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Treating PID as Its Drug Resistance Surges

Roberts, James R. MD

doi: 10.1097/01.EEM.0000526096.31911.d7

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




Pelvic inflammatory disease (PID) has a wide range of clinical manifestations, from subclinical symptoms to severe lower abdominal pain and fever. This acute infection can result in long-term infertility, predisposes patients to ectopic pregnancy, and produces chronic pelvic pain. The introduction of laparoscopy in the 1960s was a major breakthrough in understanding PID and its relationship to reproductive disability and standard antimicrobial treatments. Thanks to massive public health efforts, the rate and severity of pelvic inflammatory disease has declined in North America over the past 15 years.

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Pelvic Inflammatory Disease

Brunham RC, et al.

New Engl J Med


This rather complete review examines the guidelines for treating PID developed by the Centers for Disease Control and Prevention based on clinical trials and consensus recommendations. Treatment is almost always empirical, and involves the use of broad-spectrum antimicrobial agents to cover the likely pathogens. Any treatment should cover the principal pathogens—Neisseria gonorrhea and Chlamydia trachomatis—but other pathogens will also be successfully treated with this regimen.

Table Fi

Table Fi

Those with mild to moderate PID can be treated as outpatients. Admission is required if the symptoms are significant, the diagnosis is in question, and the patient is severely ill or has a tubal abscess. A variety of antimicrobials have been used and are outlined in the table. Generally successful outpatient therapy is a single 250-mg IM injection of ceftriaxone followed by oral doxycycline (100 mg BID) with or without metronidazole for 10 days. It is best to leave any IUD in place because removing it does not improve clinical outcome or hasten clinical resolution of symptoms.

No accurate noninvasive or minimally invasive test is available to confirm infection of the fallopian tubes with the presence of inflammatory changes that forecast long-term reproductive problems. The role of additional organisms, such as those causing bacterial vaginosis, has also been poorly defined. Less than half of women with PID had laboratory evidence of chlamydia or gonorrhea in some studies, so the exact microbiologic cause of infection may remain unclear and is probably often not used, and the addition of metronidazole therapy to PID regimens is also unclear. And then there is the role of cephalosporin-resistant gonorrhea looming on the horizon.

Comment: Women with lower abdominal pain are common patients in the emergency department. Acute PID is frequently encountered, but diagnostic and treatment decisions must be based on clinical grounds. Laboratory tests should be sent, but it is often best to treat empirically those patients with ill-defined lower abdominal pain or vaginal discharge once ectopic pregnancy and other ovarian problems have been ruled out. Overtreatment is the best option considering follow-up problems in the ED. Few women today with acute lower abdominal pain will escape transvaginal ultrasound in the ED, and, of course, it is axiomatic to obtain a pregnancy test regardless of the patient's history or denial of pregnancy. Appendicitis is the most important condition that can mimic PID.

The vaginal vault of most healthy women contains a variety of potentially pathogenic bacteria. Only the endocervical canal functions as a barrier to protect the upper genital tract, but this barrier is disrupted in the presence of sexually transmitted bacteria, providing vaginal bacteria access to the upper organs.

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

The majority of PID cases are caused by sexually transmitted pathogens or bacterial vaginosis associated with pathogens, but about 15 percent of acute PID cases are not sexually transmitted, and are associated with a variety of enteric or respiratory pathogens. The exact microbiological cause of PID will not be ascertained in the ED.

A CBC is rarely of any clinical help and often is normal in patients with mild to moderate PID. HIV screening and serologic tests for syphilis are also suggested for any women with suspicion of PID. I suspect that these are not done routinely in the ED, although the patients treated in the ED should be referred for such a subsequent evaluation. Whether patients go for such testing is unclear and variable.

The sensitivity of the ED examination in diagnosing PID is about 60-90 percent. Given the potential for serious complications if treatment is delayed, a presumptive diagnosis is sufficient to warrant empiric antimicrobial therapy for PID in the ED. Even patients with minimal or subtle findings should probably 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 evidence of cervical motion tenderness, uterine tenderness, tenderness on exam, or simply 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 upper tract infections.

The suggested CDC treatment is effective in about 90 percent of cases. There is growing concern for drug-resistant gonorrhea, and such strains have now been identified. Clinicians should be cognizant that fluoroquinolones are no longer recommended for treatment of PID due to increasing resistant rates. Treatment with cephalosporins, either ceftriaxone or cefoxitin, is equally effective. Note that if cefoxitin is used as an outpatient therapy, 1 g probenecid should be given to decrease urinary excretion. Ceftriaxone is not generally recommended for inpatients; rather, cefotetan or cefoxitin is recommended. I have never been able to understand why this is.

HIV-infected women appear to respond to therapy for PID as well as uninfected women, so recommended antibiotic regimens for HIV-infected women with acute PID are similar to those for HIV-uninfected women.

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Common Clinical Teachings: PID vs Appendicitis

PID is more likely than appendicitis to have:

  • Absence of pain migration (Appendicitis pain starts in the epigastric area and goes to the right lower quadrant.)
  • Bilateral abdominal tenderness (Appendicitis pain, of course, is on the right side.)
  • Absence of nausea and vomiting (Appendicitis frequently produces nausea and vomiting.)

These have been frequently taught at the bedside, although they are not specific enough or sensitive enough to be consistently helpful. When in doubt, perform a CT scan.

Source: Am J Emerg Med 2007;25(2):152.

Drug-resistant gonorrhea and “super gonorrhea” are on the rise and are “anything but benign.” Scientists point to oral sex as one of the more sinister transmission methods because it is difficult to detect and treat, and “these bacteria pick up resistance to antibiotics directly from other bacteria in the throat.” Thirty percent of new gonorrhea infections in the United States are resistant to at least one drug.

Source: The New York Times July 31, 2017;

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