The patient was admitted and treated initially with IV doxycycline, metronidazole, and cefazolin. On the second hospital day, when the symptoms had not improved, her medications were changed to clindamycin, gentamicin, and ampicillin. The patient was discharged on hospital day number 5, afebrile and asymptomatic, with instructions to complete a 2-week course of doxycycline 100 mg PO twice per day. In the meantime, the microbiology results demonstrated positive amplified DNA probe for N. gonorrhoeae and negative C. trachomatis.
Pelvic inflammatory disease is infection and inflammation that involves the cervix, uterus, fallopian tubes, and ovaries. In severe cases, adjacent pelvic structures including fat, fascial planes, small bowel, large bowel, and the peritoneum can become infected and inflamed. According to the Center for Disease Control (CDC), 1 million women experience acute PID per year and 150 will die of the disease itself or complications from PID (http://www.cdc.gov/std/PID/). Risk factors are the same as for any other sexually transmitted disease and include unprotected intercourse, multiple sexual partners, high frequency of intercourse, race, low socioeconomic status, prior episodes of sexually transmitted disease, and PID.1 Other risk factors that are debated to be a significant cause of PID include surgical instrumentation, use of intrauterine device, douching, cigarette smoking, and substance abuse.1-3
Pelvic inflammatory disease can present clinically with a wide spectrum of findings ranging from vague and nonspecific symptoms that are difficult to distinguish from other abdominal and pelvic pathology to the classic manifestation that includes pelvic pain, cervical motion tenderness, and pelvic mass.4 Constitutional symptom including fever, malaise, nausea, and vomiting are nonspecific and may be seen with PID. No single clinical finding is sufficiently sensitive or specific to be considered pathognomonic.
The pathogens responsible for PID are also widely variable. The sexually transmitted infections, specifically C. trachomatis and N. gonorrhoeae, are the most commonly implicated microbial organism, with chlamydia accounting for up to 40% of cases.1,3,4 In addition, aerobic and anaerobic, gram positive and negative organism, normal vaginal flora, viruses, tuberculosis, mycoplasma, and other atypical organism have been implicated as causative agents.3,4
Ultrasound should be the first line imaging modality in imaging the premenopausal female pelvis. The advantages of US include lower cost, portability, and lack of ionizing radiation. The main disadvantages are that it provides limited evaluation of the remainder of the abdomen and pelvis and is dependant on the operator and the patient's body habitus. Ultrasound findings of PID are often subtle and nonspecific and include mild enlargement or indistinctness of the uterus and ovaries, increased echogenicity of the fat in the pelvis, fluid in the endometrial canal, and/or free fluid in the cul-de-sac. More specific US findings include complex fluid collections, thickened fallopian tube wall >5mm, fluid filled fallopian tubes, and frank tubo-ovarian abscess.5 The utility of Doppler evaluation remains controversial;2 color Doppler correlates with hyperemia and is another tool that can be useful as is demonstrated in Figure 5.
The CT findings of PID can also be very subtle. This point is nicely illustrated in Figure 1, where the imaging diagnosis was nearly missed because the appearance of a young and menstruating uterus on CT can be very similar. Computed tomography was obtained in case 1 to exclude other pathology in the abdomen and pelvis, which can have similar clinical presentation. Early in the disease, the only clues can be edema in the pelvic fat planes, nonspecific free pelvic fluid, and fluid in the endometrial canal.6 Enlargement and increased number of ovarian follicles (the so-called "polycystic" appearance) is also considered a reliable finding of infection and inflammation by both US, CT, and MRI. Endometrial, ovarian, and fallopian tube enhancement is seen in the more advanced case of PID. The extreme of the spectrum, as in US, is the presence of tubo-ovarian abscess and other complex fluid collections.6 As with US, no CT finding is pathognomonic for PID. Computed tomography is often the first imaging modality used because of its wide availability and its ability to give an overview of the entire abdomen and pelvis to exclude other etiologies in the differential diagnosis such as appendicitis or diverticulitis. Computed tomography is of limited value in evaluating the ovaries, fallopian tubes, and endometrium, which are better interrogated with transvaginal ultrasound.5
No pathognomonic MRI finding has been documented. As with CT and US, tubal-ovarian abscess, dilated fluid filled tubes, increased number of ovarian cyst and free fluid in the pelvis are the characteristic findings at MRI.7 MRI, however, provides excellent soft tissue resolution and is the most sensitive imaging modality to evaluate for tissue water content (ie, inflammation). Magnetic resonance imaging has the advantage of being highly sensitive to water signal so that subtle fluid in the fallopian tubes or free fluid in the pelvis can be readily assessed. The current use of MRI is in the prevention of unnecessary laparoscopy in difficult or indeterminate cases of PID.7 Limitations of MRI include its relative expense, limited availability, and imaging time constraints that typically limit the examination to 1 specific anatomic location.
The role of laparoscopy: Laparoscopy has been the gold standard in the diagnosis of PID. This is the ultimate imaging study, as direct visualization of the female pelvic organs is performed. Obviously, this procedure is expensive and invasive and carries the risk associated with general anesthesia and surgery. The sensitivity and specificity rate of laparoscopy are 50% and 85%, respectively; when only visualization is used. The addition of biopsy improves the sensitivity and specificity of these procedure.1
The CDC recommends that empiric treatment be initiated when a patient with risk factors for sexually transmitted disease presents with uterine/adnexal tenderness or cervical motion tenderness.8 Additional criteria not necessary to initiate therapy include the following: temperature 101° F, cervical/vaginal discharge, WBCs in vaginal secretions, elevated ESR and C-reactive proteins, and microbiology positive for gonorrhoeae and chlamydia. The following are the CDC recommended oral regimen for treatment: Regimen A-ofloxacin 400 mg twice per day for 14 days or levofloxacin 500 mg once per day for 14 days with or without metronidazole 500 mg twice per day for 14 days and Regimen B-ceftriaxone 250 mg IM in a single dose or cefoxitin 2 g IM in a single dose and probenecid 1 g orally administered concurrently in a single dose or other parenteral third-generation cephalosporin (eg, 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.8 If there is no improvement, then consideration is given to intravenous therapy either as an inpatient or outpatient. There are several CDC recommended parenteral regimens (A and B and an alternative regimen) which can be used: Regimen A-cefotetan 2 g IV every 12 hours or cefoxitin 2 g IV every 6 hours plus doxycycline 100 mg orally or IV every 12 hours; Regimen B-clindamycin 900 mg IV every 8 hours plus gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours (single daily dosing may be substituted); Alternative Parenteral Regimen-ofloxacin 400 mg IV every 12 hours or levofloxacin 500 mg IV once daily with or without metronidazole 500 mg IV every 8 hours or ampicillin/sulbactam 3 g IV every 6 hours plus doxycycline 100 mg orally or IV every 12 hours.8 No large clinical trials are available to document the efficacy of this or any regimen.1,2,8 Likewise, there are no trials that demonstrate improved efficacy of inpatient versus outpatient or parenteral versus oral therapy. As illustrated in case 2, often the antibiotic treatment used is aimed to cover general abdominal processes.
The sequelae of recurrent PID is well documented and include infertility, ectopic pregnancy, chronic pelvic pain, and, as previously stated, a small risk of death.1,8 The likelihood of these complications increase with the number of episodes of PID. There are significant economic implications, and the sequela of this condition is irreversible.1
Pelvic inflammatory disease is a commonly encountered process with serious complications and challenging clinical and imaging findings. An awareness of the spectrum of imaging findings is important when correlating diagnostic data to the clinical presentation.
1. Beigi RH, Wiesenfeld HC. Pelvic inflammatory disease: new diagnostic criteria and treatment Obstet Gynecol Clin North Am
2. Ross JDC. An update on pelvic inflammatory disease Sex Transm Infect
3. Simms I, Stephenson JM. Pelvic inflammatory disease epidemiology: what do we know and what do we need to know? Sex Transm Infect
4. Barrett S, Taylor C. A review on pelvic inflammatory disease Int J STD AIDS
5. Horrow MM. Ultrasound of pelvic inflammatory disease Ultrasound Q
6. Sam JW, Jacobs JE, Birnbaum BA. Spectrum of CT findings in acute pyogenic pelvic inflammatory disease Radiographics
7. Tukeva TA, et al. MR imaging in pelvic inflammatory disease: comparison with laparoscopy and US Radiology
© 2006 Lippincott Williams & Wilkins, Inc.
8. Workowski KA, Levine WC. Sexually Transmitted Diseases Treatment Guidelines. MMWR, Center for Disease Control and Prevention. 51 (RR06); May 10, 2002:1-80.