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Pelvic Inflammatory Disease: Pearls and Pitfalls

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 24-year-old female with no significant past medical history presents to the emergency department (ED) with lower abdominal pain for five days. The pain has been associated with decreased appetite and nausea but no vomiting. It is exacerbated by sexual intercourse. Her last menstrual was period five days ago, and while she typically gets cramping, she states that this pain is more severe. Her vitals on arrival are temperature 101.2º Fahrenheit (F), heart rate (HR) 80 beats per minute (bpm), respiratory rate (RR) 14/minute, blood pressure (BP) 115/70 mmHg. Her physical examination is notable for diffuse tenderness to palpation of the abdomen, scant blood in the vaginal vault, yellow discharge from the cervical os, and severe bilateral adnexal tenderness on bimanual examination.

Background

Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI). Neisseria gonorrhea and Chlamydia trachomatis are the most commonly implicated pathogens in PID1. However, PID can also be caused by bacterial-vaginosis related organisms or, more rarely, enteric or respiratory pathogens that have colonized the lower genital tract1. Even more rarely, a chronic form of PID may be seen with tuberculosis in endemic areas or Actinomyces in women who have intrauterine devices2,3.

Any sexually active woman is at risk for PID but women with multiple sexual partners are at the highest risk4. Other risk factors include age younger than 25 years, herpes infection, HIV infection, a partner with an STI, prior PID, or prior STI. Barrier contraception is protective5. Pregnancy also decreases the risk of PID due to the mucus plug that can prevent ascending infection from the lower to the upper genital tract. Note, however, that PID can still develop in the first 12 weeks of pregnancy6. The spectrum of PID symptoms is wide with some patients going undiagnosed until they develop sequelae such as tubal factor infertility or an ectopic pregnancy. In symptomatic patients, lower abdominal pain, typically bilateral, is often the presenting symptom1. Dyspareunia and/or an onset of pain with, or shortly after, menstruation should also raise suspicion for PID7. A history of abnormal uterine bleeding, such as menorrhagia, metrorrhagia, or post-coital bleeding, is seen in one third of patients with PID8. Physical examination typically reveals lower abdominal pain, which may be unilateral or bilateral, although diffuse abdominal pain may also be seen. Cervical motion tenderness and the classic “chandelier sign” – severe pain with cervical motion such that the patient “jumps for the chandelier” on examination – may be present. Fever, rebound tenderness, and/or hypoactive bowel sounds are indicative of more severe disease and should increase suspicion for a pelvic abscess. Associated right upper quadrant pain is concerning for Fitz-Hugh-Curtis syndrome inflammation of the hepatic capsule. The most common cause of death in PID is rupture of a tubo-ovarian abscess (TOA), which has a mortality rate of 5-10%6. Serious complications include tubal factor infertility, tubal scarring leading to ectopic pregnancy, and chronic pelvic pain.

Differential Diagnosis

The differential diagnosis for pelvic and lower abdominal pain is extremely broad and varies by age. The differential in pre-menopausal women includes ectopic pregnancy, a complicated intrauterine pregnancy, ovarian cyst, ovarian torsion, endometriosis, urinary tract pathologies, appendicitis, and irritable bowel syndrome. Laboratory evaluation should include a pregnancy test in any pre-menopausal woman. In post-menopausal women, many of the gastrointestinal and urinary pathologies are still possible but there is lower risk for ovarian torsion and endometriosis. Diagnoses such as ovarian masses, endometrial cancer, and colon cancer should be considered.

Diagnosis

There is no specific lab value, physical examination finding, or imaging study that is diagnostic of PID. The diagnosis of PID is often presumptive based on clinical findings. The clinical diagnosis is only 65-90% specific, but the addition of the criteria in Table 1 increases the specificity of the clinical diagnosis1,5,9. In patients with known or suspected PID, testing for STIs, including syphilis and HIV, should be obtained. Other helpful laboratory tests include a white blood cell count, C reactive protein (CRP), and erythrocyte sedimentation rate (ESR). A positive urinalysis does not exclude the diagnosis of PID, as inflammation in the pelvis can cause white blood cells in the urine6.

 Table 1: Findings suggestive of PID1

Oral temperature >101°F (>38.3°C)
Abnormal cervical or vaginal mucopurulent discharge
Cervical friability
Abundant white blood cells on saline microscopy of vaginal secretions
Documented infection with of N. gonorrhoeae or C. trachomatis

Imaging with pelvic ultrasound may be helpful in excluding other causes of pelvic pain, including ectopic pregnancy, ovarian cysts, and ovarian torsion. It is also helpful in the diagnosis of TOA. Computed tomography (CT) or magnetic resonance imaging (MRI) may also be used, with MRI being particularly useful in characterizing complicated soft-tissue masses as would be seen with TOA6.

Management

While the clinical diagnosis is only 65-90% specific, even minimal symptoms without an alternative diagnosis warrant antibiotic therapy to reduce the risk of potentially serious complications due to the delay of or withholding therapy1. Women with IUDs do not need to have them removed prior to the start of treatment because they are rarely the cause of PID1. If symptoms fail to improve in 48-72 hours, removal of the IUD should be considered1.

Antibiotic selection should cover for N. gonorrhea and C. trachomatis. The importance of anaerobic coverage is controversial, since no trial has demonstrated improved outcomes and there is concern that the gastrointestinal side effects associated with metronidazole will lead to noncompliance10. There is currently an ongoing study on the role of anaerobic coverage in PID (Clinical Trials.gov, identifier NCT01160640).

Anaerobic coverage should be added, however, in patients who have a history of gynecologic instrumentation in the prior two to three weeks. Possible antibiotic regimens for inpatient and outpatient management are listed in Table 2.

 There has been a trend towards outpatient management of patients with mild to moderate disease. The Pelvic Inflammation Disease Evaluation Clinical Health Trial (PEACH Trial) showed similar short-term clinical and microbiologic and long-term reproductive outcomes between the inpatient and outpatient arms of the trial, with the inpatient arm experiencing high rates of phlebitis from IV doxycycline administration12.

Table 2: Inpatient and Outpatient Treatment Regimens1

Outpatient management Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)
Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)
Inpatient management Cefoxitin (2g IV q6 hours) plus doxycycline (100mg po bid for 14 days)
Cefotetan (2g IV q12 hours) plus doxycycline (100mg po bid for 14 days)
Clindamycin (900mg IV q8 hours) plus gentamicin (2mg/kg loading dose then 1.5 mg/kg q8 hours IV)

Indications for hospitalization and IV antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics1.

If a patient is treated as an outpatient, follow up in 72 hours should be arranged. Patient education is paramount, especially in adolescents where the risk of recurrence is higher and the time to pregnancy is shorter than in adult patients. Partner notification, evaluation and treatment should be encouraged. Patients should be educated about the use of barrier contraception and safe sex practices and instructed to remain abstinent from sexual activity until one week after the completion of treatment for them and their partner.

Pearls

  • Even though the presumptive clinical diagnosis is only 65-90% specific, symptoms suggestive of PID should be treated with antibiotics immediately to avoid the risk of serious sequelae, including permanent scarring that may lead to infertility and ectopic pregnancy.
  • Obtain a pelvic ultrasound to assess for TOA in patients with asymmetrical pelvic findings or clinical signs of toxicity.
  • Fluoroquinolones should not be used in known or suspected gonorrhea infection due to increasing rates of resistance.
  • IUDs do not need to be removed prior to treatment of PID.
  • Antibiotics should cover both gonorrhea and C. trachomatis.
  • Anaerobic coverage is only suggested if there has been recent gynecologic instrumentation.

 Pitfalls

  • Dismissing the pelvic pain associated with PID for dysmenorrhea.
  • Assuming a positive UA excludes the diagnosis of PID (beware sterile pyuria)
  • Failing to do a pelvic exam and STI testing on a woman with lower abdominal pain.

References / Further Reading

  1. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  2. Namavar Jahromi B, Parsanezhad ME, Ghane-Shirazi R. Female genital tuberculosis and infertility. Int J Gynaecol Obstet 2001; 75:269.
  3. Kim YJ, Youm J, Kim JH, Jee BC. Actinomyces-like organisms in cervical smears: the association with intrauterine device andpelvic inflammatory  Obstet Gynecol Sci. 2014 Sep;57(5):393-6.
  4. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory disease. Obstet Gynecol 1991; 77:425.
  5. Ross, Johnson. Pelvic Inflammatory Disease: pathogenesis, microbiology, and risk factors. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  6. Shepherd SM, Weiss B, Shoff WH. Pelvic Inflammatory Disease in Tintinalli, Judith E., Gabor D. Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division, 2016. Ch 103:668-672.
  7. Korn AP, Hessol NA, Padian NS, et al. Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. Am J Obstet Gynecol 1998; 178:987.
  8. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005; 32:400.
  9. Peipert JF, Boardman LA, Sung CJ. Performance of clinical and laparoscopic criteria for the diagnosis of upper genital tract infection. Infect Dis Obstet Gynecol 1997; 5:291.
  10. 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 2007; 44 Suppl 3:S111.
  11. Wiesenfeld, HC. Pelvic Inflammatory Disease: Treatment. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  12. Ness RB, Soper DE, Holley RL, et al. 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 2002; 186:929.

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