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Author: Richard H Beigi, MD, MSc

Section Editors: Howard T Sharp, MD, Jeanne Marrazzo, MD, MPH, FACP, FIDSA
Deputy Editor: Alana Chakrabarti, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2021. | This topic last updated: Mar 05, 2021.

INTRODUCTION
The female genital tract may be affected by ascending infection, either from sexually transmitted
infections or vaginal flora. Pelvic inflammatory disease (PID) refers to acute and subclinical
infection of the upper genital tract, involving any or all of the uterus, fallopian tubes, and ovaries;
this is often accompanied by involvement of the neighboring pelvic organs. It results in
endometritis, salpingitis, oophoritis, peritonitis, perihepatitis, and/or tubo-ovarian abscess (TOA).

PID may be complicated by a TOA, which is an inflammatory mass involving the fallopian tube,
ovary, and, occasionally, other adjacent pelvic organs (eg, bowel, bladder); TOA may also occur
without preceding PID [1]. These abscesses are found most commonly in reproductive-age
patients and typically result from upper genital tract infection. TOA typically occurs as a
complication of PID.

TOA is a serious and potentially life-threatening condition. Aggressive medical and/or surgical
therapy is required, and rupture of an abscess may result in sepsis. For patients with ruptured
abscesses, current mortality rates have not been reported, but data from the 1960s suggest the
rate may be as high as 1.7 to 3.7 percent [2-4]. The mortality rate approaches zero for abscesses
that are not ruptured.

Treatment modalities for TOA include antibiotic therapy, minimally invasive drainage procedures,
invasive surgery, or a combination of these interventions. The large majority of small abscesses
(<7 cm in diameter) resolves with antibiotic therapy alone.

The management of TOA is reviewed here. The epidemiology, diagnosis, and evaluation of TOA are
discussed separately. (See "Epidemiology, clinical manifestations, and diagnosis of tubo-ovarian
abscess".)

Other manifestations of PID are discussed separately.


:
● (See "Pelvic inflammatory disease: Pathogenesis, microbiology, and risk factors".)

● (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis".)

● (See "Long-term complications of pelvic inflammatory disease".)

● (See "Pelvic inflammatory disease: Treatment in adults and adolescents".)

CLINICAL APPROACH
Antibiotics are the mainstay of treatment for TOA. In some patients, antimicrobial therapy must be
combined with a minimally invasive drainage procedure or with surgery.

The availability of broad-spectrum antibiotics with excellent antimicrobial activity and abscess
cavity penetration has revolutionized the primary treatment of nonruptured TOA. The advent of
these antimicrobial agents reversed the dictum prior to the 1970s that all abscesses required
drainage [5-8].

Patients who are immunosuppressed should be treated in the same manner as other patients;
there are no data to support early surgical intervention in this patient population. Some data
suggest that patients with HIV infection are more likely to have a complicated clinical course.
However, treatment efficacy using the available approaches appears to be similar among HIV-
infected and non-HIV-infected patients [9,10]. As an example, studies of TOA or pelvic
inflammatory disease alone in patients with HIV infection do not suggest a benefit of early
surgical treatment. (See "Pelvic inflammatory disease: Treatment in adults and adolescents",
section on 'Patients with HIV'.)

Stable premenopausal patients — Most patients with TOA are candidates for management with
antibiotics and are able to avoid surgery. We suggest antibiotic therapy alone as a highly
successful strategy for patients who meet all of the following criteria:

● Hemodynamically stable with no signs of a ruptured TOA (acute abdomen, sepsis) that is
maintained throughout the entire treatment course.

● Continued clinical improvement while on the antibiotic regimen.

● Abscess <7 cm in diameter.

● Adequate response to intravenous antibiotic therapy.

● Premenopausal.
:
Abscess size is predictive of treatment success with antibiotics alone and of length of hospital stay.
Early observational studies have reported that patients with abscesses measuring 9 cm in
diameter on imaging appear to have a much higher likelihood of requiring surgical therapy
compared with those with smaller masses (60 versus approximately 30 to 40 percent, respectively)
[11,12]. Subsequent investigations have noted that the size of the abscess predictive of
necessitating drainage is likely more in the range of 7 cm [13].

Thus, for most patients with a TOA 7 cm, we perform surgical exploration with incision and
drainage. It is reasonable, however, to initiate antibiotic therapy alone in selected patients with
large abscesses who are hemodynamically stable and have reasons to avoid surgery (eg, a history
of pelvic surgery that suggests the presence of pelvic adhesions or desire to preserve fertility). In
our practice, we evaluate these patients on a case-by-case basis and consider them candidates for
antibiotics alone if there are no other indications for surgical intervention (eg, suspicion of abscess
rupture, lack of response to antimicrobial therapy). In these cases, the patient should be
counseled about the high risk that antimicrobial therapy will fail and that surgery will be required,
as well as the risk of a worsening clinical condition while on antibiotics alone [12]. In addition to
antibiotics, these patient may benefit from image-directed drainage procedures. Drainage may
lead to successful management, particularly when substantial amounts of inflammatory fluid can
be drained from the abscess cavity.

Stable postmenopausal patients — The majority of TOAs are diagnosed in reproductive-age


patients, but the finding of a TOA in a postmenopausal patient raises concern for the potential of
an underlying malignancy.

Case series have reported that there is a high rate of malignancy among postmenopausal patients
with TOA [14-17]. As an example, in one series, genital tract malignancy was found in 8 of 17
postmenopausal patients compared with 1 of 76 premenopausal patients [15].

Thus, postmenopausal patients with a presumed TOA should be counseled about the potential for
malignancy and the possible need for a full staging procedure. For these patients, we suggest
surgical exploration rather than treatment solely with antibiotics or a minimally invasive drainage
procedure. For patients in whom there is a low suspicion of malignancy and who have been
appropriately counseled about the possibility of malignancy, nonsurgical management is a
reasonable option, and serial imaging studies are required to demonstrate complete resolution of
the pelvic mass. If the mass does not resolve, surgery is required.

If a surgical approach is used in a postmenopausal patient, however, an intraoperative frozen


section analysis of the adnexal mass should be performed. In addition, the pelvis and abdomen
should be explored for evidence of metastatic disease. If malignancy is found, surgical staging
should be performed by a surgeon with appropriate experience.
:
Patients with sepsis and/or ruptured abscess — Rupture of a TOA is a life-threatening
emergency and requires prompt surgical intervention [2]. Even in the absence of evidence of
abscess rupture, surgical exploration and treatment are often advisable in any patient with overt
signs of sepsis and a large abscess ( 7 to 9 cm).

A ruptured TOA occurs in approximately 15 percent of cases [3,8]. Sepsis occurs in approximately
10 to 20 percent of patients with TOA [7].

Rupture is probably a misnomer, as the process is more like a leak, slow or fast; it is not typical for
the abscess to burst open. Patients with a ruptured TOA classically present with an acute
abdomen and signs of sepsis, although sepsis is not consistently present. Clinical findings
suggestive of rupture include, but are not limited to, acute peritoneal signs, hypotension,
tachycardia, tachypnea, or acidosis. (See "Epidemiology, clinical manifestations, and diagnosis of
tubo-ovarian abscess", section on 'Ruptured abscess'.)

Antibiotics should also be started as soon as possible, either before or during the urgent operative
intervention. In our experience, most patients who are acutely ill will not improve without surgical
removal of the nidus of infection. Importantly, in an unstable patient with the presumptive
diagnosis of abscess rupture, surgery should not be delayed for the administration of antibiotics.

ANTIBIOTIC THERAPY
TOA is treated with antibiotics, typically with initial therapy administered intravenously (IV) and as
an inpatient [18]. Outpatient and/or oral antibiotic therapy should be given to complete a course
of therapy only if patients show substantial clinical improvement. Patients should be closely
monitored to ensure successful treatment.

Antibiotic therapy alone is effective in approximately 70 percent of patients [5-8,11,19-21]. This


therapeutic approach is limited by the characteristics of abscesses (eg, relatively avascular, not
easily permeated by antimicrobials, low pH). The rich ovarian blood supply may contribute to the
relatively high rate of successful treatment with antimicrobial therapy.

Empiric regimen selection — Antibiotic regimens for TOA are similar to those for pelvic
inflammatory disease (PID), but there are additional considerations such as abscess wall
penetration and data specific to TOA treatment.

Treatment options include regimens using one, two, or three agents ( table 1):

● First-choice regimens:

• Cefotetan (2 g IV every 12 hours) plus doxycycline (100 mg orally or IV every 12 hours).


:
• Cefoxitin (2 g IV every 6 hours) plus doxycycline (100 mg orally or IV every 12 hours).

• Clindamycin (900 mg IV every 8 hours) plus gentamicin (2 mg/kg loading dose then 1.5
mg/kg every 8 hours IV or intramuscularly [IM]). For gentamicin dosing, single daily
dosing may be substituted (3 to 5 mg/kg IV once per day).

• Ampicillin (2 g IV every 6 hours) plus clindamycin (900 mg IV every 8 hours) plus


gentamicin (2 mg/kg loading dose then 1.5 mg/kg every 8 hours IV or IM). For gentamicin
dosing, single daily dosing may be substituted (3 to 5 mg/kg IV once per day). This is a
three-antibiotic regimen.

• Ampicillin-sulbactam (3 g IV every 6 hours) plus doxycycline (100 mg orally or IV every 12


hours).

● Second-choice regimens:

• Levofloxacin (500 mg IV once daily) plus metronidazole (500 mg IV every 8 hours).


Consideration should be given to this regimen choice in areas with non-negligible rates of
fluoroquinolone-resistant gonorrhea.

• Imipenem with cilastatin (500 mg IV every 6 hours).

Antimicrobial therapy for TOA is based upon the following considerations:

● All regimens share the common characteristics of broad coverage for all associated bacteria
(similar to treatment regimens for PID), including coverage for the sexually transmitted
pathogens (Neisseria gonorrhoeae and Chlamydia trachomatis, although these bacteria are
rarely isolated from a TOA), as well as anaerobes [5,7,8,18,20,21]. It is still inconclusive
whether additional anti-anaerobic coverage is needed above and beyond the second-
generation cephalosporin. For this reason, the Centers for Disease Control and Prevention
(CDC) guidelines for treatment of PID advise only selected use of metronidazole [18]. If
sexually transmitted pathogens are isolated from patients with TOA, clinicians should ensure
that pathogen-specific therapy is included in the treatment regimen. (See "Epidemiology,
clinical manifestations, and diagnosis of tubo-ovarian abscess", section on 'Microbiology'.)

● Regimens that include drugs with demonstrated superior abscess wall penetration and
activity within the cavity (eg, clindamycin, metronidazole, cefoxitin) are often incorporated into
the treatment regimen [22].

Within these parameters, various antibiotic regimens have been found to be effective for the
medical management of TOA. PID and TOA share many similarities, but TOA treatment
recommendations have never been exactly the same as PID recommendations. The data from
:
which treatment recommendations derive for these two conditions overlap to a great extent, and
there are also studies of only patients with TOA.

The majority of clinical data support the use of the first-choice regimens listed above and in the
table ( table 1). These include the two-antibiotic regimens also used for hospitalized patients
with PID: cefotetan plus doxycycline; cefoxitin plus doxycycline. Additional regimens found to be
effective in TOA include clindamycin plus gentamicin; ampicillin plus clindamycin plus gentamicin;
or ampicillin-sulbactam plus doxycycline. Data from head-to-head comparisons of the first-choice
agents have shown nearly equivalent efficacy for the different regimens (approximately 70
percent and including patients with different size abscesses) [6,8,11,21].

Concern had been raised about potential resistance of bowel flora to cefotetan or to the closely
related agent cefoxitin. Bowel flora are often involved in the TOA pathogenesis. This concern is
based upon findings from a randomized trial that found that ertapenem was significantly more
effective than cefotetan at preventing surgical site infection in patients undergoing elective bowel
surgery [23]. However, there is no evidence of drug-resistant pathogens impacting treatment of
TOA. In addition, guidelines from the Infectious Diseases Society of America on management of
intra-abdominal infection suggest cefoxitin as a reasonable choice for cases with mild-moderate
severity [24]. Thus, cefotetan and cefoxitin remain first-line agents for treatment of TOA.

Among the first-choice regimens, some data suggest that triple therapy is more effective than
double therapy. A small series of patients with TOA reported that the treatment success rate was
higher with a three-antibiotic regimen with ampicillin/clindamycin/gentamicin compared with two
two-antibiotic regimens (clindamycin/gentamicin or cefotetan/doxycycline; 88 versus 47 or 34
percent) [25]. Although this study did suggest higher efficacy among patients who received triple
therapy, the small study size and noncomparative nature of the investigation suggest that further
study is required before definitive conclusions can be made about superiority of three-antibiotic
regimens.

In addition to the standard regimens listed and suggested for use (due to years of data and
successful use in clinical practice), newer agents that likely also have a role in the treatment of
TOA, based on more limited investigation and known spectrum of action against pathogens
causing serious intra-abdominal infections, include ertapenem (1 gram IV every 24 hours) or
piperacillin-tazobactam (3.375 gram IV every 6 hours) [26-28].

The presence of drug hypersensitivities and risk factors for aminoglycoside toxicity (eg, renal
insufficiency) are also relevant considerations when choosing a regimen. (See "Allergy evaluation
for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with
other beta-lactam antibiotics" and "Aminoglycosides", section on 'Toxicity'.)

Directed therapy
:
Actinomyces or rare pathogens — Clinical experience suggests that pathogen-directed
therapy should be included in the regimen in cases of TOA in which a culture demonstrates
Actinomyces israelii. For patients with a TOA with this pathogen, we use one of the standard
antimicrobial regimens for TOA ( table 1) including a beta-lactam antibiotic (eg, ampicillin-
sulbactam). When the standard regimen is complete, we continue treatment with penicillin for at
least one additional month. Doxycycline may be used for patients with a penicillin allergy. There
are no high-quality data regarding duration of therapy for this pathogen; most experts suggest
three to six months of penicillin treatment.

Scattered case reports highlight the potential for an occasional unusual pathogen to be isolated
from a TOA (eg, Candida spp., Pasteurella multocida, Salmonellae) [29-31]. These cases should be
managed on a case-by-case basis, as these are not the usual endogenous genital tract flora found
in the overwhelming majority of TOAs. Consultation with an expert in infectious diseases may be
appropriate in such cases. (See "Epidemiology, clinical manifestations, and diagnosis of tubo-
ovarian abscess", section on 'Microbiology'.)

Monitoring therapy — Patients require inpatient observation during initial therapy due to the
serious nature of the infection, the potential for abscess rupture and ensuing sepsis, and
occasional diagnostic uncertainty [5-8,19,25]. The CDC recommends at least 24 hours of inpatient
observation; in our practice, we typically continue inpatient treatment and observation for 48 to 72
hours.

We generally perform daily white blood cell counts while we are monitoring response to therapy
to assure our medical management is effective. We also repeat imaging studies approximately
every three days and then less frequently if there is consistent clinical improvement. (See
"Epidemiology, clinical manifestations, and diagnosis of tubo-ovarian abscess", section on
'Imaging studies'.)

Duration of therapy — The duration of antibiotic therapy required for treatment of a TOA is
not well established. The duration depends upon several factors:

● When antibiotics alone are the chosen therapy, a minimum of 14 days is common practice.
This is consistent with the CDC guidelines on the treatment for PID [18].

● When imaging-guided drainage procedures and/or extirpative surgery are used in


combination with antimicrobial therapy, there are no data available to formally guide length
of therapy. In our experience, 10 to 14 days of total antibiotic therapy is usually effective. The
overall clinical scenario of each individual patient must also be taken into consideration in
these decisions.

Most experts recommend continuation of antibiotic therapy until the abscess has resolved on
:
follow-up imaging studies. This can sometimes require four to six weeks of total antibiotic therapy.
In cases in which the patient is improving on antibiotics alone, but the abscess has not completely
resolved, longer courses of outpatient antibiotics may be given. Cases that do not resolve with
routine therapy are best managed in collaboration with an expert in infectious diseases.

Switching to oral therapy — Finishing the course of therapy with oral antibiotics as an
outpatient is reasonable in select patients. When patients have demonstrated the criteria below,
one can consider completion of the treatment in the outpatient setting. Candidates for outpatient
therapy should meet all of the following criteria:

● Demonstrate clear clinical improvement – Afebrile for at least 24 to 48 hours, white blood cell
counts that have normalized, improving abdominal symptoms with significantly less
abdominal tenderness, etc.

● Able to tolerate oral medications.

● Able to comply with follow-up communication and appointments.

Oral antibiotic regimens for completion of TOA therapy in selected patients include ( table 1):

● Levofloxacin (500 mg orally once daily) plus metronidazole (500 mg orally twice daily).

● Ofloxacin (500 mg orally once daily) plus metronidazole (500 mg orally twice daily).

● Amoxicillin-clavulanate XR (2000 mg extended release orally twice daily).

● Clindamycin (450 mg orally four times daily) plus doxycycline (100 mg orally twice daily).

● Metronidazole (500 mg orally twice daily) plus (doxycycline 100 mg orally twice daily).

Patients who fail antibiotic therapy — After 48 to 72 hours of treatment with antibiotics alone,
patients with TOA who do not respond or worsen require either minimally invasive abscess
drainage or surgery. Antibiotics remain a cornerstone of therapy before, during, and after any
abscess drainage procedure.

The criteria used to determine failure of treatment are:

● New onset or persistent fever


● Persistent or worsening abdominopelvic tenderness
● Enlarging pelvic mass
● Persistent or worsening leukocytosis
● Suspected sepsis
:
C-reactive protein (CRP) level trends can also be used as a determinant of failed medical therapy
[32-34]. In a prospective cohort study of 94 patients with PID, CRP levels >49.3 mg/L were found to
be a strong laboratory predictor of TOA (85 percent sensitivity and 93 percent specificity), and
increasing CRP values during hospitalization were an indicator of failed medical therapy and the
need for surgical intervention [32].

There are no high-quality data to guide whether to proceed with minimally invasive imaging-
guided drainage procedures or surgery for patients who do not clinically improve. The largest
clinical series evaluating failure of antibiotics for TOA used surgical intervention as the reference
standard [6].

For patients who do not worsen, but fail to clearly improve on antibiotics alone, an imaging-
guided percutaneous drainage procedure appears to be appropriate.

For patients who are clearly clinically worsening using the clinical parameters listed, in our
institution, we generally move promptly to surgery. In addition, surgical intervention is required in
patients who are not improving on antimicrobial therapy and in whom minimally invasive
drainage is not feasible (eg, mass is multiloculated or difficult to access or a physician experienced
in these procedures is not available) [35,36].

DRAINAGE AND SURGERY


Abscess drainage or surgery is required if a patient cannot be successfully treated with
antimicrobials alone and/or there is suspicion of malignancy. This includes patients with one or
more of the following characteristics: failed antibiotic therapy, ruptured abscess, suspected sepsis,
or postmenopausal. The decision regarding drainage or surgery depends on the patient's clinical
status. Suspected intra-abdominal rupture of a TOA is a life-threatening emergency and requires
prompt surgical intervention [2]. (See 'Clinical approach' above and 'Patients who fail antibiotic
therapy' above.)

Minimally invasive drainage procedures — Since the 1970s, various methods have been used
successfully to drain intra-abdominal abscess collections without requiring surgery [5,7,8,35,36].
Procedures guided by either computed tomography or ultrasonography have been used, and a 70
to 100 percent success rate for adequate TOA drainage has been reported in case series [35-43].
As an example, a retrospective study of imaging-guided drainage procedures in 49 patients with
TOA reported successful treatment without subsequent need for surgery in 74 percent of patients
[44]. In addition, a separate small, retrospective investigation suggests that early drainage of
collections via percutaneous methods combined with antibiotic therapy may result in higher
efficacy and shorter overall treatment duration when compared with antibiotics alone [45].
Definitive conclusions await controlled study.
:
Studies have used varied anatomic approaches, including percutaneous, transvaginal, transrectal,
and transgluteal. The approach and imaging modality used vary depending upon the exact
location of the abscess, available technology, and experience of the physician performing the
procedure. In all settings, any fluid that is aspirated should be sent to the microbiology laboratory
for aerobic and anaerobic cultures.

In general, studies have reported higher success rates (defined as clinical improvement without
the need for surgery) for drainage procedures in smaller, unilocular fluid collections [46]. Thus, the
multilocular nature of many complex TOA collections may lessen the success rate in clinical
practice. Nevertheless, this innovative approach can be highly successful and will continue to grow
in popularity and efficacy as more radiologists acquire the necessary skills to perform these
procedures and as the radiologic technology continues to improve.

Prior to the availability of modern imaging-guided drainage procedures, gynecologists drained


pelvic abscesses transvaginally through a posterior colpotomy. This procedure is most appropriate
for posthysterectomy vaginal cuff abscesses that are in the lower pelvis and dissect to the
rectovaginal septum. However, the usual location of a TOA is more superior in the pelvis and
makes this a less viable drainage approach. Reports have also highlighted occasional onset of
peritonitis and sepsis after use of this approach for a TOA [7]. Thus, in most patients with TOA, this
approach should be avoided.

Surgery — Laparotomy is the surgical route used by most gynecologic surgeons for treatment of
TOA. The decision of which incision to employ is important, given the need for complete pelvic
visualization. We often use either a Maylard transverse or vertical midline incision, given the
improved exposure afforded by these incisions. (See "Incisions for open abdominal surgery".)

Some data suggest that a laparoscopic approach can be used successfully, primarily among
patients with no evidence of a ruptured abscess [3,47]. In addition, a few modestly sized case
series suggest improved outcomes while using a laparoscopic approach (compared with
laparotomy), but definitive data are lacking given there are no well-controlled prospective
investigations [48]. The choice between laparoscopy and laparotomy depends greatly on the skill
of the surgeon. Even in patients without evidence of rupture, a laparoscopic approach should be
undertaken only by an experienced laparoscopic surgeon. Surgical treatment of TOA is often a
complex procedure, given the extensive, common involvement of varied intra-abdominal organs
and inflamed nature of the involved tissues.

The importance of involvement of experienced gynecologic surgeons cannot be overstated.


Regardless of an open or laparoscopic approach, surgical cases involving TOA are notoriously
challenging, given the anatomic distortion and friable tissue planes that universally exist from the
extensive inflammatory process. It is not uncommon to also require the assistance of a surgeon
experienced with bowel surgery. Appropriate preoperative arrangements assuring availability of
:
operators possessing these skills are prudent. When the clinical scenario allows, preoperative
bowel preparation is encouraged.

The steps of surgical procedure for TOA are the following:

● Confirm the diagnosis of TOA ( picture 1).

● Remove as much of the abscess cavity and associated infectious/inflammatory fluid and
debris as possible.

● Copiously irrigate the peritoneal cavity, thereby lessening the overall infectious/inflammatory
burden to the patient.

Anaerobic and aerobic cultures should be obtained from the peritoneal cavity upon entry and of
the fluid in the abscess cavity itself. Tissue specimen cultures collected and sent from the abscess
cavity can likewise provide accurate microbiologic information. All removed tissues should be sent
for pathologic evaluation. As noted above, a TOA is sometimes associated with malignancy,
particularly in a postmenopausal patient.

The traditional approach had been to perform a total abdominal hysterectomy and bilateral
salpingo-oophorectomy (TAH-BSO) to remove all infected tissue. While in some situations this is
still the optimal approach, further investigations have validated unilateral salpingo-oophorectomy
alone as an accepted and appropriate management for unilateral TOA [2,6,7,19]. This more
conservative procedure not only has the added benefit of preserving fertility and hormonal
function but also is technically less involved with generally lower overall surgical morbidity. Thus,
we suggest a conservative approach in most patients, particularly in those who are
premenopausal and who wish to preserve fertility.

In patients who are acutely ill and who have completed childbearing, complete extirpative surgery
(TAH-BSO) is often the procedure of choice. In our experience, this more aggressive approach
hastens complete recovery compared with less extensive surgical approaches. In addition, this
eliminates the possibility of repeat surgery that is required in 10 to 20 percent of patients who
undergo more conservative surgical interventions [2,6,7,19]. Consultation with clinicians
experienced with the management of complicated cases of TOA is often helpful, if possible.

Given the high rates of wound infection from contamination of the surgical field ("dirty wound")
generated from abscess cavity disruption, we often use the following measures, when appropriate
[2,5,7,8,49]:

● Close the fascia with monofilament nonabsorbable or delayed-absorbable suture, leaving the
skin and subcutaneous wound open for at least the early postoperative period (72 hours). The
wound can then be managed with a delayed closure procedure or can heal by secondary
:
intention. Many gynecologic surgeons will opt for primary skin closure in such patients, and
this may also be a reasonable option for patients with extensive TOA surgery, although no
direct evidence suggests the superiority of either approach. (See "Complications of abdominal
surgical incisions", section on 'Delayed closure'.)

● Leave in a closed suction drain (eg, Jackson-Pratt) postoperatively until the patient
demonstrates clinical improvement and the output from the drain is minimal.

SPECIAL ISSUES

Pregnant patients — TOA has rarely been reported in pregnant patients [50-55]. The approach to
a pregnant patient with a TOA is similar to nonpregnant patients. Care should be taken to avoid
medications that are potentially teratogenic (eg, quinolones). In addition, decisions regarding
surgical care will depend in part upon the safety of surgery at a specific gestational age. (See
"Anesthesia for nonobstetric surgery during pregnancy".)

Treatment of sexual partners — For patients with TOA who test positive for sexually transmitted
infection, sexual partners should be notified of the need for evaluation and treatment. (See "Pelvic
inflammatory disease: Treatment in adults and adolescents", section on 'Management of sex
partners'.)

SOCIETY GUIDELINE LINKS


Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Gynecologic infectious
diseases (non-sexually transmitted)".)

SUMMARY AND RECOMMENDATIONS

● A tubo-ovarian abscess (TOA) is an inflammatory mass involving the fallopian tube, ovary, and,
occasionally, other adjacent pelvic organs (eg, bowel, bladder). These abscesses are found
most commonly in reproductive-age patients and typically result from upper genital tract
infection. (See 'Introduction' above.)

● Rupture of a TOA occurs in approximately 15 percent of cases. Patients suspected of having a


ruptured TOA or who present with signs of sepsis require immediate surgical exploration.
Laparotomy appears to be the best route in these emergency cases. (See 'Patients with sepsis
and/or ruptured abscess' above and 'Drainage and surgery' above.)
:
● We suggest treatment with antibiotic therapy alone ( table 1) rather than imaging-guided
drainage or surgery for premenopausal patients who meet all of the following criteria:
hemodynamically stable with no signs of a ruptured TOA, abscess <7 cm in diameter, and
adequate response to antibiotic therapy(Grade 2C). Treatment with antibiotics alone is also
reasonable in patients with an abscess that is 7 cm who meet these criteria and are aware of
the decreased efficacy of this approach in their clinical situation. (See 'Stable premenopausal
patients' above.)

● The risk of concurrent gynecologic malignancy appears to be much higher among


postmenopausal patients with TOA. For postmenopausal patients with a presumed TOA, we
suggest surgical diagnosis and/or treatment rather than treatment solely with antibiotics or a
minimally invasive drainage procedure (Grade 2C). For patients in whom there is a low
suspicion of malignancy and who have been appropriately counseled about the possibility of
malignancy, nonsurgical management is a reasonable option, and serial imaging studies are
required to demonstrate complete resolution of the pelvic mass. (See 'Stable postmenopausal
patients' above.)

● For patients treated with antibiotics alone who show no improvement, but are not worsening,
we suggest a minimally invasive abscess drainage procedure (Grade 2C). For those on
antibiotic therapy who are clinically worsening, we suggest surgical treatment (Grade 2C).
Antibiotic therapy should be maintained in combination with these additional interventions.
(See 'Patients who fail antibiotic therapy' above.)

● The choice of an open or laparoscopic surgical approach in surgery for a nonruptured TOA is
largely based on operator skill, experience, and ability to perform the necessary surgical
maneuvers given the anatomic distortion. (See 'Surgery' above.)

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REFERENCES
1. Granberg S, Gjelland K, Ekerhovd E. The management of pelvic abscess. Best Pract Res Clin
Obstet Gynaecol 2009; 23:667.

2. PEDOWITZ P, BLOOMFIELD RD. RUPTURED ADNEXAL ABSCESS (TUBOOVARIAN) WITH


GENERALIZED PERITONITIS. Am J Obstet Gynecol 1964; 88:721.

3. Rosen M, Breitkopf D, Waud K. Tubo-ovarian abscess management options for women who
desire fertility. Obstet Gynecol Surv 2009; 64:681.
:
4. Paik CK, Waetjen LE, Xing G, et al. Hospitalizations for pelvic inflammatory disease and
tuboovarian abscess. Obstet Gynecol 2006; 107:611.

5. Lareau SM, Beigi RH. Pelvic inflammatory disease and tubo-ovarian abscess. Infect Dis Clin
North Am 2008; 22:693.

6. Landers DV, Sweet RL. Tubo-ovarian abscess: contemporary approach to management. Rev
Infect Dis 1983; 5:876.

7. Sweet RL. Soft tissue infection and pelvic abscess. In: Infectious diseases of the female genit
al tract, 5th ed, Sweet RL, Gibbs RS (Eds), Lippincott Williams and Wilkins, Philadelphia 2009.

8. Wiesenfeld HC, Sweet RL. Progress in the management of tuboovarian abscesses. Clin
Obstet Gynecol 1993; 36:433.

9. Cohen CR, Sinei S, Reilly M, et al. Effect of human immunodeficiency virus type 1 infection
upon acute salpingitis: a laparoscopic study. J Infect Dis 1998; 178:1352.

10. Kamenga MC, De Cock KM, St Louis ME, et al. The impact of human immunodeficiency virus
infection on pelvic inflammatory disease: a case-control study in Abidjan, Ivory Coast. Am J
Obstet Gynecol 1995; 172:919.

11. Reed SD, Landers DV, Sweet RL. Antibiotic treatment of tuboovarian abscess: comparison of
broad-spectrum beta-lactam agents versus clindamycin-containing regimens. Am J Obstet
Gynecol 1991; 164:1556.

12. Dewitt J, Reining A, Allsworth JE, Peipert JF. Tuboovarian abscesses: is size associated with
duration of hospitalization & complications? Obstet Gynecol Int 2010; 2010:847041.

13. Fouks Y, Cohen A, Shapira U, et al. Surgical Intervention in Patients with Tubo-Ovarian
Abscess: Clinical Predictors and a Simple Risk Score. J Minim Invasive Gynecol 2019; 26:535.

14. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman. Infect Dis
Obstet Gynecol 1999; 7:248.

15. Protopapas AG, Diakomanolis ES, Milingos SD, et al. Tubo-ovarian abscesses in
postmenopausal women: gynecological malignancy until proven otherwise? Eur J Obstet
Gynecol Reprod Biol 2004; 114:203.

16. Lipscomb GH, Ling FW. Tubo-ovarian abscess in postmenopausal patients. South Med J
1992; 85:696.
:
17. Hoffman M, Molpus K, Roberts WS, et al. Tuboovarian abscess in postmenopausal women. J
Reprod Med 1990; 35:525.

18. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted
diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.

19. Ginsburg DS, Stern JL, Hamod KA, et al. Tubo-ovarian abscess: a retrospective review. Am J
Obstet Gynecol 1980; 138:1055.

20. Sweet RL, Ohm-Smith M, Landers DV, Robbie MO. Moxalactam versus clindamycin plus
tobramycin in the treatment of obstetric and gynecologic infections. Am J Obstet Gynecol
1985; 152:808.

21. Sweet RL, Schachter J, Landers DV, et al. Treatment of hospitalized patients with acute pelvic
inflammatory disease: comparison of cefotetan plus doxycycline and cefoxitin plus
doxycycline. Am J Obstet Gynecol 1988; 158:736.

22. Joiner KA, Lowe BR, Dzink JL, Bartlett JG. Antibiotic levels in infected and sterile
subcutaneous abscesses in mice. J Infect Dis 1981; 143:487.

23. Itani KM, Wilson SE, Awad SS, et al. Ertapenem versus cefotetan prophylaxis in elective
colorectal surgery. N Engl J Med 2006; 355:2640.

24. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-
abdominal infection in adults and children: guidelines by the Surgical Infection Society and
the Infectious Diseases Society of America. Clin Infect Dis 2010; 50:133.

25. McNeeley SG, Hendrix SL, Mazzoni MM, et al. Medically sound, cost-effective treatment for
pelvic inflammatory disease and tuboovarian abscess. Am J Obstet Gynecol 1998; 178:1272.

26. Pelak BA, Citron DM, Motyl M, et al. Comparative in vitro activities of ertapenem against
bacterial pathogens from patients with acute pelvic infection. J Antimicrob Chemother 2002;
50:735.

27. Solomkin J, Teppler H, Graham DR, et al. Treatment of polymicrobial infections: post hoc
analysis of three trials comparing ertapenem and piperacillin-tazobactam. J Antimicrob
Chemother 2004; 53 Suppl 2:ii51.

28. An MM, Zou Z, Shen H, et al. Ertapenem versus piperacillin/tazobactam for the treatment of
complicated infections: a meta-analysis of randomized controlled trials. BMC Infect Dis 2009;
9:193.
:
29. Hsu WC, Lee YH, Chang DY. Tuboovarian abscess caused by Candida in a woman with an
intrauterine device. Gynecol Obstet Invest 2007; 64:14.

30. Thaneemalai J, Asma H, Savithri DP. Salmonella tuboovarian abscess. Med J Malaysia 2007;
62:422.

31. Myckan KA, Booth CM, Mocarski E. Pasteurella multocida bacteremia and tuboovarian
abscess. Obstet Gynecol 2005; 106:1220.

32. Ribak R, Schonman R, Sharvit M, et al. Can the Need for Invasive Intervention in Tubo-
ovarian Abscess Be Predicted? The Implication of C-reactive Protein Measurements. J Minim
Invasive Gynecol 2020; 27:541.

33. Demirtas O, Akman L, Demirtas GS, et al. The role of the serum inflammatory markers for
predicting the tubo-ovarian abscess in acute pelvic inflammatory disease: a single-center 5-
year experience. Arch Gynecol Obstet 2013; 287:519.

34. Lee SW, Rhim CC, Kim JH, et al. Predictive Markers of Tubo-Ovarian Abscess in Pelvic
Inflammatory Disease. Gynecol Obstet Invest 2015.

35. Gerzof SG, Robbins AH, Johnson WC, et al. Percutaneous catheter drainage of abdominal
abscesses: a five-year experience. N Engl J Med 1981; 305:653.

36. Gerzof SG, Johnson WC, Robbins AH, Nabseth DC. Expanded criteria for percutaneous
abscess drainage. Arch Surg 1985; 120:227.

37. Worthen NJ, Gunning JE. Percutaneous drainage of pelvic abscesses: management of the
tubo-ovarian abscess. J Ultrasound Med 1986; 5:551.

38. Nelson AL, Sinow RM, Renslo R, et al. Endovaginal ultrasonographically guided transvaginal
drainage for treatment of pelvic abscesses. Am J Obstet Gynecol 1995; 172:1926.

39. Teisala K, Heinonen PK, Punnonen R. Transvaginal ultrasound in the diagnosis and
treatment of tubo-ovarian abscess. Br J Obstet Gynaecol 1990; 97:178.

40. Nelson AL, Sinow RM, Oliak D. Transrectal ultrasonographically guided drainage of
gynecologic pelvic abscesses. Am J Obstet Gynecol 2000; 182:1382.

41. vanSonnenberg E, D'Agostino HB, Casola G, et al. US-guided transvaginal drainage of pelvic
abscesses and fluid collections. Radiology 1991; 181:53.
:
42. Harisinghani MG, Gervais DA, Maher MM, et al. Transgluteal approach for percutaneous
drainage of deep pelvic abscesses: 154 cases. Radiology 2003; 228:701.

43. Gjelland K, Ekerhovd E, Granberg S. Transvaginal ultrasound-guided aspiration for treatment


of tubo-ovarian abscess: a study of 302 cases. Am J Obstet Gynecol 2005; 193:1323.

44. Levenson RB, Pearson KM, Saokar A, et al. Image-guided drainage of tuboovarian abscesses
of gastrointestinal or genitourinary origin: a retrospective analysis. J Vasc Interv Radiol 2011;
22:678.

45. Goharkhay N, Verma U, Maggiorotto F. Comparison of CT- or ultrasound-guided drainage


with concomitant intravenous antibiotics vs. intravenous antibiotics alone in the
management of tubo-ovarian abscesses. Ultrasound Obstet Gynecol 2007; 29:65.

46. Hiller N, Sella T, Lev-Sagi A, et al. Computed tomographic features of tuboovarian abscess. J
Reprod Med 2005; 50:203.

47. Yang CC, Chen P, Tseng JY, Wang PH. Advantages of open laparoscopic surgery over
exploratory laparotomy in patients with tubo-ovarian abscess. J Am Assoc Gynecol Laparosc
2002; 9:327.

48. Shigemi D, Matsui H, Fushimi K, Yasunaga H. Laparoscopic Compared With Open Surgery for
Severe Pelvic Inflammatory Disease and Tubo-Ovarian Abscess. Obstet Gynecol 2019;
133:1224.

49. VERMEEREN J, TE LINDE RW. Intraabdominal rupture of pelvic abscesses. Am J Obstet


Gynecol 1954; 68:402.

50. Dudley AG, Lee F, Barclay D. Ovarian and tubo-ovarian abscess in pregnancy: report of a
case and a review of the literature. Mil Med 1970; 135:403.

51. Matsunaga Y, Fukushima K, Nozaki M, et al. A case of pregnancy complicated by the


development of a tubo-ovarian abscess following in vitro fertilization and embryo transfer.
Am J Perinatol 2003; 20:277.

52. Stubbs RE, Monif GR. Ruptured tubo-ovarian abscess in pregnancy: recovery of a
penicillinase-producing strain of Neisseria gonorrhoeae. Sex Transm Dis 1985; 12:235.

53. Dicker D, Samuel N, Feldberg D, Goldman JA. Infected ectopic pregnancy presenting as
unilateral tubo-ovarian abscess. Eur J Obstet Gynecol Reprod Biol 1984; 17:237.
:
54. Davey MM, Guidozzi F. Ruptured tubo-ovarian abscess late in pregnancy. A case report. S Afr
Med J 1987; 71:120.

55. Hunt SM, Kincheloe BW, Schreier PC. Tubo-ovarian abscess in pregnancy. Obstet Gynecol
1974; 43:57.

Topic 16419 Version 29.0


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