Infect Dis Clin N Am 22 (2008) 693708

Pelvic Inammatory Disease and Tubo-ovarian Abscess

Susan M. Lareau, MD, Richard H. Beigi, MD, MSc*
Division of Reproductive Infectious Diseases, Department of Obstetrics, Gynecology and Reproductive Sciences, Magee-Womens Hospital of the University of Pittsburgh Medical Center, 300 Halket Street, Pittsburgh, PA 15213, USA

Pelvic inammatory disease (PID) is polymicrobial infection in women characterized by inammation of the upper genital tract, including endometritis, salpingitis, and pelvic peritonitis, and occasionally leading to the formation of a tubo-ovarian abscess (TOA). PID primarily aects young, sexually active, reproductive-aged women. The spectrum of disease is caused most commonly by sexually transmitted diseases (STDs), such as Chlamydia trachomatis and Neisseria gonorrhoeae, although many studies show that 25% to 50% of cases fail to document one of these sexually transmitted pathogens [14]. PID can be classied as acute, subacute, or subclinical. Estimates of the prevalence of PID are not exact because of a variety of factors and likely under-represent the true prevalence of disease. Nevertheless, PID and its associated short- and long-term sequelae, including but not limited to tubal factor infertility, ectopic pregnancy, and chronic pelvic pain and their associated treatments, are signicant and are estimated to be in excess of one billion dollars in annual health care costs [5]. Epidemiology The incidence of PID steadily increased in the1970s in direct correlation to rising rates of STDs. The incidence peaked in 1982 with an estimated 1 million cases diagnosed annually and 14.2 % of reproductive-aged women in the United Sates reported having received treatment for PID [6,7]. Historically, rates of PID increased in Europe after World War II with the majority associated with N gonorhoeae infections. The rising rates are linked predominantly to more frequent diagnosis with improved health care

* Corresponding author. E-mail address: rbeigi@mail.magee.edu (R.H. Beigi). 0891-5520/08/$ - see front matter 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.idc.2008.05.008

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systems and not necessarily attributed to an increasing burden of disease [8]. Westrom [8] evaluated the change in prevalence from 1960 to 1979 in Lund, Germany, and found the rates of PID in this area paralleled the change in much of the world. Rates of PID steadily increased from 1965 to 1979 with a 1.5-fold increase from 1960 to 1979. Rates increased most signicantly in the 20- to 24-year-old and the 25- to 29-year-old groups with only a slight increase in the 35- to 39-year-old age group. Washington and colleagues [6] saw similar trends in the United States from 1975 to 1981 in a study monitoring the trends in hospitalization for PID. An estimated 267,200 women were hospitalized annually during that time, a rate of 5.3 per 1000 women. Prevalence of PID in the United States peaked in 1982 occurring in one of every seven women [7]. The prevalence appears to be declining with approximately 106,000 women seeking care in a physicians oce for PID in 2006, down from 424,000 in 1983 [9]. The incidence and prevalence of PID in the general population is notoriously dicult to assess, and current gures likely underestimate the burden of disease in several ways. Attempts have been made to estimate the prevalence of PID through use of hospital data, including discharge rates, emergency room visits, physician oce visit data, and patient self-reporting. Additionally, researchers estimate the prevalence of PID in relation to that of gonorrhea or chlamydia infections. All eorts at characterizing the rates of PID are complicated by several factors, including high rates of subclinical PID, increasing rates of outpatient diagnosis, and inaccuracies in diagnosis. Risk factors Several risk factors for PID are clearly identied whereas many remain controversial. Relevant risk factors include demographics, sexual behaviors, and patterns of contraceptive use. PID is highly correlated with sexual activity at a younger age, having several sexual partners, nonuse of barrier contraception, and infection with C trachomatis and N gonorhoeae [1012]. Jossens and colleagues [12] evaluated a population in San Francisco General Hospital and found less than 12 years of education, more than one male sexual partner in the last 30 days, age at rst voluntary intercourse less than 18, prior gonorrhea infection, and intercourse during menses to be risk factors for development of PID. Additionally, use of no birth control method and not using barrier method contraception were highly associated with PID. PID is inversely proportional to age, as shown by Westrom [8] in 1980, with the highest rates of PID in the 15- to 19-year-old group. Several biologic and social factors likely contribute to the higher rates of PID in young women. It is theorized that the cervicovaginal environment in young women tends to increase their risk for developing PID. The new high estrogen environment along with the presence of cervical ectopy with a relatively large transformation zone of exposed columnar epithelium may facilitate the attachment of C trachomatis and N gonorrhoeae, increasing a young womans

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risk for cervical and upper tract disease. Additionally, adolescent women are more likely to engage in high-risk sexual behavior, including having several sexual partners and partners who are more sexually experienced, thus increasing the risk for acquiring STDs. Many have considered vaginal douching a risk factor for PID [11,13,14]. Douching is known to alter the vaginal ora, which is hypothesized to confer an increased risk for PID. Many suspect that douching may increase the risk for PID by forcing vaginal microbes into the upper genital tract. A meta-analysis investigating the relationship between vaginal douching and PID documented a pooled overall relative risk of 1.73 among women who douche [14]. Douching is also a risk factor for the development of bacterial vaginosis, shown in some investigations to be associated with PID [15]. The interaction between bacterial vaginosis and PID is inconclusive, however, and merits ongoing investigation. Microbiologic etiology PID is believed to be caused by the ascension of lower genital tract organisms into the upper tract, including the uterus, fallopian tubes, and peritoneal cavity. The polymicrobial etiology of PID can be delineated articially into two main causative categories: sexually transmitted pathogens and lower genital tract ora. Sexually transmitted infections can be recovered from the upper tract in women who have PID, including C trachomatis (10.0%) and N gonorrhoeae (43.6%). Both organisms are isolated in 12.2% of cases [16]. Other STDs also may contribute to the development of PID but in smaller numbers. Infections from sexually transmitted viruses, including herpes simplex virus and cytomegalovirus, have an unclear association with PID [11]. Jossens and colleagues [16] demonstrated that 30% of PID cases are caused by non-STD, endogenous organisms, including anaerobes and facultative bacteria. Anaerobes, such as Prevotella, Bacterioides, and Peptostreptococcus, are frequently isolated in cases of acute PID [17]. Moreover, microora associated with bacterial vaginosis frequently are isolated from the upper genital tract in women who have PID [15,17]. The polymicrobial nature of this infection is what forms the foundation of treatment regimens (discussed later). Complications of pelvic inammatory disease PID can be considered a spectrum of disease ranging widely in presentation from acute to subclinical infection. Acute PID typically is characterized by abdominal/pelvic pain and tenderness, fever, leukocytosis, and an ill-appearing patient. National Hospital Discharge Survey data show that approximately 50,000 women were hospitalized in 2005 with acute PID [9]. Nearly 30% of those hospitalized have a TOA, one of the most serious complications of PID [18,19]. Mortality attributed to PID is encouragingly low in industrialized nations, with a rate of 0.29 deaths per 100,000 women in the United States in 1979 [20].

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Perihepatitis, also known as Fitz-HughCurtis syndrome, complicates from 1% to 30% of cases of PID [11]. Women may present with right upper quadrant pain and tenderness and, if evaluated surgically, are found to have adhesions between the liver capsule and the anterior abdominal wall. This is found most commonly in PID associated with C trachomatis and N gonorrhoeae [11,21]. Laparoscopic evaluation can conrm the diagnosis with the classic violin string adhesions between the liver and the anterior abdominal wall. Occasionally, elevated liver function tests are noted and the diagnosis may be confused with cholecystitis. There are no known long-term complications of Fitz-HughCurtis that have been observed. The majority of the morbidity and public health care burden attributed to PID comes from the long-term sequelae of the disease, including tubal factor infertility, ectopic pregnancy, and chronic pelvic pain from adhesive disease. The costs to patients and society of all PID-associated conditions is dicult to assess but estimated at $1.88 billion per year in 1998 [5]. Recent projections by Yeh and colleagues [22] suggest each case of PID carries a lifetime cost of $1060 to $3180. During 1998, an estimated $166 million was spent on treatment of chronic pelvic pain, $295 million was spent on treatment of ectopic pregnancies, and $360 million was spent on infertility treatments as a direct result of previous PID infection [5]. Diagnosis It has been demonstrated that no single subjective complaint, physical examination nding, or laboratory nding is highly sensitive or specic for the diagnosis of PID. Thus, the diagnosis of PID requires careful consideration of the combination of patient risk factors, physical examination ndings, laboratory ndings, and overall clinical presentation. Because of this, the diagnosis of PID is imprecise, with the clinical diagnosis of PID having a positive predictive value of only 65% to 90% in even the most experienced practitioners hands. PID traditionally is diagnosed in women who have a combination of abdominal tenderness, cervical motion tenderness, and bilateral adnexal tenderness and who fulll at least one minor diagnostic criteria (documentation of a cervical infection with C trachomatis or N gonorrhoeae, mucopurulent cervicitis, temperature O38.3 C, elevated erythrocyte sedimentation rate or C-reactive protein, or presence of an inammatory mass on pelvic sonography). Updated guidelines from the Centers for Disease Control and Prevention (CDC) liberalized the criteria for diagnosis in 2002 to include the many women who have subclinical PID. These guidelines were developed with the understanding that many women are demonstrated to have evidence of upper genital tract inammation without meeting the strict criteria set out in the 1998 guidelines and that undertreatment of PID carries signicant consequences [23]. Updated guidelines were expanded to include treatment of women at risk for STDs

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who present with lower abdominal or pelvic pain and experience pelvic tenderness on exam for whom no other cause of the pain is identied (Box 1) [24]. The diagnosis of PID often is complicated by the many gynecologic and nongynecologic disorders that can present with similar complaints of lower abdominal pain. A careful history and physical examination alone often help clarify the diagnosis. Women who have PID often present with complaints of slowly developing dull abdominal pain, fevers, and vaginal discharge. Often the symptoms occur after menstruation, worsen over 2 to 3 days, and persist for less than 3 weeks [10,11,25,26]. Many clinicians often are faced with the dilemma of distinguishing PID and appendicitis. Bongard and colleagues [27] evaluated 118 women who presented with an unclear diagnosis of appendicitis or PID. Women who had PID tended to present to the hospital later after the onset of symptoms than those who had appendicitis (median 48 hours versus 21 hours), were more likely to complain of vaginal discharge or bleeding (not statistically signicant), and had diuse or bilateral lower abdominal pain. Additionally, women who had PID were more likely to have cervical motion tenderness or bilateral adnexal tenderness on examination. In contrast, women presenting with appendicitis were more likely to complain of nausea or vomiting but no more likely to complain of anorexia than women who had PID. Women who had appendicitis also were more likely to have solely right lower quadrant pain and tenderness. Laboratory evaluation can be of assistance and often is used in the diagnosis of PID. Measurement of the peripheral white blood cell count is, however, nonspecic and elevated in only 44% of women who have PID. Markers of inammation, such as elevations in C-reactive protein or erythrocyte sedimentation rate, show good sensitivity (74%93%) and specicity (25%90%) in predicting PID [25,2831]. These tests, however, often take signicant time to result and are used less commonly in the acute setting. Vaginal wet smears recently have been evaluated and found to have a high sensitivity for upper genital tract infection (87%91%) if three or more white blood cells are seen per high-power eld [32,33]. Additionally, the absence of white blood cells on a vaginal wet smear has a high negative predictive value (94.5%) for the absence of upper genital tract infection,

Box 1. 2006 Centers for Disease Control and Prevention guidelines for diagnosis of pelvic inammatory disease .empiric treatment of 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 other cause for the illness other than PID can be identied, and if one or more of the following minimum criteria are present: cervical motion tenderness or uterine tenderness or adnexal tenderness.

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making it a potentially useful tool to rule out PID in women who have an otherwise unclear diagnosis [32]. Transvaginal ultrasound commonly is used as an initial tool for evaluation of PID given its ready availability and low cost. Timor-Tritsch and colleagues [34] systematically evaluated 74 patients who had acute, chronic, and no PID and described their ultrasound ndings. The most common nding among women with PID was incomplete septum of the fallopian tube wall (92%), which is indicative of a swollen, tortuous tube. Thick walls (100%) and a cogwheel structure (86%) on cross-section of the fallopian tube were markers of acute disease. Thin walls (97%) and the appearance of nodules within the wall (beads on a string) (57%) often were associated more with subacute disease. Patients who have TOA had complete obliteration of the normal architecture of one or both of the adnexa. Often a mass is noted, within which they were unable to distinguish tube and ovary. Ultrasound has proved useful in diagnosis of TOA and PID complicated by hydrosalpinx or pyosalpinx. Although transvaginal ultrasound has excellent specicity (97%100%), it has a relatively poor sensitivity overall (32% 85%) [35,36]. Transvaginal ultrasound can be helpful in the presence of ndings; however, the diagnosis of PID is clinical and a normal ultrasound should not alter the level of suspicion for the diagnosis. Endometrial biopsy can be a sensitive and specic test for PID; however, the time required to process a biopsy specimen and receive a clinically useful result makes it an unrealistic diagnostic aid in the acute setting. Endometrial biopsy, however, can be helpful in certain less acute clinical scenarios to conrm or negate a suspected diagnosis, with the presence of leukocytes and plasma cells 70% to 90% sensitive and 67% to 90% specic for the diagnosis of PID [37]. Laparoscopic evaluation of the pelvic organs is considered the gold standard for diagnosing PID. Typical ndings include edematous, erythematous fallopian tubes, often with purulent exudate emanating from the mbrial end. Peritubal adhesions also often are present [11,26]. Recent data have called into question, however, the usefulness of visual pelvic inspection alone. Sellors and colleagues [37] demonstrated that visualization alone had an only 50% sensitivity and 85% specicity rate for PID compared with pathologic evaluation of a mbrial biopsy. Laparoscopy is not used routinely to diagnose PID given the cost and risks associated with surgery; it is a useful tool, however, in the evaluation of patients who appear ill and have an unclear diagnosis. Additionally, laparoscopy can facilitate drainage and culture of an abscess for those found to have a TOA or inammatory mass. Treatment Treatment regimens for PID include broad-spectrum antibiotics, reecting the polymicrobial nature of the infection, and always must include coverage for N gonorrhoeae and C trachomatis. Treatment recommendations recently have been altered slightly to reect the emerging ouroquinolone

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resistance seen among certain strains of N gonorrhoeae. Treatment goals include resolution of the acute symptoms with an attempt to prevent the long-term sequelae caused by the inammation and infection. The CDC has published several recommended treatment regimens for inpatient and outpatient treatment (Box 2). Treatment must include adequate coverage for the most common causative agents (discussed previously) and is universally recommended to continue for a total of 14 days. The overall clinical cure rates with the CDC recommended regimens are greater than 90% [10]. Therefore, failure to improve on one of these regimens suggests noncompliance, incorrect diagnosis, or the presence of an inammatory mass, prompting further investigation. Azithromycin recently has been evaluated as part of a treatment regimen for PID in several trials [3840]. Clinical cure rates with azithromycin were found equivalent and compliance was much improved over a standard 2-week, multidrug regimen. Results of the recent trials seem promising and warrant consideration; however, formal recommendations to include azithromycin as part of PID treatment regimens currently await CDC evaluation and endorsement. The safety, ecacy, and role of outpatient treatment recently were demonstrated in the Pelvic Inammatory Disease Evaluation and Clinical Health (PEACH) trial. This was a randomized, multicenter trial that evaluated treatment ecacy and fertility outcomes in women who had mild to moderate PID, comparing inpatient to outpatient management [41]. The investigators found no dierence in resolution at 30 days, with 54.1% of the outpatient group and 62.4% of the inpatient group achieving microbiologic cure. They also documented similar rates of clinical cure between the two groups, with 79.4% of the outpatient group and 81.6% of the inpatient group achieving a clinical cure at 30 days with resolution of their tenderness on examination. Longer-term outcomes also were similar in the two groups when evaluated for PID recurrence, chronic pelvic pain, infertility, ectopic pregnancy, and tubal obstruction as noted on hysterosalpingogram after 3 years [41]. An ongoing follow-up evaluation of the original PEACH cohort addressing outcomes at 84 months was recently published. There was no dierence in the proportion of women achieving pregnancy, live birth, ectopic pregnancy, PID recurrence, or chronic pelvic pain [42]. Based on available data, it seems that clinicians can comfortably manage patients with mild to moderate PID as outpatients without any clear negative consequences on fertility or other outcomes included in these analyses. Even with the larger numbers of patients who have mild to moderate PID treated as outpatients, it remains important to identify those patients who may be better served by management with parenteral antibiotics and inpatient observation. Guidelines previously suggested that all adolescents who have PID be admitted secondary to likely noncompliance with antibiotic regimens and increased concerns for future fertility. This position has been reconsidered, however, and adolescents no longer require routine

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Box 2. Centers for Disease Control and Prevention recommended treatment regimens for pelvic inammatory disease (2006) Parenteral Recommended treatment regimen A Cefotetan 2 g intravenously (IV) every 12 hours OR Cefoxitin 2 g IV every 6 hours PLUS Doxycycline 100 mg orally or IV every 12 hours Recommended treatment regimen B Clindamycin 900 mg IV every 8 hours PLUS Gentamicin loading dose IV or intramuscularly (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 Ampicillin/sulbactam 3 g IV every 6 hours PLUS Doxycycline 100 mg orally or IV every 12 hours Oral/outpatient 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 OR 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 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

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If parenteral cephalosporin therapy is not feasible, use of uoroquinolones (levooxacin 500 mg orally once daily or ooxacin 400 mg twice daily for 14 days) with or without metronidazole (500 mg orally twice daily for 14 days) may be considered if the community prevalence and individual risk for gonorrhea is low. Testing for gonorrhea should be instituted before administration of therapy and the patient managed appropriately if the test is positive.
Data from Centers for Disease Controls and Prevention. Updated recommended treatment regimens for gonococcal infections and associated conditions United States, April 2007. Available at: http://www.cdc.gov/std/Treatment/2006/ updated-regimens.htm. Accessed September 23, 2008.

hospitalization. The nal decision to hospitalize should be left to treating physicians with attention to the CDC recommendations (Box 3). HIV and pelvic inammatory disease Many studies have investigated the interplay between HIV and PID. Clinicians often recommend women who have HIV be hospitalized and treated with parenteral antibiotics, largely because of concern for slower clinical resolution of disease and increased risk for development of TOA. A large trial of 349 women in the United States showed that women who had HIV and PID tended to present with a lower white blood cell count (7411 versus 11,266) and seemed to have a longer hospital course (10.5 versus 6.4 days) compared with women who did not have HIV. Women who were HIV

Box 3. Recommendations for hospitalization of women who have pelvic inammatory disease  Surgical emergencies (eg, appendicitis) cannot be excluded  The patient is pregnant  The patient does not respond clinically to oral antimicrobial therapy  The patient is unable to follow or tolerate an outpatient oral regimen  The patient has severe illness, nausea and vomiting, or high fever  The patient has a TOA
Data from Centers for Disease Control and Prevention. Sexually transmitted disease treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR-11):1-94.

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positive also experienced higher rates of febrile morbidity and required more frequent antibiotic changes. There was no dierence found, however, in the frequency of TOA formation or the need for surgery [43]. More recently, Mugo and colleagues [44] measured the eects of HIV-1 on treatment outcomes in women who had mild, moderate, or severe PID. They found that women who were HIV infected and had severe PID took slightly longer than women who were HIV negative to meet criteria for clinical improvement (6 days versus 5 days). Women who had mild or moderate disease showed no dierence in time to clinical improvement. In addition, the women who had HIV were no more likely to require surgery or need additional parenteral antibiotics. The general consensus is that women who had HIV and PID may be somewhat more likely to require prolonged therapy and may have slightly more complicated courses when compared with their HIV-negative counterparts. Nevertheless, they seem to respond to the same recommended antibiotic regimens and should be treated with standard CDC-directed therapy. Tubo-ovarian abscess TOA is one of the most severe complications of PID and can lead to signicant morbidity and occasional mortality. TOA is an inammatory mass involving the fallopian tube, ovary, and often surrounding structures. Clinical presentation of TOA is similar to that of PID with the addition of a pelvic mass often noted on examination or imaging. Landers and Sweet found that 50% of women who had TOAs presented with fever and chills. Women also frequently presented with nausea (26%), vaginal discharge (28%), and abnormal vaginal bleeding (21%). Although the classic presentation of TOA includes abdominal pain, pelvic mass on examination, fever, and leukocytosis, Landers and Sweet [19] found that 35% of women who had a TOA were afebrile and 23% had a normal white blood cell count. Tubo-ovarian abscess is noted in nearly one third of women hospitalized with PID equating to nearly 100,000 women hospitalized each year [18,19,45]. Risk factors for TOA are similar to those for PID, including multiple sexual partners, sexual activity at a younger age, and lack of barrier contraception use [45]. Several imaging modalities have proved eective for the diagnosis of TOA, including CT, ultrasound, scintigraphy, and radionuclide scanning. Modalities using radionuclide markers may be of some use; however, they are technically dicult and there often is a delay in the results. CT and ultrasound still are the most accepted and most readily available imaging modalities for the recognition and delineation of TOAs. Looking more closely at these two modalities, CT seems to have an improved sensitivity (78%100%) over ultrasound (75%82%) but comes at a higher nancial cost [46,47]. If CT is chosen to evaluate possible TOAs, ideally it should be performed with oral and IV contrast. A recent study by Hiller and colleagues [48] evaluated the appearance of TOA on CT scan, clarifying the most common ndings. On CT imaging, TOAs

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tend to have a thick, uniform, enhancing abscess wall (95%) and to be multilocular (89%) with an increased uid density (95%). The most common ndings also included thickening of the mesosalpinx (91%), inltration into the pelvic fat (91%), bowel thickening (59%), and thickening of the uterosacral ligaments (64%). Pyosalpinx was noted 50% of the time. Ultrasound frequently is used as an initial tool for evaluation of PID and is helpful in distinguishing PID and TOA. Patients who have TOA frequently have complete obliteration of the normal architecture of one or both of the adnexa. Often a cystic or multiseptated mass is noted, within which tube and ovary are unable to be distinguished. Speckled uid also is seen commonly on ultrasound and correlates with purulent material within the abdomen or cul-de-sac [47]. Landers and Sweet [19] evaluated a series of 98 cases of suspected PID by ultrasound. Thirty-one cases were surgically conrmed to have TOAs and 29 (90%) of these were diagnosed correctly on ultrasound preoperatively. The transvaginal ultrasound identied a complex adnexal mass or a cystic-type mass with multiple internal echoes. The two cases not identied on ultrasound had simple cystic masses. The microbial etiology of TOAs typically is polymicrobial with a mixture of anaerobic, aerobic, and facultative organisms being isolated. It is believed that N gonorrhoeae also is a signicant contributing causative agent but is rarely isolated from the abscess cavity. Landers and Sweet [19] demonstrated, however, that N gonorrhoeae, although rarely recovered from the abscess cavity (3.8%), frequently is recovered from the endocervix (31%) in cases of TOA. The organisms recovered from TOAs mirror those found in PID not complicated by TOA, such as Escherichia coli, Prevotella, Bacterioides, and Pepotostreptococcus species [18,19]. In vivo studies suggest that infection with N gonorrhoeae may facilitate the invasion of the upper tract by lower genital tract ora [49]. Treatment of TOA historically was surgical with most women having a total abdominal hysterectomy and bilateral salpingo-oophorectomy. Management of TOAs has changed drastically in the past three decades with the advent of broad-spectrum antibiotics and continues to evolve with improved imaging and drainage techniques. Studies have demonstrated an overall 16% to 95% success rate with conservative medical management of TOAs with the majority of studies demonstrating a success rate of 70% or greater [45]. Primary treatment has shifted from surgery to antimicrobial chemotherapy with surgery reserved for patients who have suspicion for ruptured TOAs or a poor response to antibiotics. The success of medical management has been demonstrated to be inversely proportional to the size of the TOA. Reed and colleagues [50] evaluated 119 women who had TOAs and found that women who had TOAs greater than or equal to 10 cm had a greater than 60% chance of requiring surgery. In this same study, women who had a mass 4 to 6 cm had less than 20% chance of requiring surgery. Although these data suggest that surgical intervention for large TOAs likely is necessary, the decision to proceed with surgical management of a TOA should be based on the overall clinical presentation, in addition to patient response to antibiotic treatment.

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Rupture of a TOA is a surgical emergency with women commonly presenting with signs and symptoms of diuse peritonitis, which subsequently can progress to overwhelming sepsis. Before the use of broad-spectrum antibiotics in the 1950s, ruptured TOA carried an 85% to 100% mortality rate [51,52]. As clinicians used more aggressive surgical management and improved antibiotic chemotherapy, the mortality rate decreased drastically to 3.1% [51]. Older reports demonstrated improved survival rates with total hysterectomy and bilateral salpingo-oophorectomy when compared with fertility-conserving surgery. Given that TOAs occur most commonly in young, reproductive-aged women, however, an eort has been made to treat TOAs with conservation of fertility. Landers and Sweet [19] showed more recently that aggressive, fertility-sparing surgery with unilateral adnexectomy is successful when combined with intensive medical management. The demonstration of high rates of successful medical management of TOAs calls into question the dictum that all abscesses necessitate drainage. Antibiotic choice is based on the common causative agents and the ability of the chosen antibiotic to penetrate the abscess cavity. The CDC recommendations for parenteral treatment of PID (see Box 2) provide excellent coverage for TOAs, incorporating coverage for B fragilis, gram-negative and gram-positive aerobic microbes and N gonorrhoeae. Often, metronidazole or clindamycin are chosen given their anaerobic spectra of action and their success in abscess wall penetration. In addition, newer broad-spectrum single agents antibiotics are used with some success (ie, imipenem-cilastatin, piperacillin-tazobactam, and ampicillin-sulbactam). Given the complexity of the infection, women often require prolonged treatment with parenteral antibiotics. It is generally agreed that women who have TOAs require hospital admission, at least at the outset of therapy. They should be monitored carefully for an adequate response to antibiotics and any signs of rupture of the TOA and discharged after sucient response to parenteral antibiotics is demonstrated (ie, resolution of pain and tenderness, defervescence of fever, normalization of leukocytosis, and stability or decrease in the size of the mass noted on imaging studies). Improved radiologic technology has led to increased use of percutaneous drainage procedures, sparing many women longer, more complex surgical procedures. Historically, patients underwent a posterior colpotomy with direct drainage of a cul-de-sac abscess. Current technology has made this practice less necessary, allowing clinicians to drain abscesses more easily and eectively using ultrasound or CT guidance. In certain situations, however, drainage of an abscess in the pelvic cul-de-sac through a posterior colpotomy is a simple and eective way of treating low-lying pelvic abscesses. Pelvic and abdominal abscesses can be drained with imaging-guided techniques abdominally, vaginally, transgluteally, or transrectally. The majority of minimally invasive drainage, however, is performed transvaginally or transabdominally.

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Gjelland and colleagues [53] reviewed 302 cases of patients who were administered antibiotics and subsequently underwent transvaginal, ultrasound guided drainage. Treatment was successful in 93.4% of women, with 62.3% having complete resolution of their pain within 48 hours of the rst drainage. Temperature also normalized within 48 hours in 77.4% of patients. Approximately 6% of women ultimately required surgery. The location of the abscess and accessibility determines the mode of drainage. Others have reported high success rates with various methods of minimally invasive drainage. Patients who have complicated pelvic abscesses, however, often have multiloculated collections, which may lower success rates in clinical practice. In addition, no large-scale randomized trials have been performed to help clarify the precise role of imaging-guided drainage procedures in the management of TOAs. Nevertheless, minimally invasive drainage remains a valid option in the management of women with TOAs. If a decision for abscess drainage is made, the choice of surgery versus guided drainage should be individualized and based on local expertise and surgical capabilities. Summary PID remains an important and prevalent pelvic infection among reproductive-aged women. PID is responsible for severe acute morbidity and signicant long-term sequelae, including tubal factor infertility, ectopic pregnancy, and chronic pelvic pain. The medical and economic burden of PID is substantial. The diagnosis, although imprecise, is predominantly clinical and should be considered in reproductive-aged women with appropriate risk proles and clinical presentations. The presence of a TOA represents a serious infection and often mandates hospital admission, prolonged parenteral antibiotic treatment, and occasional surgical extripation. Clinicians caring for women must remain vigilant in the diagnosis and treatment of PID and TOA. References
[1] Mardh P-A, Lind I, Svensson L, et al. Antibodies to Chlamydia trachomatis, Mycoplasma hominis and Neisseria gonorrheoae in serum from patients with acute salpingitis. Br J Vener Dis 1981;57:1259. [2] Sweet RL, Schachter J, Robbie MO. Failure of beta-lactam antibiotics to eradicate Chlamydia trachomatis in the endometrium despite apparent clinical cure of acute salpingitis. JAMA 1983;250:26415. [3] Wasserheit JN, Bell TA, Kiviat NB, et al. Microbiological causes of proven pelvic inammatory disease and ecacy of clindamycin and tobramycin. Ann Intern Med 1986;104:18793. [4] Sweet RL, Schachter J, Landers DV, et al. Treatment of hospitalized patients with acute pelvic inammatory disease: comparison of cefotetan plus doxycycline and cefoxitin plus doxycycline. Am J Obstet Gynecol 1988;158:73643. [5] Rein DB, Kassler WJ, Irwin KL, et al. Direct medical cost of pelvic inammatory disease and its sequelae: decreasing, but still substantial. Obstet Gynecol 2000;95:397402.

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