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Section 9.5. Management of Tubo-ovarian Abcesses
https://t.me/med1917
Daniel S. Seidman, Bulent Berker, and Camran Nezhat
Tubo-ovarian abscess (TOA) is a severe sequela of pelvic inflammatory disease (PID) and occurs in almost one third of patients
hospitalized with PID.[1] PID remains the most common gynecologic reason for admission to the hospital in the United States,
accounting for 49 per 10,000 recorded hospital discharges. The
exact incidence of PID, however, is unknown because the disease cannot be diagnosed reliably from clinical symptoms and
signs.[2] Yet, it is estimated that PID affects at least once about
10% to 15% of young women in the United States. Moreover,
because most PID is asymptomatic, this figure almost certainly
underestimates the true prevalence among women of reproductive age.[3]
Tubo-ovarian abscess is part of a spectrum of inflammatory
disorders of the upper female genital tract comprising PID that
includesanycombinationofendometritis,salpingitis,pelvicperitonitis, and TOA.[4]Symptomaticor subclinical pelvicinfections
may progress rapidly into a TOA, which can rupture and cause
peritonitis.[5]
Sexually transmitted organisms, especially Neisseria gonor-
rhoeae and Chlamydia trachomatis, are implicated in many cases
of PID.[6] These microorganisms are rarely isolated from TOAs,
but they are involved in the initiating event, that is, the invasion of the fallopian tube epithelium. This results in tissue damage and necrosis providing an ideal environment for subsequent
anaerobic invasion and growth. Othermicroorganismsthat comprise the vaginal flora, including anaerobes, Gardnerella vagi-
nalis, Haemophilus influenzae, enteric gram-negative rods, and
Streptococcus agalactiae, have also been associated with PID.
In addition, cytomegalovirus, Mycoplasma hominis, and Ureaplasma urealyticum may be the etiologic agents in some cases of
PID.[4]
Risk factors associated with the development of PID include
inconsistent barrier contraception, possibly vaginal douching,
and the use of oral contraceptivepills possibly masking the clinical
severity of the disease. The small risk associated with the IUD
is limited to the first few weeks after insertion.[1] Postpartum
endometritis may also lead to PID.
The sequelae of PID may cause infertility, tubal pregnancy,
chronic pelvic pain, and recurrent upper genital tract infection.
The extent of tubal damage and pelvic adhesions depends on the
severity of the infection, the number of PID episodes, and the
etiology. Peritonitis is associated with a 17% risk of infertility
compared with 3% for a mild infection. With each successive
episode, the risk of infertility increases. The risk of ectopic pregnancy is six to 10 times higher in women who have had PID.
Chronic pelvic pain occurs in 15% to 18% of patients after PID
because of adhesions. About 25% of these patients will have at
least one recurrent infection.[4]
DIAGNOSIS
Precise diagnosis of acutePID is the cornerstone of the treatment
for the condition.[7] However, acute PID is difficult to diagnose
because of the wide variationinthesymptoms and signs.[4] Delay
in diagnosis and effective treatment is of concern because it may
contribute to inflammatory sequelae in the upper reproductive
tract, including TOA. Among women with PID, many report
subtle, nonspecific symptoms, such as dyspareunia, postcoital
spotting, and abnormal uterine bleeding. In these situations, a
bimanual examination could reveal cervical motion or adnexal
tenderness. Even in the presence of “classic” symptoms and signs,
such as lower abdominal pain, cervical motion and adnexal tenderness, elevatedwhitecellcount,fever,anda massonultrasound,
other diseases are part of a differential diagnosis. The clinical
diagnosis of acute PID is imprecise. Data indicate that a clinical
diagnosis of symptomatic PID has a positive predictive value for
salpingitis of 65% to 90% compared with laparoscopy.[3,4]
Additional criteria that support a diagnosis of PID include
oral temperature above 101
vaginal discharge, elevatederythrocyte sedimentation rate andCreactive protein, andlaboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis.[4] However, recent
critical review has suggested that there is insufficient evidence to
support existing diagnostic criteria, which have been based on a
combination of empirical data and expert opinion.[8] It hasbeen
suggested that a new evidence base is urgently needed, but this
will require either a new investigation of the association between
clinical presentationand PIDbased on a laparoscopic “gold standard” or the development of new diagnostic techniques.[8]
The most specific criteria for diagnosing PID are histopathologic evidence of endometritis on an endometrial biopsy specimen and laparoscopic abnormalities consistent with PID.[4]
Laparoscopy, allowing direct visualization of the fallopian tubes,
is usually considered the best single diagnostic test to obtain a
more accurate diagnosis of salpingitis and a more complete bacteriologic diagnosis.[3] However, this diagnostic tool is invasive
and often not readily available, and its use is not easy to justify
when symptoms are mild or vague. Moreover, laparoscopy will
not detect endometritis and may not detect subtle inflammation
of the fallopian tubes. Consequently, a diagnosis of PID usually
is based on clinical findings.
Laparoscopy is still considered a useful tool in selected cases,
allowing rapid and precise identification of the infectious agent
and extent of disease so that appropriate therapy can be instituted. Molander et al. [9] evaluated the efficacy of acute-phase
operative laparoscopy in 33 womenwith clinically suspectedPID.
LaparoscopyconfirmedthediagnosisofPIDin20 patients (61%);
◦
F (38.3◦C), abnormal cervical or
237
238 — Daniel S. Seidman, Bulent Berker, and Camran Nezhat
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11 women (33%) had other disease, and two (6%) had no evidence of disease. The authors concluded that acute-phase operative laparoscopy provided a final diagnosis in all but three of 33
patients (91%).[9]
In a subsequent study, these authors tried to assess the diagnostic accuracy of the laparoscopic diagnosis of PID.[10] They
studied the observer agreement with laparoscopic diagnosis of
PID using photographsamong three seniorconsultantsand three
residents. The overall accuracy of the laparoscopic diagnosis of
PID was 78%, the sensitivity was 27%, and the specificity was
92%. The overall intraobserver reproducibility of the diagnosis
of PID was only fair, and it was clearly better among the consultants thanamong the residents. When specific diagnostic features
(e.g., tubal erythema, edema, adhesions, cul-de-sac fluid) were
separately analyzed, the results were no different, suggesting only
poor to fair reproducibility.Theinvestigatorsthereforeconcluded
that based on photographic images, the observer reproducibility
and the overall diagnostic accuracy of the laparoscopic diagnosis
of PID are unsatisfactory when histopathologically proven PID
is used as the gold standard.[10]
Imaging
Pelvic sonography is almost universally performed in patients
with a clinical diagnosis of PID. Though the study may be normal or sometimes nonspecific, there are a variety of findings
that are characteristic of this process. The experienced sonographer is able to evaluate the features of PID, salpingitis, pyosalpinx, tubo-ovarian complex, and TOAs.[11] Sonography may
also help distinguish acute from chronic abnormalities in the fallopian tubes.[11] Transvaginal sonogram (TVS), showing thickened fluid-filled tubes with or without free pelvic fluid or a tuboovarian complex, is considered one of the most reliable criteria
for diagnosing PID.[4] Newer diagnostic techniques that have
been evaluated include Doppler ultrasound and MRI.[1]
Timor-Tritsch et al. [12] tried to identify sonographic markers of PID and to place these in a clinical context. They found
that the best marker of tubal inflammatory disease, either acute
or chronic, was the presence of anincomplete septum ofthe tubal
wall, which was present in 92% of the total cases. A thick wall
and the “cogwheel” sign were sensitive markers of acute disease,
whereas a thin wall and “beads-on-a-string” sign were indicators
of chronic disease. Palpable findings andsurgical history werenot
discriminatory, but were present in three quarters and one third
of their study population, respectively. Three false-positive cases
were identified, including an ovarian cystadenoma, an appendiceal mucocele, and one case with peri-ovarian fluid accumulation. Timor-Tritsch and his colleagues [12] concluded that a
tubo-ovarian complex and TOA should be considered separate
entities that differin their clinicalimplications. TVS allows oneto
distinguish between them. Furthermore, they found that distinguishing TVS characteristics are also of benefit for the diagnosis
of acute versus chronic salpingitis.
The usefulness of power Doppler TVS in the diagnosis of
PID was evaluated by Molander et al. [13]. Conventional TVS
and power Doppler TVS were performed. All patients with suspected acute PID underwent laparoscopy to confirm the diagnosis. Power Doppler was used to assess the vascularity of any
adnexal mass. The diagnosis of PID was confirmed by laparoscopy
in 20 (67%) of the 30 women with clinically suspected acute
PID. Specific TVS findings, including wall thickness 5 mm or
greater,cogwheel sign, incomplete septa, and thepresence of culde-sac fluid, discriminated women with acute PID from the control women with hydrosalpinx formation. Power Doppler TVS
revealed hyperemia in all women with acute PID, but in only two
women with hydrosalpinx, a statistically significant difference.
Pulsatility indiceswere significantly lower in the acute PIDgroup
than in the control group. The authors concluded that power
Doppler TVS was 100% sensitive and 80% specific in the diagnosis of PID, with an overall accuracy of 93%. Specific sonographic
landmark findings and power Doppler findings were noted to
augment the clinical diagnosis of PID and allow simple classification of the severity of the disease.[13]
Varras et al. [14] tried to identify the different sonographic
markers on gray-scale and color Doppler sonography in TOA.
They retrospectively analyzed the ultrasound records of a group
of 25 women in whom the presence of TOA was confirmed by
surgery and histopathology. A mass was found in all cases. The
maximumdiameterofthemasswas5cm intwocases andbetween
5 cm and 10 cm in 23 cases. The mass was demonstrated at the
anatomic position of the ovary in 21 cases (84%) and at the culde-sac in four cases (16%). The mass was a simple cyst in two
cases (8%), in four cases it was cystic with diaphragms (16%), in
four cases it was a thickened tube-shaped structure with multiple
internal echoes (16%), and in 15 cases it was a mixture of cystic
and solid elements (60%). Pyosalpinges with fluid–fluid levels
were found in two cases. Fluid in the cul-de-sac was observed at a
rate of 48%. Color Doppler sonography demonstrated abundant
blood flow in the borders and the septa of the TOAs in 90% of
the studied cases. Varras et al. [14] concluded that the ultrasonographic findings of TOAs are not specific. They suggested that
the presence of a mass at the anatomic position of the ovary or at
the cul-de-sacin combination with an increased number ofwhite
blood cells, elevated erythrocyte sedimentation rate, and clinical
findings may be helpful for a correct diagnosis. In addition, they
pointed out that color Doppler flow may help characterize the
nature of the pelvic mass by detecting a significant rich blood
flow in most cases of TOAs.[14]
CT is ordered with increasing frequency in patients with
unexplainedlowerabdominalpain.Itisimportanttocorrelate the
TVSfindings with those of the pelvic CT.[11] In cases of suspected
TOA, CT and MRI findings may be helpful in demonstrating the
extent of the disease, characterizing the lesions, and making a
specific diagnosis.[15] These expensive imaging modalities may
be of greatest value when used in cases of rare but specific causes
of TOA, such as actinomycosis, tuberculosis, and xanthogranulomatous inflammation.[16]
TOA and Endometriosis
Women with stages III through IV endometriosis were observed
to be more likely to develop TOAs compared with those without
endometriosis.[17] This association was most strongly noted in
nulliparous women or those who had delivered no morethan two
children. It was suggested that this association with parity may
be related to endometriosis suppression, the prolonged duration
of menstrual-free periods in multiparous women, or changes in
the local immunity of the pelvic cavity.[17]
The presence of an ovarian endometrioma is a well-known
risk factor for the development of a TOA or an ovarian
Management of Tubo-ovarian Abcesses — 239
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abscess.[18] In a review of the medical records of 6557 gynecologic inpatients, the incidence of TOAs was found to be significantly higher in patients with endometrioma compared with
patients without endometrioma (2.3% vs. 0.2%). The causes of
the abscesses in the seven cases with endometrioma were contamination during surgery (one case), contamination during a
transvaginal endometrioma aspiration (one case), an ascending
infection (one case), and unknown in four cases.[18]
Tubo-ovarian abscess is a rare but well-recognized complication of in vitro fertilization (IVF) treatment.[19] The increased
risk for TOA during IVF may occasionally be a result of reactivation of a latent pelvic infection, due to previous PID, following TVS-directed follicleaspiration and transcervical embryo
transfer.[20] However, among women undergoing transvaginal
oocyte pickup for IVF, when severe endometriosis or an ovarian
endometrioma are present, there appears to be an increased risk
for TOA. Latemanifestation of pelvic abscess supports the notion
that the presence of old blood in an endometrioma provides
a culture medium for bacteria to grow slowly after transvaginal inoculation.[21] However, it is not yet clear whether more
vigorous antibiotic prophylaxis and better vaginal preparation
before oocyte pickupcan prevent the risk ofTOA developing after
the procedure in patients with severe endometriosis and ovarian
endometrioma.[22,23] It has been suggested that both the pseudocapsule of the endometrioma and the old blood inside it may
prevent antibiotic prophylaxis from overcoming the transvaginal
bacterial inoculation.[21] Small pools of old blood formed in the
peritoneal cavity of patients with endometriosis may act as an
isolated culture medium for the inoculated bacteria.
The altered immune system of patients with endometriosis may adversely affect the immune response to inoculated
bacteria.[22] This altered immune response may explain the
occurrence of PID in milder forms of endometriosis. It should be
noted, however, that although it has long been hypothesized that
dysregulation of the immune system plays a role in the pathogenesis of endometriosis, no report has so far linked the risk of
infection in these patients to the altered immune system.[24]
TOA and Gynecologic Cancer in
Postmenopausal Women
A significant associationbetween TOAsinmenopause and malignancy has been established.[25] Amongpostmenopausalwomen,
Protopapas et al. [25] found a strong relationship between TOAs
and concomitant gynecologic malignancy including a variety of
cancers. The incidence of gynecologic cancer in postmenopausal
patients who develop TOAs ranged from 25% to 47%.[25–27]
The cases of gynecologic cancer included adenocarcinoma of the
cervix, endometrial cancer, andepithelialovariancancer. Primary
carcinoma of the fallopian tube may also present as TOA.[28,29]
TOAs represent a rather unusual entity in postmenopausal
women when compared with those observed in women of reproductive age. A recent study has also suggested that there may be a
new trend in theepidemiology of TOAoccurring in older women,
who do not present with the traditional risk factors for PID and
TOA.[30] In postmenopausal women, the clinical picture is different from the typical occurrence of abdominal or pelvic pain,
fever (temperature ≥38.5
◦
C), chills, and increased vaginal secretions. Postmenopausal women rarely report a history of acute
PID,andmanypatientspresentwithvagueandnonspecificsymp-
toms. Protopapas et al. [25] observed that moderate or severe
abdominal pain was present in the majority of their patients,
whereas pyrexia (temperature ≥38
◦
C) was absent in59%ofcases.
Thus, in the postmenopausal patient,low abdominal pain accompanied by signs of peritoneal irritation, even when high fever is
absent, may suggest serious acute surgical conditions.[25]
The existence of a gynecologic malignancy may predispose a
patient to the development of a TOA for several reasons.[25] An
advanced cervical or endometrial carcinoma may cause obstruction and subsequent entrapment of bloodand uppergenital tract
secretions, creating an optimal anaerobic environment that may
lead to the development of pyometra and/or a bilateral or unilateral TOA. A fallopian tube or ovarian carcinoma may cause
excessivelocal destruction of normal anatomy, permitting anaerobic growth, which is optimized in conditions of low oxidation–
reduction potential, low oxygen tension, and ample nutrient supply, all of which are provided by ischemic and necrotic neoplastic
tissue.[25]
All postmenopausal women presenting with TOAs should
therefore be thoroughly investigated to exclude a concomitant
pelvic malignancy. Conservative treatment of TOAs has no place
in menopause. Laparoscopy has a major role in investigating
the nature of suspicious masses in postmenopausal women with
PID.
It should be remembered that not only can the presentation
of a carcinoma of the gynecologic tract mimic a TOA [29], but
patients presenting with abdominalpainanda pelvic mass resembling an ovarian tumor may actually be found to suffer from a
TOA. A pelvic TOA mimicking a pelvic malignancy may occur
not only in postmenopausal women [31,32], but also in sexually
inactive girls.[33]
TREATMENT
It is generally assumedthatifPID is inadequately treated, this may
lead to a complicated course occasionally involving the development of TOA. Moreover, because PID has high morbidity, management must be prompt to prevent long-term complications;
about 20% of affected women become infertile, 20% develop
chronic pelvic pain, and 10% of those who conceive have an
ectopic pregnancy.[2] Repeated episodes of PID are associated
with a four- to sixfold increase in the risk of permanent tubal
damage.[2] Empirical treatment of PID with broad-spectrum
antibiotics is thus always recommendedin women who are at risk,
if lower abdominal tenderness, adnexal tenderness, and cervical
motion tenderness are present.[4] Initial treatment is provided on
an outpatient basis. There are no apparent differences in clinical
outcomes, whether a woman with PIDis treated as an inpatientor
an outpatient.[1] Combination drug regimens, including antibiotics against the most common factors underlying acute PID,
seem to prevent most late sequelae in cases with mild or moderate salpingitis. However, thisis not the casein women witha tubal
or pelvic abscess.[4] Patients who do not improve under antibiotic therapy usuallyrequirehospitalization,additional diagnostic
tests, and surgical intervention.[4]
The classic treatment of TOA used to be total abdominal
hysterectomy with bilateral salpingo-oophorectomy, a procedure
that promised rapid cure due to complete evacuation of infected
tissue but had devastating consequences for young women.
240 — Daniel S. Seidman, Bulent Berker, and Camran Nezhat
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Table 9.5.1: Management of Tubo-ovarian Abscess
Administration of broad-spectrum antibiotics
Transvaginal or percutaneous drainage
Ultrasound-guided intracavitary instillation of antibiotics
Laparoscopic draining and irrigation of abscess
Laparoscopic removal of infected tube or adnexa
With the advancement in broad-spectrum antibiotics and the
availability of accurate imaging techniques, treatment of TOA
has changed dramatically. Because most women with TOA are of
reproductive age, the primary aimof management is to be as conservative as possible. Organ-preserving approaches are currently
advocated for the management of TOA (Table 9.5.1).
Transvaginal ultrasound–guided aspiration combined with
antibiotics iscurrently recommended asa first-line procedurefor
TOAs.[34] It hasbeen shown tobe an effectiveand safe treatment
regimen. In a recent study from Norway, surgery was performed
in only 20 women (6.6%) following 449 transvaginal aspirations
performed on302 women. The mainindications for surgery were
diagnostic or therapeutic uncertainty, such as suspected residual
TOA abscess or pain. No procedure-related complications were
diagnosed.[34]
In a randomized prospective study of 40 women diagnosed
as suffering from TOA of less than 10 cm maximal diameter,
intensive antibiotic therapy alone was compared with antibiotic therapy in association with early ultrasound-guided vaginal
drainage.[35] Early transvaginal drainage of the abscess resulted
in a favorable short-term response in 90% of the cases, whereas
this was 65% in the control group.[35]
One-step sonographically guided aspirationof TOA followed
byintracavitary antibioticinstillation hasalsobeenshowntooffer
an easy and safe alternativetherapy in patients in whom treatment
with systemic antibiotics has failed.[36]
Laparoscopic management of TOA was introduced almost
three decades ago.[37,38] Laparoscopic procedures in women
with TOA comprise pelvic irrigation in all patients and lysis of
adhesions in most cases.[9] They usually also include laparoscopic draining and irrigation of the TOA or complete removal
of the inflamed tube or adnexa.[9]
German investigators compared the outcome of operative
laparoscopyfor TOAwith incision of theabscesscavity and lavage
(organ-preserving treatment) onlyversus laparoscopicsalpingectomy or salpingo-oophorectomy (ablative treatment).[39] In
their retrospective analysis, 35 patients not wishing to have
children underwent salpingectomy or salpingo-oophorectomy,
whereas 25 patients wishing to remain fertile were treated by
means of an organ-preserving procedure. Apart from one postoperative readmission because of lower pelvic pain in the organpreserving group, there were no operative complications or serious systemic sequelae. In contrast, there was a significantly
higher incidence of intraoperative and postoperative complications when ablative treatment was performed: one intestinal perforation requiring subsequent laparotomy, four serosal lesions,
two lesions of the greater omentum, two lacerated collaterals
of the internal iliac artery, one postoperative fever higher than
◦
C for 2 days, two bowel obstructions, one thrombosis of the
38
upper leg, and one thrombosis of the lower leg. The authors concluded that when laparoscopic treatment of TOA is performed,
organ-preserving treatment should be chosen, irrespective of the
patient’s age or desire to have children, because of the risk of
complications.[39]
Raiga and coauthors[40]studied39patientswhoweretreated
for adnexal abscesses. Those authors showed that laparoscopic
surgery is a safe and efficient technique for treating this condition. No immediate reoperation was necessary within the first
2 months after the initial laparoscopic procedure. At a secondlook laparoscopy, adhesiolysis was required in all of the patients.
A salpingostomy was done in 17 women, and six others were
referred for IVF. Subsequently, 12 of 19 patients who did not
use any contraception became pregnant. Although laparoscopy
remains the technique of choice in the initial management of
adnexal abscesses, the anatomic results observed at second-look
laparoscopy suggest that a second-look procedure should be considered for patients who desire future pregnancy, if they are not
referred to IVF treatment. Moreover, laparoscopic removal of the
tube may be warranted in some patients undergoing IVF treatment, as subsequent development of hydrosalpinges following
inflammatory involvement of the tube may adversely affect the
success of IVF.[41]
A recent retrospective study compared laparoscopic surgery
in 19 women and conventional exploratory laparotomy in 37
women for managing patients with TOA.[42] Laparoscopic
surgery wasassociatedwith a significantly decreasedhospitalstay,
a lower percentage of wound infections, and a shorter time for
fever to subside. Open laparoscopy thus seems to be a good alternative to traditional laparotomy in managing patients with TOA.
A laparoscopic study of acute PID was conducted in Nairobi,
Kenya, among 133 patients with acute salpingitis.[43] TOAs were
found significantly more frequently among HIV-1–infected compared with HIV-1–uninfected women (33% vs. 15%). TOAs were
also significantly more common among women with low CD4
cell counts. Thus, in patients with laparoscopically verified acute
salpingitis, the likelihood of TOA was related to HIV-1 infection
and advanced immunosuppression.
THE LAPAROSCOPIC TECHNIQUE
The laparoscopic management of TOA as undertaken by Nezhat
et al. [44] is performed in the following manner: Two 5-mm trocars are inserted in the lower quadrants, and a suction–irrigator
probe and grasping forceps are inserted through the trocars. The
pelvis, upper abdomen, and pelvic viscera are examined for free
or loculated purulent material, and the course of both ureters
is identified. Collections are dispersed gently with the suction–
irrigator, and purulent fluid is aspirated. Cultures are taken from
the inflammatory exudate. If necessary, the suction–irrigator is
used to bluntly mobilize the omentum, small bowel, rectosigmoid, and tubo-ovarian adhesions (Figure 9.5.1).[45] After the
abscess cavity is localized, it is drained and the suction–irrigator
separates the bowel and omentum completely from the reproductive organs. TOAs are separated by using a combination of
blunt lysis and hydrodissection. Adhesions caused by acute PID
are soft and can be disrupted by gentle blunt dissection and
hydrodissection.Hydrodissection is done by placing thetip of the
Management of Tubo-ovarian Abcesses — 241
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Tubo-ovarian abscess
Abscess involving
most of ovary
Figure 9.5.1. The abscess is localized and is exposed for drainage. The cut surface of the tubo-ovarian abscess is shown.
suction–irrigator between the tissues. The pressure of the fluid
spray andthe gentle forceof the instrument create aplane for dissection (Figure 9.5.2). The 5-mm graspers provide traction and
countertraction, improving observation oftheaffectedarea.After
the abscess is mobilized, it is drained (Figure 9.5.3). Its walls are
removed in sections by using the 5-mm graspers (Figure 9.5.4).
Though technically arduous, meticulous dissection of the
abscess from the surrounding structures is important for success. Once the ovary is mobilized, rents or holes in it are irrigated
copiously. Sutures are not required to repair the ovary. Graspers
are inserted into the tubal ostium to spread it and free agglutinated fimbriae. Chromopertubation is not suggested because
Hydrodissection for
adhesion separation
edema in the interstitial tissue of the tube occludes the lumen.
At the end of the procedure, the peritoneal cavity is irrigated
with lactated Ringer’s solution until the effluent is clear (Figure
9.5.5). The upper abdomen is irrigated also, and the remainder of the irrigation fluid is aspirated while the patient is in the
reverse-Trendelenburg position. Between 300 mL and 400 mL of
irrigation fluid isleft in the pelvis to separate these organs during
the early healing phase. Hydrodissection and gentle blunt dissection decrease the potential for intestinal injury; the laser and
electrosurgery should be used sparingly.
In contrast to the adhesions associated with an acute abscess,
chronic TOAshave dense walls.The bowel oftenadheres to pelvic
Drainage of
abscess cavity
Figure 9.5.2. Hydrodissection and gentle blunt dissection reduce the
potential for intestinal injury.
Figure 9.5.3. The abscess cavity is drained and irrigated.
242 — Daniel S. Seidman, Bulent Berker, and Camran Nezhat
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Abscess wall is removed
in pieces from attached organs
Figure 9.5.4. Sections of the abscess wall are removed in pieces using
a 5-mm grasper.
organs and is dissected with difficulty; the adnexa appear as a
dense mass, making it difficult to distinguish between the pyosalpinx and the ovary. Adhesiolysis technically is difficult and is
associated with a high risk of complications.
SUMMARY
Recent epidemiologic studies indicate that the clinical panorama
of PID is changing, with fewer patients hospitalized for PID but
Copious lavage of both
the pelvis and abdomen
Figure 9.5.5. The pelvis is irrigated.
a higher percentage of patients developing TOA.[45] This may
be attributed to changing risk factors, such as endometriosis,
now recognized to influence the incidence ofTOAs.Furthermore,
although the direct medical costs of PID and its sequelae may be
decreasing, they remain substantial.[46]
The initial management ofTOAconsistsof conservative medical treatment with broad-spectrum antibiotics. However, it is
now widely accepted that drainage of the abscess by transvaginal
ultrasound or CT-guided aspiration or under direct laparoscopic
guidance should be considered early after the diagnosis. Laparoscopic surgical intervention in selected cases allows for prompt
management of TOAs and may prevent considerable short- and
long-term morbidity.
All postmenopausalwomen presenting with a clinicalpicture
suggestive of TOA should be thoroughly investigated to exclude a
concomitant gynecologic or other pelvic malignancy. Even when
such an association has not been confirmed after an extensive
preoperative diagnostic work-up, conservative treatment has no
place in such cases as it may lead to an unnecessary delay in the
diagnosis of anoccultcanceror of a life-threatening acute surgical
condition.
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14. Varras M, Polyzos D, Perouli E, Noti P, Pantazis I, Akrivis CH.
Tubo-ovarian abscesses: spectrum of sonographic findings with
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surgical and pathological correlations. Clin Exp Obstet Gynecol.
2003;30:117–121.
15. Ha HK,Lim GY,ChaES,et al.MRimagingoftubo-ovarianabscess.
Acta Radiol. 1995;36:510–514.
16. Kim SH, Kim SH, Yang DM, Kim KA. Unusual causes of tuboovarian abscess: CT and MR imaging findings. Radiographics.
2004;24:1575–1589.
17. Chen MJ, Yang JH, Yang YS,HoHN. Increasedoccurrenceof tuboovarian abscesses in women with stage III and IV endometriosis.
Fertil Steril. 2004;82:498–499.
18. Kubota T, Ishi K, Takeuchi H. A study of tubo-ovarian and ovarian abscesses, with a focus on cases with endometrioma. J Obstet
Gynaecol Res. 1997;23:421–426.
19. Orvieto R. Bleeding and PID following ART. In: Allahbadia GN,
Merchant R, eds. Contemporary Perspectives on Assisted Reproduc-
tive Technology. New Delhi: Elsevier; 2006:217–221.
20. Varras M, Polyzos D, Tsikini A, Antypa E, Apessou D,
Tsouroulas M. Ruptured tubo-ovarian abscess as a complication of IVF treatment: clinical, ultrasonographic and histopathologic findings. A case report. Clin Exp Obstet Gynecol. 2003;30:
164–168.
21. Younis JS, Ezra Y, Laufer N, Ohel G. Late manifestation of pelvic
abscess following oocyte retrieval, for in vitro fertilization, in
patients with severe endometriosis and ovarian endometriomata.
J Assist Reprod Genet. 1997;14:343–346.
22. Moini A, Riazi K, Amid V, et al. Endometriosis may contribute
to oocyte retrieval-induced pelvic inflammatory disease: report of
eight cases. J Assist Reprod Genet. 2005;22:307–309.
23. TsaiYC, LinMY,ChenSH, etal.Vaginaldisinfectionwithpovidone
iodine immediatelybeforeoocyteretrievaliseffective in preventing
pelvic abscess formation without compromising the outcome of
IVF-ET. J Assist Reprod Genet. 2005;22:173–175.
24. Dmowski PW, Braun DP. Immunology of endometriosis. Best
Pract Res Clin Obstet Gynaecol. 2004;18:245–263.
25. Protopapas AG, Diakomanolis ES, Milingos SD, et al. Tuboovarian abscessesinpostmenopausalwomen:gynecologicalmalignancy until proven otherwise? Eur J Obstet Gynecol Reprod Biol.
2004;114:203–209.
26. Heaton FC, Ledger WJ. Postmenopausal tuboovarian abscess.
Obstet Gynecol. 1976;47:90–94.
27. Hoffman M, Molpus K, Roberts WS, Lyman GH, Cavanagh D.
Tuboovarian abscess in postmenopausal women. JReprodMed.
1990;35:525–528.
28. Halperin R, Zehavi S, Gayer G, Herman A, Schneider D. Fallopian
tube carcinoma presenting astubo-ovarianabscess: a report oftwo
cases with literature review. Int J Gynecol Cancer . 2005;15:1131–
1134.
29. Verit FF, Kafali H. Primary carcinoma of the fallopian tube mimicking tubo-ovarian abscess. Eur J Gynaecol Oncol. 2005;26:225–
226.
30. Halperin R, Levinson O, Yaron M,BukovskyI, Schneider D. Tuboovarian abscess inolderwomen:is the woman’sage a risk factorfor
failed response to conservative treatment? Gynecol Obstet Invest.
2003;55:211–215.
31. Seoud MA, Kanj SS, Habli M, Araj GF, Khalil AM. Brucella pelvic
tubo-ovarian abscess mimickingapelvic malignancy. Scand J Infect
Dis. 2003;35:277–278.
32. Gungor T, Parlakyigit EE, Dumanli H. Actinomycotic tuboovarian abscess mimicking pelvic malignancy. Gynecol Obstet
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abscess mimickingovarian tumor in a sexually inactive girl. J Pedi-
atr Adolesc Gynecol. 2004;17:351–352.
34. Gjelland K, Ekerhovd E, Granberg S. Transvaginal ultrasoundguided aspiration for treatment of tubo-ovarian abscess: a study
of 302 cases. Am J Obstet Gynecol. 2005;193:1323–1330.
35. Perez-Medina T, Huertas MA, Bajo JM. Early ultrasound-guided
transvaginal drainage of tubo-ovarian abscesses: a randomized
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36. Caspi B, Zalel Y, Or Y, Bar Dayan Y, Appelman Z, Katz Z. Sonographically guided aspiration: an alternative therapy for tuboovarian abscess. Ultrasound Obstet Gynecol. 1996;7:439–442.
37. Anducci JE. Laparoscopy in the diagnosis and treatment of
pelvic inflammatory disease with abscess formation. Int Surg.
1981;66:359.
38. Henry-Suchet J, Soler A, Loffredo V. Laparoscopic treatment of
tubo-ovarian abscesses. JReprodMed. 1984;8:579.
39. Buchweitz O, Malik E, Kressin P, Meyhoefer-Malik A, Diedrich K.
Laparoscopic management of tubo-ovarian abscesses: retrospective analysis of 60 cases. Surg Endosc. 2000;14:948–950.
40. Raiga J, Canis M, Le Bouedec G, et al. Laparoscopic management of adnexal abscesses: consequences for fertility. Fertil Steril.
1996;66:712.
41. Johnson NP, Mak W, Sowter MC. Surgical treatment for tubal
disease in women due to undergo in vitro fertilisation. Cochrane
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42. Yang CC, Chen P, Tseng JY, Wang PH. Advantages of open laparoscopic surgery over exploratory laparotomy in patients with tuboovarian abscess. J Am Assoc Gynecol Laparosc. 2002;9:327–332.
43. Cohen CR, Sinei S, Reilly M, et al. Effect of human immunodeficiency virus type 1 infection upon acute salpingitis: a laparoscopic
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A. Operations of the follopian tube. In Operative Gynecological
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46. Sorbye IK, Jerve F, Staff AC. Reduction in hospitalized women
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47. Rein DB, Kassler WJ, Irwin KL, Rabiee L. Direct medical cost of
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substantial. Obstet Gynecol. 2000;95:397–402.
Section 9.6. Surgical Management of Polycystic
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Ovarian Syndrome
Michelle Tham and Alan B. Copperman
Polycystic ovarian syndrome (PCOS) is the most common manifestation of hormonal dysfunction in reproductive-age women
today. The prevalence of PCOS is reported to be anywhere from
4% to 12%, with mild racial variations.[1] It is a complex disorder affecting multiple organ systems whose historical roots lie
in Stein and Leventhal’s 1935 case reports [2] describing seven
womenwithaconstellationofclinicalsymptomsincludingamenorrhea, infertility, obesity, hirsutism, and polycystic-appearing
ovaries. What initially may have been considered primarily a
reproductive disorder has since evolved into a disease entity that
profoundly affects the cardiovascular, metabolic, and endocrine
systems.
DIAGNOSIS
In 1990, the National Institutesof Health sponsored a conference
to systematically describe polycysticovariansyndrome,laying the
foundation for amore dynamic definitionby the 2003Rotterdam
European Society of Human Reproduction/American Society for
Reproductive Medicine (ESHRE/ASRM) PCOS consensus workshop. Diagnostic criteria now include two of the following three
cardinal features:
1. oligo- and/or anovulation
2. clinical and/or biochemical signs of hyperandrogenism
3. polycystic ovaries (via ultrasound)
The diagnosis is also contingent on ruling out other endocrinologic disorders,such as hyperprolactinemia, ovarian hyperthecosis, congenital adrenal hyperplasia (CAH), Cushing’s syndrome,
an androgen-secreting neoplasm, or acromegaly.[3] Initial laboratory assessment of the patient with suspected PCOS should
serve to narrow the differential diagnosis and includes serum
total testosterone, 17α-hydroxyprogesterone (to rule out CAH
from 21-hydroxylase deficiency), and dehydroepiandrosterone
(DHEA) levels. A 24-hour urine collection to measure free cortisol will assist in diagnosing Cushing’s syndrome.
PCOS is associated with insulin resistance, and measurements of fasting glucose levels and insulin may also be performed, although the specificity of these tests tends to be poor.
The gold standard of the hyperinsulinemic euglycemic clamp is
not commonly used in clinical practice. Classically, PCOS has
also been associated with an elevated luteinizing hormone (LH)–
to–follicle-stimulating hormone (FSH) ratio; however, the actual
levels of these pituitary peptides do not correlate with the severity of the disease and it is not mandatory to measure them to
establish a clinical diagnosis.
PATHOGENESIS
At its core, PCOS is an ovarian dysfunction. The precise pathogenesis of this entity, however, involves far more than ovarian
structure. The hyperandrogenic state seems to be the product
of increased LH secretion in combination with enhanced ovarian theca cell responsiveness. The etiology of the increased LH
levels has been purported to be secondary to increased pulse
frequency of gonadotropin-releasing hormone (GnRH). This
increased pulse frequency may be the result of an inherent defect
in the GnRH pulse generator or of low circulating levels of
progesterone from few ovulations leading to decreased negative
feedback.[4]
In combination with elevated ovarian production of androgen, the amount of circulating sex hormone–binding globulin
(SHBG) also plays a role in pathogenesis. There is an inverse
relationship between insulin and SHBG. Insulin inhibits hepatic
production ofSHBG. Intuitively, inthe hyperinsulinemic state of
PCOS, SHBG is decreased and there are resultant higher levels of
free testosterone. Adrenal androgen is also a contributing factor
to PCOS, as approximately 50% of women will have enhanced
production. It is unclear whether the adrenal dysfunction is critical to the progression of the disorder.
CLINICAL FEATURES
The characteristically androgen-dominated hormonal milieu of
PCOS dictates clinical manifestations. Symptoms usually begin
at menarche, and an early pubarche may in fact be a portent of
PCOS in adulthood. Chronic anovulation and resultant lack of
menses may leadto endometrial hyperplasia and in its worstconsequence, carcinoma. Infertility isalsocommonin PCOS patients
because of the decreased frequency of ovulatory cycles. There
have been recent associations among PCOS, insulin resistance,
and recurrent early pregnancy loss, although the mechanism is
unclear.
Hirsutism is another cardinal phenotypic feature of PCOS.
Increased hair growth in PCOS patients is often found on the
side of the face, upper lip, and chin. There may be a male pattern
escutcheon and in severe cases, temporal balding and hair on the
chest.
PCOS patientsgenerally have enlargedovaries with increased
central stroma andan abundance of peripheral cystic follicles (see
Figure 9.6.1). It is unclear whether there are simply a baseline
elevated number of follicles or if the rate of their programmed
cell death is retarded.[1] The hyperplastic ovarian stroma occupies approximately 25% of the medullary portion of the ovary.
244
Figure 9.6.1. Typical appearance of an ovary in a woman with poly-
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cystic ovarian syndrome.
Ultrasound criteria have been defined and include 12 or more
follicles 2 to 9 mm in diameter in each ovary and/or increased
ovarian volume (≥10 ml).[5]
Insulin resistance and a predisposition for type 2 diabetes
are also part of the clinical syndrome. This may correlate with
the approximately 50% of PCOS patients who are obese with
the classic android pattern of increased waist-to-hip ratio and a
higher proportion of visceral fat. Although clinically most PCOS
patients do fall into a classic mold, there are always nonobese,
fertile outliers who may have lesser manifestations of the disease
process.
TREATMENT
Treatment of polycystic ovaries should be targeted toward the
patient’s primary complaint, be it infertility, clinical signs of
hyperandrogenism, or prolonged amenorrhea. Ina large percentage of cases, treatment is ultimately focused on balancing the elevated circulating androgens and restoring the normal endocrine
axis either via weight reduction or pharmacologic assistance.
In the patient not desiring fertility, oral contraceptive agents
assist in decreasing ovarian steroidogenesis and increasing SHBG.
Clinically, oral contraceptive pills may diminish hirsutism and
protect the endometrium by inducing regular shedding.
Oral antihyperglycemics such as metformin have also proven
to be useful. Although there are conflicting data, most studies
have shown associated decreased androgen levels, improvement
in response to clomiphene citrate, and restoration of ovulation.
One recent randomized, double-blinded placebo trial, however,
failed to show effects of metformin on weight loss or menstrual
frequency in obese PCOS patients and suggested that weight loss
alone for that subset was the only successful factor.[6] Further
efforts are being made to identify prognostic indicators to determine which modality is most likely to succeed in an individual
patient.
The majority of women (70%) with PCOS who exhibit infertility as a result of chronic anovulationwill respond to clomiphene
citrate. Approximately 50% of these women will eventually then
Surgical Management of Polycystic Ovarian Syndrome — 245
go on to conceive.[7] Gonadotropin therapy has traditionally
been thenext step intherapy for those who fail clomiphene; however,theability to achieve monofollicular ovulation is challenging
and there is considerable risk for ovarian hyperstimulation syndrome. In fact, recent data reported from our center comparing
controlled ovarian hyperstimulation with IVF for patients with
PCOS showed three times the pregnancy rate and less than one
third the higher-order multiple gestation rate with IVF.[8] We
concluded that though traditionally considered a more “aggressive” treatment of infertility, in patients with PCOS, IVF might
actually be expensive and invasive but more “conservative.”
Because of that increased risk, therehave been some advocates
for mechanical destruction of excess ovarian tissue. Decreasing
functional ovarian mass may diminish intraovarian androgen
production and possibly encourage increased FSH levels. This
theory datesbacktoStein and Leventhal’soriginal work involving
wedge resection of the ovary (though surgical management of
this disease began to fall out of favor in the early 1980s). The
technique, however, had been shown to be effective in as many
as 90% of reported cases.[9] Unfortunately, although improving
the hormonal milieu and often restoring ovulatory function, the
technique often caused severe pelvic adhesions and subsequently
resulted in mechanical infertility due to tubal disease.
Over the past two decades, laparotomy has largelybeen abandoned in these patients, and laparoscopy has taken its place.
In fact, laparoscopic-assisted ovarian diathermy (most often via
monopolar electrocautery) has been reported in more than 1000
patients, with variable success rates. Though too few to establish a consensus on the technique, the randomized trials that do
exist comparing laparoscopic diathermy and gonadotropin therapy show similar rates of conception.[7] Laparoscopic ovarian
drilling also offers the benefit of altering the hormonal composite of PCOS patients after surgery. There is often a reported
decrease in serum LH, androgen concentration, and DHEA levels. This reduction in the intraovarian androgen levels allows for
the development offunctionalfollicles.[10] Inhibin levels alsofall
more permanently,butthe overall improvementin hormonal status does not seem to affect the peripheral sensitivity to insulin.
Although electrocautery is the most well studied, laser drilling
and multiple biopsy technique have also been employed. In the
electrocautery technique, the ovary is first isolated with laparoscopic grasping forceps. An insulated 8-mm monopolar needle
is introduced at a 90
◦
angle to the ovarian cortex and a series of
puncture sites are created. A cutting current of 100 W is used to
initially enter the cortex and is followed by 2 seconds of coagulation current at 40 W. The whole length of the needle may be
placed into the ovary. Based on ovarian site, anywhere from 10
to 15 puncture sites may be made to adequately destroy ovarian
tissue. The surface of the ovary is then irrigated with crystalloid
before removing the trocars. Of note, the use of the laser has
diminished secondary to anecdotal increases in adhesion formation and increased surface damage to the ovarian cortex.
Although laparoscopic ovarian drilling is efficacious and carries with it the benefit of multiple ovulatory cycles, relatively
short operative time, a decrease in spontaneous abortions, and
a lowered risk of multiple gestations, there may be disadvantages as well. A recent article suggested that bilateral ovarian
drilling may result in diminished ovarian reserve. The authors
suggested that unilateral drilling might have comparable results,
without deleterious long-term effects.[11] Evenwith laparoscopy,
246 — Michelle Tham and Alan B. Copperman
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however, significant postoperative tubo-ovarian adhesions, and
thus compromisedfertility,mayresult.With thesepotentialiatrogenic effects on the patient, selection for this technique should
be carefully assessed before proceeding.
Perhaps Stein and Leventhal’s initial paper was our best clue
for a cure. Wedge resection via laparotomy restored fertility
in their case studies, corroborating their theory of mechanical
crowding of the diseased ovary with follicles lacking the signal for programmed cell death. The true pathogenesis of PCOS,
however, remains elusive. Whether a selection or combination of
oral antihyperglycemics, selective estrogen receptor modulators,
aromatase inhibitors, oral contraceptives, dietary modification,
and/or mechanical ablation of excess ovarian tissue is the best
treatment is still uncertain and must be individualized. What
is clear is that a multisystem approach to this complex disease
state must be employed for cardioprotection, optimal fertility,
and long-term diminished risk for neoplastic processes.
REFERENCES
1. Chang RJ. Chapter 19. Polycystic ovarian syndrome and hyperandrogenic states. In: Strauss J, Barbieri R, eds. Yen and Jaffe’s Repro-
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632.
2. Stein IF,LeventhalML.Amenorrheaassociatedwithbilateralpolycystic ovaries. Am J Obstet Gynecol. 1935;29:181–191.
3. The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus
Workshop Group. Revised 2003 consensus on diagnostic criteria
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4. Ehrmann D. Polycystic ovarian syndrome. N Engl J Med.
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5. Balen AH, Laven JS, Tan SL, Dewailly D. Ultrasound assessment
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6. Tang T, Glanville J, Hayden CJ, White D, Barth JH, Balen AH.
Combined lifestyle modification and metformin in obese patients
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7. Farquhar CM, Williamson K, Gudex G, Johnson NP, Garland
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8. Grunfeld L, Mukherjee T, Sandler B, Scott RT, Copperman AB.
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11. Kandil M, Selim M. Hormonal and sonographic assessment of
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