Pelvic Inflammatory Disease

OVERVIEW: What every practitioner needs to know

Are you sure your patient has pelvic inflammatory disease? What are the typical findings for this disease?

Pelvic inflammatory disease (PID) refers to an inflammatory process of the upper genital tract in females caused by an ascending infection. PID is a spectrum of disorders and can affect any or all of the genital structures from the cervix to the uterus, tubes or peritoneum (endocervicitis, endometritis, salpingitis or peritonitis). While PID is considered to be a disease primarily affecting sexually-active females, PID can occur in sexually inactive girls and women. PID is unusual, but has been reported, in premenarchal girls.

Acute PID can be difficult to diagnose because of the wide variation in presenting symptoms. Lower abdominal or pelvic pain is the most common presenting symptom of PID, but patients with PID may also have abnormal vaginal discharge, nausea or vomiting, low back pain, irregular bleeding (either intermenstrual or postcoital bleeding), or dysuria. Fever is present in less than one-half of patients.

What other disease/condition shares some of these symptoms?

Due to the range in symptoms that patients with PID can experience, there are a number of other clinical concerns that providers most consider when evaluating a patient who might have this diagnosis:

Pregnancy: always perform a pregnancy test when evaluating a patient with suspected PID

-Ectopic

-Intrauterine

Gynecologic Pathology:

-Bacterial vaginosis

-Yeast vulvovaginitis

-Uterine fibroids

-Endometriosis

-Ovarian cysts

-Ovarian torsion

Genitourinary disorders:

-Urinary tract infections

-Nephrolithiasis

-Pyelonephritis

-Gastrointestinal illness

-Diverticulitis

-Appendicitis

-Gastroenteritis

-Cholecystitis

-Inflammatory bowel disease

What caused this disease to develop at this time?

There are several important risk factors for PID, including exposure of the upper genital tract to microbial pathogens and epidemiologic factors.

PID risk factors include:

Neisseria gonorrhoeae (GC) and Chlamydia trachomatis (CT)

Non gonococcal, non-chlamydial pathogens

Bacterial vaginosis

Sexual Activity

Douching

Recent instrumentation of the uterus

Disruption of the endocervical barrier

Neisseria gonorrhoeae and Chlamydia trachomatis are thought to be important causative agents of pelvic inflammatory disease. Nationally, between 5.1-11.0% of 15 to 24 year old patients screened for Chlamydia at family planning clinics will test positive for Chlamydia. Often the infection can be clinically silent and the patient will present with PID.

Non gonococcal, non-chlamydial pathogens that may cause PID include any of the normal flora of the vagina (streptococci, staphylococci, Enterobacteriaceae like Klebsiella, Escherichia coli and Proteus spp as well as anaerobic bacteria) or other sexually transmitted pathogens like Mycoplasma genitalium. Recent studies suggest that the proportion of PID cases attributed to CT and GC is declining with <50% of patients diagnosed with clinic PID testing positive for CT or GC.

Sexual activity:

Beyond the microbial milieu, several epidemiologic factors of women and their sexual partner(s) are associated with a risk of PID. A woman’s age and her age at first intercourse are associated with PID. Women under age 25 account for the majority of cases of PID, primarily due to an increased risk of acquisition of gonorrhea and chlamydia in sexually active adolescents. There is a higher prevalence of PID treatment reported among females who had their first vaginal intercourse at younger ages, particularly <15 years. Patients with a history of PID are at risk of recurrent PID. In a case-control study of urban women, prior involvement with a child protection agency, prior suicide attempt, alcohol use before intercourse and current chlamydial infections were also identified as risk factors for PID.

Finally, hygienic factors may play a role in the development of PID. Douching is known to increase the risk for PID, presumably by altering the normal vaginal flora.

Sexual partners contribute to a risk of PID as well. Patients with a greater number of male sex partners in the last 12 months had higher proportions of ever being treated for PID and adolescents with PID were more likely to have older sex partners.

Recent instrumentation of the uterus:

Instrumentation of the uterus, which disrupts the cervical mucous barrier, increases the risk of PID, including procedures such as termination of pregnancy, hysterosalpingogram, and placement of an intrauterine device. While there was a historic association between intrauterine devices and PID, modern intrauterine devices likely cause little or no increased risk for PID beyond the first 3 weeks after insertion of the IUD.

Disruption of the endocervical barrier can lead to PID:

Typically, the endocervical canal and its mucus plug provide a barrier between the upper genital tract and potentially pathogenic bacteria of the vagina. When disruption of the endocervical barrier occurs, either due to a change in the character of cervical mucus or due to an alteration of the normal vaginal ecosystem, the risk for PID increases. PID can occur from ascending infection, but can also occur from direct spread for another organ, i.e., appendicitis. Typically PID which spreads from a contiguous organ will be more likely to be unilateral than bilateral.

Bacterial vaginosis is associated with PID:

Bacterial vaginosis is a non-inflammatory condition in which the anaerobic bacteria of the vagina predominate over the normally dominant hydrogen peroxide-producing lactobacilli. This alteration of the typical balance of microflora can lead to the degradation of the cervical mucus plug and naturally occurring antimicrobials, thereby increasing susceptibility to ascending infection. Bacterial vaginosis may be present in up to two thirds of cases of PID. It probably increases the risk of PID but is not solely causative.

PID is a clinical diagnosis based on exam findings, not laboratory studies. However, some studies may be helpful in suggesting the diagnosis, including gonorrhea and chlamydia testing, vaginal culture and wet mount (saline microscopy), white blood cell count, sedimentation rate or endometrial biopsy, but treatment should not be delayed for the results of laboratory studies if there is a clinical suspicion, with the only possible exception being a pregnancy test as positive pregnancy will influence the treatment regimen.

Pregnancy test:

A urine hCG test should be obtained immediately to test for pregnancy as treatment will be influenced if pregnancy testing is positive.

Serum and vaginal studies of infection:

Due to the sequelae of untreated PID resulting, treatment should be initiated when PID is clinically suspected; however the following tests may aid in the evaluation of a patient in whom PID is being considered:

Gonorrhea and chlamydia testing

Vaginal culture and microscopy

Serum testing

HIV testing

HIV testing:

Full screening for sexually transmitted infections, including HIV, should be recommended. HIV does not cause PID per se, but women with HIV are more likely to have abscess formation and require surgical intervention than HIV negative women.

Gonorrhea and chlamydia testing:

Due to the proportion of PID caused by gonorrhea and chlamydia, urine or cervical gonorrhea and chlamydia testing is recommended in the initial evaluation; however, empiric diagnosis and treatment should not be delayed for laboratory results.

Unfortunately, culture for chlamydia has low sensitivity for chlamydial infection. Endocervical or vaginal nucleic acid amplification tests have the highest sensitivity for chlamydia and gonorrheal infection, over 90%. If the patient refuses speculum examination, the patient or physician can collect a vaginal swab. If needed, the patient can collect a direct urine sample (non clean catch) to test for chlamydia and gonorrhea. Although this is less sensitive for chlamydial infection (80.6%), the urine nucleic acid amplification test is still more sensitive than culture and is non invasive.

Vaginal culture and microscopy:

Given that PID is typically a polymicrobial infection, a culture will detect additional organisms which are not tested with the nucleic acid amplification test.

It should be noted that the absence of vaginal white blood cells on saline microscopy of vaginal fluid makes the diagnosis of PID less likely (negative predictive value of 94.5% in one study) and women with normal serum WBC, wet mount WBC and serum ESR are very unlikely to have upper genital tract disease.

Serum tests:

An elevated serum white blood cell count, erthyrocyte sedimentation rate or C-reactive protein, laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis can support the diagnosis, but PID cannot be excluded if these factors are absent.

Electrolytes and a serum creatinine should be obtained in patients who appear septic or hemodynamically unstable.

Endometrial biopsy:

Invasive testing can be performed if a diagnosis is uncertain or if the patient has failed to respond to appropriate therapy. Endometrial biopsy demonstrating the presence of plasma cells in endometrial stroma and neutrophils in the endometrial epithelium is considered one of the most specific studies for confirming PID, but treatment can be initiated without such invasive procedure.

Ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI) have all been considered in the evaluation of PID, but none are required. The CDC considers ultrasound or MRI showing thickened, fluid-filled tubes with or without free pelvic fluid or tuboovarian complex suggesting pelvic infection among the most specific criteria for diagnosing PID, but neither is necessary to make the diagnosis and begin treatment. Such imaging would be warranted if there were a pelvic mass on examination, the patient was not responding to appropriate antibiotic therapy or if there were other pathology suspected as possible diagnoses (ie. if the patient’s clinical history was suspicious for appendicitis).

Laparoscopy can also be used to help diagnose PID.

Additional Ultrasound findings in PID:

Other findings suggestive of PID on ultrasound include tubal wall thickness greater than 5 mm, incomplete septae within the tube, fluid in the cul-de-sac and a cogwheel appearance on the cross-section tubal view. In addition, ultrasound can also help to identify the presence or absence of tuboovarian abscess, a potential complication of PID.

Additional MRI findings in PID:

MRI can also be used to detect tubal wall thickening, pyosalpinx (fallopian tube filled with purulent fluid), tuboovarian abscess or free fluid, but is more expensive and not as readily available as ultrasound.

CT findings in PID:

CT scan findings of PID include inflammatory changes or thickening of the pelvic viscera and adjacent abdominal organs. Also, CT can be useful for evaluating the appendix or contiguous organs in non-sexually active or prepubertal patients, where the source of primary infection may be gastrointestinal etiology. However, the patient is exposed to radiation with this modality of imaging.

Laparoscopic findings in PID:

Direct imaging during laparoscopy, revealing features of PID such as salpingitis or peritonitis with fibrinoid exudates on the serosal surfaces of the pelvic organs can also be helpful in diagnosing PID, but is clearly associated with high cost and potential for surgical risk.

Please see the previous information regarding the minimum criteria and signs that support a diagnosis of pelvic inflammatory disease.

If you are able to confirm that the patient has pelvic inflammatory disease, what treatment should be initiated?

For women with presumed PID (genital tract inflammation with pelvic organ tenderness), empiric, broad spectrum antibiotic treatment of likely pathogens, particularly N. gonorrhoeae and C. trachomatis and the common polymicrobial vaginal flora, should be initiated. While it is not necessary to await the results of laboratory or imaging studies before starting treatment, it is important to collect diagnostic tests for gonorrhea and chlamydia before beginning therapy. Testing for pregnancy is important, both to determine the appropriate treatment location (inpatient or outpatient) and to guide antimicrobial choices (to limit teratogen exposure in the case of positive pregnancy testing).

2015 CDC criteria for inpatient therapy:

The CDC recommends inpatient therapy for women with any of the following criteria:

surgical emergencies (e.g., appendicitis) cannot be excluded;

the patient is pregnant;

the patient is unable to tolerate or does not respond clinically to oral antimicrobial therapy;

the patient has severe illness, nausea and vomiting, or high fever; or

the patient has a tubo-ovarian abscess (at least 24 hours of inpatient observation is recommended)

Inpatient or parenteral regimens:

For women who meet criteria for inpatient or parenteral therapy, the following treatment regimens are recommended by the CDC:

Parenteral Regimen A

Parenteral Regimen B

Alternative Parenteral Regimen

Recommended Parenteral Regimen A:

Cefotetan 2 g IV every 12 hours

Cefoxitin 2 g IV every 6 hours

PLUS

Doxycycline 100 mg orally or IV every 12 hours (oral and IV administration offers similar bioavailability; however because of pain associated with IV infusion, oral administration is preferred and IV routes are recommended for patients unable to tolerate oral therapy)

Discontinue IV therapy 24 hours after clinical improvement and continue oral doxycycline 100 mg twice daily for a total of 14 days of therapy.

For patients with tuboovarian abscess, oral clindamycin or metronidazole should be administered with doxycycline for continued therapy rather than doxycycline alone.

Parenteral Regimen B:

Clindamycin 900 mg IV every 8 hours

PLUS

Gentamicin loading does IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours. Single daily dosing (3-5 mg/kg) can be substituted.

Discontinue IV therapy 24 hours after clinical improvement and continue oral doxycycline 100 mg twice daily or clindamycin 450 mg twice daily for a total of 14 days of therapy.

For patients with tuboovarian abscess, oral clindamycin or metronidazole should be administered with doxycycline for continued therapy rather than doxycycline alone.

Alternative Parenteral Regimens: (may be selected depending on patient’s allergy profile)

Clinical trials have demonstrated effective cure rates with the following regimens.

Ampicillin/Sulbactam 3 g IV every 6 hours

PLUS

Doxycycline 100 mg orally or IV every 12 hours

Azithromycin 500mg IV daily for 1-2 doses, then 250mg orally daily for 5-6 days

WITH or WITHOUT

Metronidazole 500mg orally twice a day for 12 days

Outpatient regimens:

Outpatient, oral therapy can be considered for women with mild-to-moderately severe acute PID who do not have the exclusion criteria noted above with one of the following CDC-recommended regimens. Outcomes are similar between women treated with outpatient versus IV therapy, however, patients who do not respond to outpatient therapy in 72 hours should be admitted for inpatient treatment.

Recommended Outpatient Regimen:

Ceftriaxone 250 mg IM in a single dose

PLUS

Doxycycline 100 mg orally twice a day for 14 days

WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days

Alternative outpatient regimen:

Cefoxitin 2 g IM in a single dose and Probenecid, 1 g orally administered concurrently in a single dose

PLUS

Doxycycline 100 mg orally twice a day for 14 days

WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days

Alternative outpatient regimen:

Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime) PLUS

Doxycycline 100 mg orally twice a day for 14 days

WITH or WITHOUT

Metronidazole 500 mg orally twice a day for 14 days

Special patient populations:

There are some patient characteristics that are important when considering treatment of PID.

Special Patient Populations:

Pregnant women

Patients with tuboovarian abscess

Patients with an intrauterine device

Treatment of male partners

Pregnant women:

It should be noted that PID is relatively uncommon in pregnant women. However, in pregnant women with PID, the regimen of choice is clindamycin PLUS gentamycin.

Patients with tuboovarian abscess:

While there is considerable overlap between PID and tuboovarian abscess (pathogenesis, risk factors, antibiotic therapy), the management of tuboovarian abscess should be considered separately.

Patients with an intrauterine device:

If a patient with an IUD develops PID, evidence suggests that treatment outcomes do not generally differ between patients who retained the IUD and those who had it removed. However, IUD removal before treatment is associated with faster improvement in pelvic pain, vaginal discharge, dysuria/frequency, dyspareunia, abdominal tenderness and cervical tenderness (p < 0.05 for all comparisons). For patients with retained IUD who do not show clinical improvement in 48-72 hours after initiation of treatment, IUD removal should be considered.

Treatment of male partners:

Male sexual partners should be treated if they have had sexual contact with the patient within 60 days of a patient’s symptoms onset or if their most recent sexual intercourse was more than 60 days before, the most recent sexual partner should be treated. Treatment should be empiric with regimens effective against gonorrhea and chlamydia (e.g., one time treatment with azithromycin 1 gram orally and ceftriaxone 250 mg intramuscular) no matter what pathogen is isolated in the patient with PID.

Immediate treatment and counseling:

After determining that a patient has PID, treatment should be initiated with one of the above regimens. Fluid administration is warranted for patients with nausea and vomiting or any signs of hypovolemia or sepsis.

Because PID can be a consequence of sexually transmitted infections and because untreated PID is associated with future infertility, the counseling of patients with a new diagnosis of PID should be approached thoughtfully and respectfully. Care should be taken to avoid obtaining or disclosing confidential information about a patient’s sexual history or relationships in front of an adolescent’s care providers, parents or friends. When PID is suspected, it is helpful to interview the patient alone, both to obtain a history and to determine what information can comfortably be shared with support persons.

If an adolescent requires admission or treatment, it is reasonable to consider referring to the diagnosis more generally as “an infection” and to explain the polymicrobial nature of the condition, rather than to focus on the correlation to sexual behaviors. Counseling regarding risk taking behaviors and ameliorating risks of PID should be done privately.

While infertility is a potential consequence of PID, it is not a certain outcome. For patients in whom pregnancy is not desired, it is important to emphasize the need for contraception after treatment of PID. In addition, progestin containing contraceptives decrease the risk of recurrence of PID. Women with a history of PID should be counseled that the risk of ectopic pregnancy is increased and that early sonographic confirmation of an intrauterine pregnancy is recommended if pregnancy is suspected.

Longer term treatment:

Patients should show clinical improvement (defervescence; reduction of pain) within 72 hours of treatment initiation. Hospitalization and additional evaluation is warranted for patients who do not improve in this time period. If the patient has been treated as an outpatient, she should be seen 72 hours after initiation of treatment to ensure that she is improving clinically. Imaging, such as an ultrasound or CT scan, should be performed if there no clinical improvement or worsening.

Even if clinical improvement is demonstrated, all patients with clinically suspected PID should receive a minimum total therapy of 14 days as guided by the above regimens. To minimize disease transmission, all patients should be counselled to abstain from sexual intercourse until treatment is complete. All patients should be strongly encouraged to use condoms with every episode of intercourse, but may want to consider using a progesterone containing contraceptive, which in some studies has been shown decrease the risk of ascending infection.

Choice of regimens:

Due to the need for surveillance for antibiotic resistance, the authors recommend following the most recent CDC guidelines for treatment.

Any of the treatment options can be associated with side effects, particularly GI side effects. Compliance is also a concern and the importance of completing a 14 day course should be emphasized for any patients undergoing therapy for PID.

Chronic pelvic pain may result from PID. If PID ascends to the tubes (salpingitis), the risk of tubal factor infertility and ectopic pregnancy is increased. It is estimated that up to 10-15% of women with PID may become infertile. The risk of infertility is increased in patients that delay treatment of PID, have repeated episodes of PID or who have increased severity of salpingitis when laparoscopically graded.

What will you tell the family about prognosis?

As above (see Immediate treatment and counseling), particularly in sexually active patients, the counseling regarding the diagnosis and prognosis should be performed in a manner that protects the patient’s confidentiality. As most patients will still retain fertility after treatment, the patient should not be told that she is infertile.

What will you tell the family about risks/benefits of the available treatment options?

The patient’s family can be told that the patient has an infection and that a major benefit of treatment is rapid improvement in pain and symptoms if the diagnosis is accurate. The major risk of antibiotic treatment is allergic reaction. The benefit of treatment is that early and aggressive treatment of PID is associated with fewer complications compared to untreated PID or PID where there has been a delay in treatment. This includes decreased a risk of infertility and tuboovarian abscess and need for operative drainage. In pregnancy, without treatment of proven gonorrhea and chlamydia, some newborns will develop a serious eye infection which can lead to blindness.

PID, the infection of the upper genital tract of women occurs when bacteria from the vagina or ectocervix (outside of the cervix) ascend into the upper reproductive organs (endocervix, uterus, tubes, ovaries) or peritoneum. Many cases of PID are a result of sexually transmitted infections, primarily gonorrhea or chlamydia or both, but several organisms can cause PID and often multiple organisms cause the disease (polymicrobial infection). PID most commonly occurs through ascending infection, and much less commonly occurs through contiguous spread from other pelvic organs.

Detailed epidemiology

Incidence, seasonal variation, age distribution:

The CDC estimates that more than 750,000 women experience an episode of acute PID each year. Sexually active women, particularly those under age 25, are at greatest risk of developing PID. Adolescent girls are thought to be at greatest risk because of sexual risk taking behaviors, including concurrent sexual partners, and because of biological factors including increased cervical ectopy increase the risk of sexually transmitted infections.

Mode of transmission:

PID is typically caused when pathogenic bacteria ascend into the upper genital tract of women. It has been estimated that 85% of cases of PID are associated with sexually transmitted bacteria or bacterial vaginosis-associated organisms. Less than 15% of cases are associated with colonization of the upper genital tract with respiratory or enteric flora from distant or peritoneal infection.

Predisposing exposures:

Exposure to sexually transmitted infections, primarily N. gonorrheoea and C. trachomatis is a risk factor for the development of PID. Microorganisms of normal vaginal flora (e.g., anaerobes, G. vaginalis, Haemophilus influenza, Streptococcus agalactiae, enteric Gram-negative rods), M. hominis, U. urealyticum, M. genitalium and cytomegalovirus have also been associated with PID.

Activities that may increase the risk of PID include sexual practices that increase the risk of sexually transmitted infection acquisition, such as not using condoms, having multiple concurrent sexual partners, or initiation of sexual activity at a young age.

Vaginal douching has also been implicated as a risk factor for PID.

Genetics:

While PID is widely accepted to be an infectious condition, there is some evidence in human and animal studies that there may be some genetic susceptibility to PID and its sequelae. This may be mediated through gene polymorphisms in proteins involved in recruitment and activation of monocytes and T-lymphocytes or major histocompatibility complex (MHC) alleles or antibodies to chlamydial heat shock protein.

As noted before, PID may be due to an ascending infection after disruption of the endocervical barrier, thereby exposing the upper genital tract to potentially pathogenic bacteria. Alternatively, PID may result when infection from a nearby organ spreads laterally.

Subclinical PID can be defined as women who have histopathological evidence of upper genital tract infection and inflammation in the absence of acute signs or symptoms of PID. These women may only be identified when they have studies performed for other indications (for instance, endometrial biopsy performed for abnormal bleeding; laparoscopy for an ovarian cyst) or if they present with a complication of PID like tubal factor infertility. The demographic and microbiologic characteristics of women with subclinical and acute PID are similar.

To prevent the development of the sequelae of PID, either acute or subclinical, it is important to counsel patients regarding risk reducing behaviors and to encourage screening of patients at risk for PID.

Potential long-term consequences of PID include increased risk of future episodes of PID, infertility, increased risk of ectopic pregnancy, and chronic pelvic pain.

Short-term consequences include potential need for hospitalization, missed school or work or increased severity of disease if untreated as well as tuboovarian abscess, tuboovarian abscess rupture and sepsis or perihepatitis (Fitz-Hugh-Curtis syndrome).

There are no known laboratory tests that have not been discussed above.

Prophylactic drugs or vaccines:

There are no known prophylactic medications or vaccines for the prevention of PID. However, some evidence shows that using progesterone containing oral contraceptives or Depo Provera can decrease the risk of PID. This is most likely related to the effect that progesterone has on thickening cervical mucous and decreasing uterine bleeding by inactivating the endometrium. Likewise, other conditions that increase cervical mucous, like pregnancy, may also help to prevent PID.

Behavioral Factors:

At present there is a two-tiered approach to the prevention of PID: 1) avoiding the acquisition of sexually transmitted infections and 2) increasing the early detection and treatment of lower genital tract infection to prevent the risk of ascending infection. There are a number of habits that may decrease risk of sexually transmitted infection, including abstaining from sexual intercourse, or to be in mutually monogamous relationship with an uninfected partner and always using male condoms correctly.

It has been shown that identifying, testing and treating women at high risk of cervical chlamydial infection have been shown to reduce the incidence of PID. It is assumed that treatment of other vaginal or cervical infections (e.g., bacterial vaginosis and N. gonorrhea) may likewise reduce the risk of developing PID. There is some evidence that a single screening for cervical chlamydia infection might not be associated with a decreased risk of PID at one year, so the optimal strategy for early screening is not certain.

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Fang, J, Husman, C, DeSilva, L, Chang, R, Peralta, L. “Evaluation of self-collected vaginal swab, first void urine, and endocervical swab specimens for the detection of Chlamydia trachomatis and Neisseria gonorrhoeae in adolescent females”. J Pediatr Adolesc Gynecol. vol. 21. 2008 Dec. pp. 355-60.

Howard, EJ, Xu, F, Taylor, SN, Stoner, BP, Mena, L, Nsuami, MJ, Powell, S, Lillis, R, Martin, DH. “Screening methods for Chlamydia trachomatis and Neisseria gonorrhoeae infections in sexually transmitted infection clinics: what do patients prefer”. Sex Transm Infect. vol. 87. 2011 Mar. pp. 149-51.

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. vol. 30. 2012. pp. 1114-7.

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. vol. 31. 2003. pp. 45-54.

Brunham, RC, Gottlieb, SL, Paavonen, J. “Pelvic Inflammatory Disease”. N Engl J Med. vol. 372. 2015. pp. 2039-2048.

Historically, many patients with pelvic inflammatory disease were treated as inpatients. More recently, it has been shown that there are similar outcomes for patients with mild to moderate severity who are treated as outpatients.

The increasing availability of nucleic acid amplification testing for N. gonorrhea or C. trachomatis has expanded the number of ways in which these sexually transmitted infections can be diagnosed, including self-collected urine or vaginal samples as well as provider-obtained samples. This, in turn, would allow for treatment of these infections and potentially, prevention of pelvic inflammatory disease. There is evidence to support that detection rates of gonococcal or chlamydia infections are similar between self-collected urine or vaginal samples and provider-obtained samples; however, self-collection may not be preferred by all patients.

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Pelvic Inflammatory Disease

OVERVIEW: What every practitioner needs to know

Are you sure your patient has pelvic inflammatory disease? What are the typical findings for this disease?

What other disease/condition shares some of these symptoms?

What caused this disease to develop at this time?

If you are able to confirm that the patient has pelvic inflammatory disease, what treatment should be initiated?

What is the evidence?

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