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InFocus: Acute PID Common in the ED, but Diagnosis is Often an Educated Guess

Roberts, James R. MD

doi: 10.1097/01.EEM.0000524789.44185.6f

Dr. Robertsis a professor of emergency medicine and toxicology at the Drexel University College of Medicine in Philadelphia. Read the Procedural Pause, a blog by Dr. Roberts and his daughter, Martha Roberts, ACNP, PNP, at, and read his past columns at




Thanks to massive public health efforts, the rate and severity of pelvic inflammatory disease have declined in North America over the past 15 years, but it's still out there. The spectrum of this infection-induced inflammation encompasses the female upper reproductive tract, endometrium, fallopian tubes, ovaries, and pelvic peritoneum (peritonitis).

PID has a wide range of clinical manifestations, from subclinical ones and vaginal discharge to intermenstrual bleeding and severe lower abdominal pain and fever. PID can result in long-term infertility, predispose women to ectopic pregnancy, and produce chronic pelvic pain in addition to the discomfort and clinical manifestations of the acute infection. The introduction of laparoscopy in the 1960s was a major breakthrough in understanding PID and its relationship not only to reproductive disability but to standard antimicrobial treatments.

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Pelvic Inflammatory Disease

Burnham RC, et al.

New Engl J Med


This is a rather complete review of PID published in a recent issue of the New England Journal of Medicine.

Physiology and Microbiology: Acute PID is the result of spontaneous ascension of microbes from the cervix or vagina to the endometrium, fallopian tubes, and adjacent structures. Most commonly it is caused by Neisseria gonorrhoeae (GC) or chlamydia, but numerous other organisms are associated with acute PID. Most infections are due to sexually transmitted pathogens or from bacterial vaginosis, but respiratory or enteric organisms are culprit in approximately 15 percent of cases. Anaerobic or facultative bacteria found in the vaginal flora are often associated with gonorrhea and chlamydia infections, so PID is truly a polymicrobial process. Numerous other organisms are identified in more than 50 percent of patients with gonococcal PID when stringent microbiologic techniques are employed.

The inflammation resulting from infection on the epithelia surface of the fallopian tubes and peritoneal surfaces leads to scarring, adhesions, and obstruction of the fallopian tubes. Infection-induced changes in the fallopian tubes can result in infertility or predispose those infected to ectopic pregnancy.

Clinical Manifestations and Diagnosis: Classically the onset of severe lower abdominal pain during or shortly after menses has been a classic characteristic used to identify acute PID. The disease can occur anytime in the menstrual cycle, however, and can be quite ill-defined and subtle. Other symptoms include abnormal vaginal discharge, intermenstrual bleeding, dyspareunia, and dysuria. Systemic manifestations, such as fever, nausea, and vomiting, are not prominent features of PID, and suggest an alternative diagnosis. Asymptomatic infections of the upper genital tract have been well documented, leading to long-term reproductive complications in the absence of acute symptoms. Tubal-related infertility has also been attributed to mild or asymptomatic pelvic inflammatory disease. Clinicians often miss subacute cases, but should have a low threshold for considering the diagnosis and initiating empiric treatment.

The clinical diagnosis of PID is based on pelvic pain, accompanied by cervical motion tenderness, adnexal tenderness, or uterine compression tenderness. Those infected often demonstrate cervical mucopus, a yellow-green mucus discharge from the endocervix in addition to tenderness and pain. The clinical diagnosis of acute PID is imprecise, however, and there is no single diagnostic gold standard.

The most accurate way to diagnose PID is via laparoscopic confirmation; this procedure is rarely performed in individuals with suggestive signs and symptoms or those with mild disease. Transvaginal ultrasound (US) and MRI can also reveal findings highly specific for salpingitis. US is commonplace, but MRI is not routinely performed; both can be used to investigate for alternative diagnoses, such as ovarian cyst, endometritis, ectopic pregnancy, diverticulitis, and acute appendicitis. Interestingly, these diseases are found in up to 25 percent of women who are initially thought to have acute PID by clinical exam.

Patients suspected of having PID should undergo cervical fluid analysis by nucleic acid amplification testing (NAAT) for gonorrhea or chlamydial infection. A pregnancy test should be routine to rule out ectopic pregnancy in women with acute lower abdominal pain. Tests for HIV and syphilis should also be considered, but are not always performed in the ED.

Comment: Women with lower abdominal pain are common denizens of the ED, and ferreting out the etiology of symptoms is a daily mandate for the emergency clinician. Acute PID is frequently encountered, but diagnostic and treatment decisions are usually based on clinical data combined with an educated guess. Acute PID is difficult to diagnose with certainty because of the wide variation in symptoms and signs associated with this condition, as well as the overlap of the clinical presentation with other conditions. Many women with PID have subtle or nonspecific symptoms or, in retrospect, are asymptomatic. Delay in diagnosis and treatment probably contributes to inflammatory sequelae in the upper reproductive tract, including infertility, ectopic pregnancy, and chronic pelvic pain. Unfortunately, no single historical, physical, or laboratory finding is sensitive and specific for diagnosing acute PID.

PID is largely a best-guess clinical call that is over- and underdiagnosed, and there appears to be no true gold standard upon which to rest one's diagnosis. Many episodes of PID go unrecognized, and although some cases are asymptomatic, others are not diagnosed because the patient or clinician fails to recognize the implications of mild or nonspecific symptoms or signs (e.g., abnormal bleeding, dyspareunia, and vaginal discharge).

Per the Centers for Disease Control and Prevention, “Presumptive treatment for PID should be initiated in sexually active young women and other women at risk for STDs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following minimum clinical criteria are present on pelvic examination: cervical motion tenderness or uterine tenderness, or adnexal tenderness.” (PID Fact Sheet, CDC, Jan. 27, 2017;

One or more of the following additional criteria can be used to enhance the specificity of the minimum clinical criteria and support a diagnosis of PID:

  • Oral temperature higher than 101°F (>38.3°C)
  • Abnormal cervical mucopurulent discharge or cervical friability
  • Presence of abundant numbers of WBC on saline microscopy of vaginal fluid
  • Elevated erythrocyte sedimentation rate
  • Elevated C-reactive protein
  • Laboratory documentation (nucleic acid amplification test [NAAT]) of cervical infection with N. gonorrhoeae or Chlamydia trachomatis.

Although of minimal importance and usually nonspecific, laboratory tests should be sent, but it is best to treat empirically for ill-defined lower abdominal pain once ectopic pregnancy and other ovarian problems have been ruled out. Blood cultures are not indicated. Sed rate and C-reactive protein testing have been suggested, but are of little help to the evaluating clinician. A negative GC/chlamydia test should not dissuade your diagnosis of PID.

Few women with acute lower abdominal pain in the ED will escape transvaginal US. It is not a definitive test for PID, but it can be used to detect tubo-ovarian abscess, ectopic pregnancy, and other conditions. Finding enlarged adnexa is associated with PID, but is nonspecific. Of course, it is axiomatic to obtain a pregnancy test regardless of the patient's history or denial of being pregnant.

The polymicrobial aspect of PID is well referenced. Clinically, therefore, PID is considered a mixed infection. The role of Mycoplasma genitalium sexually transmitted infection has been emerging, but the proportion of PID associated with it is uncertain. The polymicrobial etiology of PID has been shown in a variety of studies, and 50 percent of patients with gonococcal PID in one report had a mixed infection. (Obstet Gynecol 1981;58[1]:62.)

The gold standard for diagnosing chlamydia and gonorrhea used to be bacterial culture—attempting to grow bacteria from samples taken directly from the cervix or urethra. These days, however, urine testing is considered a better option. The performance of NAATs, testing urine for bacterial DNA, is better than other tests available for diagnosing chlamydial and gonococcal infections for overall sensitivity, specificity, and ease of specimen transport. The results are not initially available to the ED, however.

The majority of PID cases are caused by sexually transmitted pathogens or bacterial vaginosis-associated pathogens, but about 15 percent of acute PID cases are not sexually transmitted and are associated with enteric or respiratory pathogens. The exact microbiological cause of PID will not be ascertained in the ED. Most importantly, a negative GC/chlamydia test does not rule out PID. Treatment is directed toward GC/chlamydia, and a positive test is important for follow-up and for identifying other conditions that need to be treated.

HIV screening and serologic tests for syphilis are also suggested for any women with suspicion of PID. I suspect that these are also not done routinely in the ED, another reason patients treated in the ED should be referred for subsequent evaluation. Whether they go for such testing is variable. After many years of cajoling, our stubborn hospital lab was convinced to perform STAT RPR and HIV tests. The days of clinicians doing laboratory tests in the ED, such as wet mount microscopy or gram stain on vaginal discharge, are long gone due to strict rules on such testing outside the lab. The finding of WBCs in saline microscopy of vaginal discharge is thought to be sensitive for PID, and the absence of WBC should suggest an alternative diagnosis. This is not really specific for diagnosing PID, however.

The sensitivity of the ED examination in diagnosing PID is about 60-90 percent. Given the potential for serious sequelae if the diagnosis is delayed, an ED presumptive diagnosis is sufficient to warrant empiric antimicrobial therapy. Even patients with minimal or subtle findings should be treated because the potential consequences of withholding therapy are great, and follow-up is erratic. Probably the only thing required for the empiric treatment of PID is a presumptive clinical diagnosis in sexually active young women who present with lower abdominal pain and have cervical motion tenderness, uterine tenderness, or simply a mucopurulent cervical discharge.

One should be careful about telling these patients that they have a sexually transmitted disease until further information is known, but treatment should not be withheld or delayed in patients with minimal findings. Overtreatment will occur in a number of cases, but the suggested interventions are usually benign. Of course, even though chlamydia and gonorrhea are targets for treatment, a negative screen for these pathogens does not rule out PID.

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A Mixed Infection

PID treatment is aimed at gonorrhea and chlamydia, but this is a mixed infection. Regarding the bacterial etiology of PID, the CDC states, “Sexually transmitted organisms, especially N. gonorrhoeae and C. trachomatis, are implicated in many cases. Recent studies suggest that the proportion of PID cases attributable to N. gonorrhoeae or C. trachomatis is declining; More than 50 percent of women who are diagnosed with acute PID test positive for one of these organisms. Microorganisms that comprise the vaginal flora (e.g., anaerobes, G. vaginalis, Haemophilus influenzae, enteric gram-negative rods, and Streptococcus agalactiae) have been associated with PID. Cytomegalovirus (CMV), Mycoplasma hominis, Ureaplasma urealyticum, and M. genitalium might also be associated with some PID cases. Newer data suggest that M. genitalium might play a role in the pathogenesis of PID and might be associated with milder symptoms, although one study failed to demonstrate a significant increase in PID following detection of M. genitalium in the lower genital tract.” (2015 Sexually Transmitted Disease Treatment Guidelines: Pelvic Inflammatory Disease; CDC;

Next month: Treating PID.

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