Elevated C-reactive protein level
  • White blood cells on saline wet mount of vaginal secretion
  • Laboratory documentation of cervical infection with N gonorrhoeae or C trachomatis

Causes

• N gonorrhoeae and C trachomatis traditionally have been considered the etiologic agents of pelvic inflammatory disease, alone or combined.
• A sexually transmitted disease (STD) organism is not recovered in a third of women with pelvic inflammatory disease.
• Facultative anaerobes consistent with the endogenous vaginal and perineal flora have also been identified as potential etiologic agents in pelvic inflammatory disease. These include the following flora:
  • Gardnerella vaginalis
  • Streptococcus agalactiae
  • Peptostreptococcus species
  • Bacteroides species (other than Bacteroides fragilis)
  • Genital Mycoplasma and Ureaplasma species, coliforms
• Other nongenital pathogens, such as Haemophilus influenzae and Haemophilus parainfluenzae, may be the causes of some pelvic inflammatory disease cases.
  • Actinomyces species have been linked to some pelvic inflammatory disease cases associated with intrauterine device (IUD) usage.
  • In less-developed countries, pelvic inflammatory disease may be due to a granulomatous salpingitis caused by Mycobacterium tuberculosis and Schistosoma species.

Differential Diagnoses

Workup

Laboratory Studies

• All female patients of childbearing age with lower abdominal pain require a pregnancy test. Pelvic inflammatory disease (PID) is the most common incorrect diagnosis in missed ectopic pregnancies. Although it is rare to have pelvic inflammatory disease in pregnancy, the disease can occur in the first 12 weeks of gestation before the decidua seals off the uterus from ascending bacteria.
• Complete blood cell count
  • Fewer than 50% of women with acute pelvic inflammatory disease have a white blood cell (WBC) count more than 10,000.
  • An elevated WBC count is not a CDC criterion for diagnosing pelvic inflammatory disease.
• The erythrocyte sedimentation rate (ESR) is included in the CDC's additional criteria for pelvic inflammatory disease. However, ESR may not be particularly helpful in the ED where other diagnoses that also may elevate ESR are present or under consideration.
• Perform a urinalysis on all patients with lower abdominal pain to exclude cystitis or pyelonephritis.
• Obtain gonorrhea and chlamydia cultures or other detection assays, (eg, enzyme-linked immunosorbent assay [ELISA], fluorescent antibody tests, DNA probes) on all patients during the pelvic examination.

Imaging Studies

• Pelvic ultrasonography
  • On transvaginal ultrasonography, acute pelvic inflammatory disease can present as tubal wall thickness greater than 5 mm, incomplete septae within the tube, fluid in the cul-de-sac, and the cogwheel sign (a cogwheel appearance on the cross-section tubal view). One study found that using color flow Doppler in conjunction with transvaginal ultrasonography was 100% sensitive for diagnosing pelvic inflammatory disease.¹ Further studies are needed to confirm this result.
  • Although pelvic ultrasonography is not used in the routine diagnosis of uncomplicated pelvic inflammatory disease, it is a valuable adjunct in the diagnosis of tubo-ovarian abscess.
  • Ultrasonography can also help diagnose other entities on the differential, including ovarian cyst and ovarian torsion.
• Magnetic resonance imaging is useful in diagnosing pelvic inflammatory disease, but it is not a practical tool due to its limited availability and significant cost. Although the cost of MRI is prohibitive, it is a more sensitive and specific imaging modality compared with ultrasonography in diagnosing pelvic inflammatory disease. On MRI, pelvic inflammatory disease can present as a fluid-filled fallopian tube or free fluid in the pelvis with polycysticlike ovaries.

Other Tests

• Venereal Disease Research Laboratory (VDRL) test
• Rapid plasma reagent test
• HIV test

Procedures

• Some experts believe that pelvic inflammatory disease is rare without a coexisting purulent endocervical infection and recommend a wet-mount examination from the os to look for numerous WBCs.

Treatment

Emergency Department Care

• All patients with pelvic inflammatory disease (PID) require antibiotics. The CDC recommends several parenteral and oral regimens in the 2002 Guidelines for Treatment of Sexually Transmitted Diseases.² These regimens are listed in Medication. A recent study demonstrated that, in conjunction with ceftriaxone, 1 g of azithromycin weekly for 2 weeks is equivalent to a 14-day course of doxycycline for treating mild pelvic inflammatory disease. The ease of dosing and less prohibitive cost makes azithromycin an attractive choice.
• Treatment should not be postponed due to the evidence that prevention of long-term sequelae is linked with timely administration of appropriate antibiotics.
• Analgesics
• Intravenous fluids, if dehydrated
• Recent studies indicate that oral outpatient treatment is as effective as inpatient parenteral treatment for mild-to-moderate cases of pelvic inflammatory disease. However, the CDC has established the following criteria for hospitalization based on observational data and consensus opinion:
  • Surgical emergencies, such as appendicitis, cannot be excluded.
  • Pregnancy
  • The patient does not respond clinically to oral antimicrobial therapy.
  • The patient is unable to follow or tolerate an outpatient oral regimen.
  • The patient has severe illness, nausea, vomiting, or high fever.
  • The patient has a tubo-ovarian abscess.
  • The patient is immunodeficient (eg, HIV infection with low CD4 counts, immunosuppressive therapy) or has another disease.

Consultations

• A gynecologist should be consulted if the patient is pregnant or a candidate for admission or if the diagnosis is unclear.
• Surgical consultation is indicated if acute appendicitis or other surgical emergency is being considered.

Medication

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Cefoxitin (Mefoxin) or cefotetan (Cefotan) plus doxycycline (Bio-Tab, Doryx)

Parenteral regimen A.
Cefoxitin and cefotetan are second-generation cephalosporins indicated for the management of infections caused by susceptible gram-positive cocci and gram-negative rods. Many infections caused by gram-negative bacteria that are resistant to some cephalosporins and penicillins respond to cefoxitin. Doxycycline inhibits protein synthesis and, thus, bacterial growth, by binding with the 30S and, possibly, the 50S ribosomal subunits of susceptible bacteria.
The parenteral therapy may be discontinued 24 h after a patient improves clinically. Continue doxycycline PO for 14 d. When tubo-ovarian abscess is present, clindamycin or metronidazole often is added to the doxycycline for better anaerobic coverage.

Dosing

Adult

Cefoxitin 2 g IV q6h or cefotetan 2 g IV q6h plus doxycycline 100 mg PO/IV q12h

Pediatric

<8 years: Not recommended
>8 years: Not established

Interactions

Consumption of alcohol within 72 h of cefotetan may produce disulfiramlike reactions; cefotetan may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) or aminoglycosides may increase nephrotoxicity; bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Reduce dosage by half if <10-30 mL/min CrCl and by a quarter if <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy; photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Clindamycin (Cleocin) plus gentamicin (Gentacidin, Garamycin)

Parenteral regimen B.
Clindamycin is a lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.
Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM.
If tubo-ovarian abscess is present, clindamycin is recommended instead of doxycycline.

Dosing

Adult

Clindamycin 900 mg IV q8h plus gentamicin
Loading dose 2 mg/kg IV/IM, followed by a 1.5 mg/kg maintenance dose IV/IM q8h; single dosing of gentamicin may be substituted; parenteral therapy may be discontinued 24 h after clinical improvement; continue doxycycline 100 mg PO bid or clindamycin 450 mg PO qid for 14 d

Pediatric

Not established

Interactions

Increases duration of neuromuscular blockade, induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin; coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Contraindications

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in severe renal and hepatic dysfunction; associated with severe and possibly fatal colitis; narrow therapeutic index (not intended for long-term therapy); caution in myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission

Ampicillin and sulbactam (Unasyn) plus doxycycline (Doryx)

Ampicillin and sulbactam is a combination antimicrobial agent that uses a beta-lactamase inhibitor with ampicillin. It covers skin, enteric flora, and anaerobes. It is not ideal for nosocomial pathogens.
Doxycycline inhibits protein synthesis and, thus, bacterial growth, by binding with the 30S and, possibly, the 50S ribosomal subunits of susceptible bacteria.

Dosing

Adult

Ampicillin and sulbactam 3 g IV q6h plus doxycycline 100 mg PO/IV q12h

Pediatric

<8 years: Not recommended
>8 years: Not established

Interactions

Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of PO contraceptives; bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Evaluate rash and differentiate from hypersensitivity reaction; photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Ceftriaxone (Rocephin) or cefoxitin (Mefoxin) plus doxycycline (Doryx)

This regimen is theoretically limited by poor anaerobic coverage. Depending on the clinical situation, consider adding metronidazole. Use of PO cephalosporins is not recommended for PID, only for cervicitis and urethritis.

Dosing

Adult

Ceftriaxone 250 mg IM once or cefoxitin 2 g IM plus probenecid 1 g PO in single dose once concurrently plus doxycycline 100 mg PO bid for 14 d

Pediatric

<8 years: Not recommended
>8 years: Not established

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity; bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; caution in breastfeeding women and those with allergy to penicillin

Follow-up

Further Inpatient Care

• Clinical improvement should occur within 3 days of initiating therapy.
• Consider further diagnostic tests, laparoscopy, or both if symptoms do not improve or worsen.
• Surgical intervention may be indicated in patients with an enlarging pelvic mass despite medical therapy, intraperitoneal bleeding secondary to erosion into a vessel, or abscess rupture.
• Remove IUDs following institution of antibiotics.

Further Outpatient Care

• Patients should continue oral antibiotics for a full 2 weeks.
• Follow-up is suggested in 3 days to monitor clinical improvement.
• Sexual abstinence is advised until cure is achieved.
• Treatment of sexual contacts is essential to prevent reinfection.
• The CDC recommends the treatment of partners who have had sex with the patient during the 60 days preceding onset of symptoms.

Transfer

• Transfer is advised only if a patient is stable and only if the hospital is incapable of managing acutely ill patients with gynecological emergencies.

Deterrence/Prevention

• All patients should routinely receive sexual counseling, including advice to practice safe sex with the use of condoms. Other areas of discussion include limiting the number of sexual partners and avoiding contact with high-risk partners. Adolescents should be advised to delay the onset of sexual activity until the age of 16 years or older, as they are at an increased risk for pelvic inflammatory disease.
• Barrier contraceptives (eg, diaphragms with spermicidal agents) and oral contraceptives are thought to reduce the risk for developing pelvic inflammatory disease.
• Intrauterine devices (IUDs) predispose patients to pelvic inflammatory disease, predominantly during the first few months after insertion.
• Frequent vaginal douching was considered to be a risk factor for pelvic inflammatory disease, but recent studies reveal no clear association.⁴

Complications

• Ectopic pregnancy is 6 times more likely in women who have had pelvic inflammatory disease than in those who have not.
• Tubal damage and scarring can result in infertility. One study demonstrated infertility in 8% of women after a single episode of pelvic inflammatory disease and in 40% of women after 3 or more episodes.
• One investigator found chronic pelvic pain in up to 18% of women after pelvic inflammatory disease had resolved.

Prognosis

• The prognosis is good if diagnosed and treated early.
• A poor prognosis is related to late therapy and continued unsafe lifestyle.

Patient Education

• Emergency physicians should emphasize behavioral and contraceptive methods to prevent the acquisition of sexually transmitted diseases (STDs).
• HIV testing should be recommended.
• Patients must be encouraged to complete the recommended antibiotic treatment for the full 14 days.
• Sexual partners of patients diagnosed with pelvic inflammatory disease must be treated to prevent reinfection.
• For excellent patient education resources, visit eMedicine's Women's Health Center, Sexually Transmitted Diseases Center, and Pregnancy and Reproduction Center. Also, see eMedicine's patient education articles Pelvic Inflammatory Disease, Birth Control Overview, Birth Control FAQs, and Female Sexual Problems.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose and treat patients with pelvic inflammatory disease (PID) in a timely manner
• Failure to test for pregnancy and potentially to misdiagnose ectopic pregnancy
• Failure to obtain a medication allergy history
• Failure to test for syphilis
• Failure to advise that sexual partners must be treated

References

1. Molander P, Sjoberg J, Paavonen J, Cacciatore B. Transvaginal power Doppler findings in laparoscopically proven acute pelvic inflammatory disease. Ultrasound Obstet Gynecol. Mar 2001;17(3):233-8. [Medline].

2. CDC. Sexually transmitted diseases treatment guidelines 2002. Centers for Disease Control and Prevention. MMWR Recomm Rep. May 10 2002;51(RR-6):1-78. [Medline].

3. 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. April 13 2007;56(14):332-336.

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

5. CDC. 1998 guidelines for treatment of sexually transmitted diseases. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep. Jan 23 1998;47(RR-1):1-111. [Medline].

6. FDA. Center for Drug Evaluation and Research. Drugs to be discontinued. Available at www.fda.gov/cder/drug/shortages/#disc. Accessed May 2, 2007.

7. Hillis SD, Joesoef R, Marchbanks PA. Delayed care of pelvic inflammatory disease as a risk factor for impaired fertility. Am J Obstet Gynecol. May 1993;168(5):1503-9. [Medline].

8. Hollier LM, Workowski K. Treatment of sexually transmitted diseases in women. Obstet Gynecol Clin North Am. Dec 2003;30(4):751-75, vii-viii. [Medline].

9. McCormack WM. Pelvic inflammatory disease. N Engl J Med. Jan 13 1994;330(2):115-9. [Medline].

10. Meyers DS, Halvorson H, Luckhaupt S. Screening for chlamydial infection: an evidence update for the U.S. Preventive Services Task Force. Ann Intern Med. Jul 17 2007;147(2):135-42. [Medline].

11. Ness RB, Hillier SL, Kip KE. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet Gynecol. Oct 2004;104(4):761-9. [Medline].

12. Ness RB, Trautmann G, Richter HE, et al. Effectiveness of treatment strategies of some women with pelvic inflammatory disease: a randomized trial. Obstet Gynecol. Sep 2005;106(3):573-80. [Medline].

13. Rice R, Schwartz D, Knapp J, et al. Pelvic inflammatory disease. In: Morse, Moreland, Holmes, eds. Atlas of Sexually Transmitted Diseases and AIDS. 1996:134-47.

14. Sam JW, Jacobs JE, Birnbaum BA. Spectrum of CT findings in acute pyogenic pelvic inflammatory disease. Radiographics. Nov-Dec 2002;22(6):1327-34. [Medline].

15. Soper DE. Pelvic inflammatory disease. Infect Dis Clin North Am. Dec 1994;8(4):821-40. [Medline].

16. Suss AL, Homel P, Hammerschlag M, Bromberg K. Risk factors for pelvic inflammatory disease in inner-city adolescents. Sex Transm Dis. May 2000;27(5):289-91. [Medline].

17. Walker CK, Wiesenfeld HC. Antibiotic therapy for acute pelvic inflammatory disease: the 2006 Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis. Apr 1 2007;44 Suppl 3:S111-22. [Medline].

18. Westrom L, Joesoef R, Reynolds G, Hagdu A, Thompson SE. Pelvic inflammatory disease and fertility. A cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sex Transm Dis. Jul-Aug 1992;19(4):185-92. [Medline].

19. Wiesenfeld HC, Sweet RL, Ness RB, Krohn MA, Amortegui AJ, Hillier SL. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis. Jul 2005;32(7):400-5. [Medline].

Keywords

pelvic inflammatory disease, PID, infertility, infections of female upper genital tract, endometritis, tuboovarian abscess, peritonitis, Chlamydia trachomatis, C trachomatis, Neisseria gonorrhoeae, N gonorrhoeae, Peptococcus, Peptostreptococcus species, Bacteroides species, genital Mycoplasma, Ureaplasma species, gut coliforms, chronic pelvic pain, vaginal discharge, low back pain, irregular vaginal bleeding, gonococcal PID, mucopurulent cervical discharge, uterine tenderness, adnexaltenderness, sexually transmitted disease, STD, Gardnerella vaginalis, Streptococcus agalactiae, Haemophilus influenzae, Haemophilus parainfluenzae, Actinomyces species, granulomatous salpingitis, Mycobacterium tuberculosis, Schistosoma species

Contributor Information and Disclosures

Author

Iris Reyes, MD, Advisory Dean; Director of Quality Improvement, Associate Professor, Department of Emergency Medicine, University of Pennsylvania
Iris Reyes, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Ritu Kumar, MD, Resident, Department of Emergency Medicine, Hospital of the University of Pennsylvania
Ritu Kumar, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Student Association/Foundation, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Stephanie Abbuhl, MD, Vice Chair, Associate Professor, Department of Emergency Medicine, University of Pennsylvania School of Medicine; Attending Physician in Emergency Services, Hospital of the University of Pennsylvania
Stephanie Abbuhl, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Mark Zwanger, MD, MBA, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University
Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)