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13 Complicated Pelvic Inammatory Disease
13.4.2.4 Puerperium
Puerperium appears to be the least likely time to
develop a TOA because ascending infection, the
major pathophysiology in developing PID in
most women rarely occurs during this phase. The
co-existence of vaginal colonization and delivery
has been associated with severe infections, such
as endometritis, salpingitis, and TOA [112].
Vaginal S. pneumoniae colonization was present
during CS.Neither the antenatal amoxicillin for
group B Streptococcus prophylaxis nor intraoperative prophylaxis with cefazolin prevented
maternal and neonatal infection [113]. In 1870,
Lauchlan Aitken made a different statement:
“That suppuration is more common in the puer-
peral than in any other variety of pelvic inammation – whether in the serous membrane or
cellular tissue– is a fact disputed by no one; and
I think it also probable, that not only is
suppuration much the most common termination
in such cases, but also that the matter forms much
more rapidly” [114]. One explanation could be
that TOA started during pregnancy but was diagnosed in the puerperium.
13.4.2.5 Tubal Sterilization
The incidence of TOA is minimal because the
procedure blocks communication between the
genital tract and the pelvic cavity [115].
Theoretically, this blockage should prevent an
ascending transmission of any organisms, if present, from the genital tract proximal to the site of
tubal sterilization into the peritoneal cavity. This
is supported by clinical evidence that complete or
even partial tubal occlusion appears to lessen the
severity of infection [115]. Three possible explanations of TOA after previously occluded tubes
have been proposed [115] as follows:
• Persistent tract or reconnection between the
two tubal segments,
• Factors related to the operative procedure,
• Systemic factors such as a hematogenous or
lymphatic bacterial spread with an immunocompromised state.
Time intervals from tubal occlusion to TOA
range widely, from as early as 36h to 12years
[115].
13.4.2.6 Genital Anomalies
Structural genital anomalies are risk factors for
pelvic abscess during pregnancy [56, 106, 116].
It is unknown whether (1) anomalies themselves
or (2) invasive procedures directed to correct
these anomalies or to enable pregnancy are the
real cause/risk factor of the pelvic abscess.
13.4.2.7 Infective Non-Gynecologic
Etiology
The etiologies may include infective nongynecologic conditions such as ruptured colonic
or Meckel’s diverticulitis or acute appendicitis
(Table13.4). It is specied whether the abdominal operation itself is a risk factor [56, 106] or
operation due to intra-abdominal infective cause
such as TOA results in infective complication
[117]. Even TOA of unknown origin has been
reported [14].
13.4.3 Ovarian Abscess
An OA is a primary infection of the ovary without the involvement of the fallopian tube, whereas
a TOA involves both the fallopian tube and the
ovary.
The ratio of ovarian to tubo-ovarian abscess
increases in pregnancy [58].
The possible factors for OA include the disruption of the ovarian capsule, giving bacteria
access to the ovarian stroma, and hematogenous
Table 13.4 Differential diagnoses of pelvic inammatory disease in pregnancy
Gynecologic/obstetric Non-gynecologic
Ectopic pregnancy Perityphlitic abscess
Threatened abortion Acute appendicitis
Endometrioma Meckel’s diverticulitis
Adnexal torsion Colonic diverticulitis
Hemorrhagic cyst Urinary tract infection
Ovarian hematoma Iliopsoas abscess
Ovarian vein thrombosis Crohn’s disease
Placental abruption Urolithiasis
Chorioamnionitis
Pelvic neoplasm
Uterine horn abscess

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341
and lymphatic spread [25]. Nevertheless, the
most common mechanism is an alteration of the
ovarian capsule at ovulation or penetration during surgery or surgical procedures. Patients with
OA commonly have a history of salpingitis,
endometriosis, pelvic adhesions, hydrosalpinx,
or pelvic surgery [70, 93].
The interval between capsule disruption and
clinical presentation varies depending on the bacterial load, type of bacterium, its virulence, and
whether the infection occurred secondary to
direct contamination at surgery, or spread through
devitalized tissue, most commonly after vaginal
hysterectomy, ovarian cystectomy, CS, during
pregnancy, the use of an IUD [25, 118], or
transvaginal/percutaneous needle aspiration of an
endometrioma [96, 119]. Nevertheless, despite
the advantages of image-guided vaginal oocyte
collection, there are inherent risks, such as injury
to blood vessels and hemoperitoneum, trauma to
pelvic organs, infection or exacerbation of PID,
rupture of endometriotic cysts, ureteral lesions,
and hyperstimulation [71, 120–122].
OA after TVOR or transcervical ET occurs in
0.2–2.2% [68, 70, 71, 123]. Risk factors include
(1) ovarian or pelvic endometrioma (most common) [87, 94, 96, 105], with old blood providing
a rich culture medium for bacterial proliferation
[88], (2) previous (operated or non-operated)
ectopic pregnancy [124, 125], and 3) follicle
aspiration even without any subtle pelvic pathology [71].
The etiology of OA in pregnancy is uncertain
and different from that in the nonpregnant state.
Ascending infection is the most important mode
of infection in nonpregnant women. Barriers to
ascending infection in pregnancy include cervical mucus plug, intact fetal membranes, and the
decidua covering the openings of the fallopian
tubes. Several classications and mechanisms
[51, 126] are proposed for infection of ovaries
during pregnancy (see Sect. 13.4.2). Data conrming these facts are that OA readily occurs in
the puerperium if there is an infection of the birth
canal during or following parturition. Also, it is
likely that the ovary becomes infected independently of the gravid state or that the infection
exists before the pregnancy. During the last
decades, the more common cause is TVOR as a
part of IVF pregnancy (see Sect. 13.4.2.1) [73,
94, 127].
13.4.4 Intramyometrial Abscess
The etiology of this exceptionally rare abscess
location (two cases) failed to reveal a cause [82].
13.5 Microbiology
The most common isolate was N. gonorrhoeae
[54]. Bacterial conrmation of pelvic infection is
rarely available after transvaginal punctures,
including E. coli [128] and subclinical infection
with C. trachomatis [129], and rare isolate in
general population Atopobium vaginae [130], S.
aureus, and mixed anaerobic bacteria [94].
Anaerobic opportunists of the vagina are found
with pelvic abscesses after TVOR. E. coli, B. fra-
gilis, Enterococcus spp., and Peptococcus spp.
are common [70, 71]. There are also case reports
with other microorganisms, such as
Fusobacterium necrophorum, during puerperium
[131]. TOAs are usually polymicrobial.
Organisms isolated from TOAs belong to the facultative anaerobe Enterobacteriaceae family (E.
coli, Proteus spp., Klebsiella spp.) and anaerobic
Peptostreptococcus spp., Streptococcus spp. or
Actinomyces spp. in nonpregnant women [27,
106, 108, 132, 133].
During the rst half of the twentieth century,
tuberculous salpingitis with intrauterine pregnancy was more frequent [111]. Today, these are
rare.
13.6 Clinical Presentation
13.6.1 Suppurative Salpingitis
13.6.1.1 Acute Suppurative Puerperal
Salpingitis
Aleck W. Bourne described the clinical presentation of all stages of acute puerperal salpingitis in
1921 [43]. It differs in many aspects from that of

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13 Complicated Pelvic Inammatory Disease
non-puerperal origin. Essentially, the tubes are
abdominal and not pelvic organs, which are usually affected before reaching their normal positions in the pelvic cavity. Like acute appendicitis,
pain precedes everything and is rapidly followed
by a slowly rising temperature becoming 38.9–
39.4°C on the third or fourth day, with a pulse
the following suit. Vomiting is not a feature in
early cases. Occasional, indicative symptom consists of retention of urine or painful micturition.
This is common when cellulitis develops
secondarily to the salpingitis involving the upper
part of the broad ligament and extending forward
beneath the round ligament around the bladder.
Without operative treatment, fever is persistent
with chronic pain and wasting.
In the early stages, the abdomen is not rigid.
There is nothing but tenderness accurately localized to a point about 2in. below and external to
the umbilicus, i.e., over the posterior part of the
lateral brim of the pelvis. The uterine fundus rises
about 5cm above the symphysis. It may or may
not be tender at rst, but later it becomes so,
especially if adhesions become attached to the
uterine corn or secondary cellulitis develops.
After a week or more, nding a mass in the
hypogastrium to one side of the uterine fundus is
not unusual. Except for cellulitis, which is felt
immediately above Poupart’s ligament, such a
tumor is nearly always due to adherent omentum
and coils of the distended gut. Later, as suppuration spreads, there is rigidity and tenderness of
the whole hypogastrium, with extension upwards
over the ovarian veins if these vessels have
thrombosis.
By way of the vagina, the signs are difcult to
appreciate, for the primary changes are not in the
pelvis, and the gentlest manipulation causes pain.
The uterus can feel enlarged, with limited mobility soon developing and complete xity. In the
rst few days, it is symmetrically in the pelvis.
However, later it may be displaced laterally by
secondary cellulitis, and the displacement is
toward the affected side.
During the rst week, there may be little or
nothing felt in the lateral fornices. However, later
an indenite tender mass can be felt very high up
in the posterolateral region, largely made up of
the ovary surrounded by adherent coils enclosing
pus. The accessible part of Douglas’ pouch seldom, if ever, contains anything by the vagina.
The posterior portion of the lower part of the
uterine body may give the impression of a tumor
because it tends to bulge backward immediately
above the cervix. The best palpation of the pelvis
is obtained by rectal examination. High up on one
or both sides, the early composite swelling can be
made out early, becoming larger and more distinct as time passes.
A swelling high up in the broad ligament disturbing the position of the uterus is probably a
mass of secondary cellulitis.
13.6.2 Tubo-Ovarian Abscess
Pregnancy is said to protect against pelvic infections. Clinicians are unlikely to suspect a pelvic
abscess as a cause of an acute abdomen in pregnancy. A detailed history should search for [27,
72] the following:
• Previous episodes of PID,
• Unexplained spontaneous abortions,
• Intrauterine device.
The clinical presentation between ruptured
and unruptured TOA differs. In unruptured cases,
the rst signs of the disease are sometimes mild
and not specic, and the ndings may be altered
signicantly by the size of the gravid uterus [56,
93]. The time of symptom onset is highly vari-
able, ranging from 5days to 287days of gestation [60]. Recurrent abdominal or pelvic pain
symptoms in the postoperative and interpregnancy periods suggest the chronic nature of the
disease. However, the courses of antibiotics and
the low virulence of the organisms result in
chronic pelvic infection. History of pelvic pain
can be present for several months or years [13]. A
history of PID is present in only 50% of patients.
The infection may are up and present at any
time during pregnancy. Pain is mostly gradual in
onset, but it nally has become so severe that the
patient cannot be out of bed. While at rest, intermittent cramping, like menstrual cramps, could

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be present. There are no gastrointestinal symptoms [13]. There is no vaginal bleeding, and the
membranes are intact, but cervical discharge is
often present [116], especially with gonorrheal
cervicitis [126]. Patients with TOAs typically
present with pelvic or abdominal pain and fever.
A signicant proportion of women with TOA is
afebrile [13] (many of these have normal WBC
counts) [2].
Classic clinical presentation of TOA is
abdominal pain, cervical motion tenderness, and adnexal tenderness, as well as
one of the following:
• Fever >38°C (101°F),
• Abnormal cervical discharge,
• Elevated ESR or CRP or positive cervical cultures for N. gonorrhea or C.
trachomatis.
The abdominal examination can reveal a
suprapubic or low abdominal mass. It can be
mildly tender with cystic consistency. Vaginal
tenderness during palpation of the fornix is elicited on the side of abdominal pain [31]. If no
classical clinical features of acute peritoneal or
pelvic infection are present, it is mostly not suspected preoperatively and can be found only during emergent or elective CS [134]. In ruptured
cases, peritonitis results in pyrexia and sometimes vomiting [14].
With localized TOA, pelvic mass can be
found. It could be a hydrosalpinx, tubo-ovarian
complex, or other complex adnexal mass.
Ruptured TOA results in generalized tenderness
over the entire uterus. The uterus is very irritable,
and minimal stimulation produces contractions.
Abdominal wall guarding on the side of the rupture is present.
If rupture has occurred, peritonitis may lead to
septic shock. Pelvic examination usually reveals
extreme pelvic tenderness (cervical motion tenderness), and mass may be present. The cervix is
closed if there are no signs of preterm labor. The
vaginal examination can reveal evidence of a pre-
vious gonorrheal infection, such as the swelling
of Bartholin’s orices and granulation of the vaginal mucosa [30].
A pelvic infection becomes clinically evident
within hours up to a few days after TVOR.The
time from TVOR to the manifestation of a frank
pelvic abscess is highly variable. Diagnosis of
PID after IVT-ET mainly occurs within the rst
week after the procedure [68–70, 93] and in
<25days in 50% [73]; however, there are cases
with symptoms even postpartum [107]. PID after
IVT-ET with underlying endometriosis has the
same symptoms and signs, including cervical and
adnexal tenderness, the rise of body temperature
to >37.8°C for 48 h, cervical discharge, WBC
count >12,000/μL, and elevated ESR.
13.6.3 Ovarian Abscess
Clinical presentation depends on whether the
abscess is unruptured or ruptured. Women with
OA during pregnancy may present a wide range
of clinical symptoms with an unruptured abscess.
Presentation depends on the type of the bacteria,
the load of the bacteria, whether the infection is
mono- or polymicrobial, and the patient’s
immune status. Most cases (with or without subsequent pregnancy) present with indolent onset
of abdominal or pelvic pain [87]. The interval
between TVOR and symptom onset is generally
short but highly variable and occasionally prolonged (mean, 38.5 days; median, 22.5 days;
range, 1–320 days) [87]. If pregnancy follows
TVOR, OA develops within 4weeks in 50% of
patients and the remaining 50% from 4weeks to
the postpartum period [87]. (Low-grade) fever is
present in 95% of patients [73, 87] but could be
the only symptom in 50%.
Detailed history reveals the risk factors for
TOA (see Sect. 13.6.2). Palpable mass can be
detected. On speculum examination, the cervix
and vagina are healthy. In cases with impeding
rupture, diffuse lower abdominal pain may
worsen to severe pain associated with anorexia,
nausea, and vomiting in case of rupture. A woman
with a ruptured OA presents with features of diffuse peritonitis [27].

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13 Complicated Pelvic Inammatory Disease
13.7 Dierential Diagnosis
Table 13.4 summarizes gynecologic and nongynecologic causes of inammatory conditions in
the pelvic region and lower abdomen. Differential
diagnosis is somewhat different between early
(ectopic pregnancy, threatened abortion) and
advanced (placental abruption, chorioamnionitis,
ovarian vein thrombosis) pregnancy (see Sect.
15.6). Sometimes, it is difcult to differentiate
between types of PID, such as TOA and uterine
horn abscess. The most common differential diagnoses are acute appendicitis/perityphlitic abscess
and ectopic pregnancy [37, 54]. Sigmoid diverticulitis should be excluded with left lower quadrant abdominal pain [135, 136].
13.8 Diagnosis
Before the widespread use of US, preoperative or
prelabor diagnosis was rare. English literature of
19 cases until 1977 found that the diagnosis was
made preoperatively in only one case (5.3%)
[106]. In most cases, the diagnosis was made during emergent CS when complicated PID causes
fetal distress, preterm labor, or preterm premature rupture of membranes [134] or symptoms
and signs of acute abdomen.
13.8.1 Laboratory Findings
Leukocytosis is a prerequisite of OA, and the ESR
and CRP are elevated [73, 87]. A Papanicolaou
smear is a simple and effective method for diagnosing uterine actinomycosis in pregnancy [28].
Dining from adnexal tumors can be difcult for a
loculated disease on imaging, and CA 125 is not
tumor-specic (see Sect. 8.4.1).
13.8.2 Abdominal Ultrasound
Abdominal US should be the rst diagnostic
imaging modality for suspected PID [15, 137].
Transvaginal sonography (TVUS) allows detailed
visualization of the uterus and adnexa, including
the ovaries. The fallopian tubes are usually visible only when abnormal and distended, primarily
from postinammatory obstruction. Common
TVUS characteristics of TOA are large, solid,
and cystic mass with an irregular contour in the
adnexal region. Free uid in the cul-de-sac indicated ruptured PID (Fig.13.3).
Transabdominal sonography (TAUS) is less
sensitive in late gestation when an enlarged
uterus interferes with adequate compression of
the abdominal wall with the probe. TAUS is complementary to the TVUS because it provides a
Fig. 13.3 Transvaginal
sonography of a solid and
cystic mass
(6.7cm×5.6cm×5.1cm)
with an irregular contour in
the left adnexal region at
31weeks of IVF pregnancy. (Reproduced with
permission from [60])

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345
Fig. 13.4 Transabdominal sonography of a 12.5cm right ovarian cyst in pregnancy. (Reproduced with permission
from [138] under the CC Attribution License)
more global view of the pelvic contents
(Fig. 13.4), whether TAUS (bladder lling
required) or TVUS (bladder lling not required)
is performed rst and whether the complementary examination is needed for a nal diagnosis
[137, 139].
Serial TAUS can detect mass enlargement,
presumptive of TOA [66, 107]. Free intraabdominal uid has a high probability of ruptured TOA. The sensitivity of US for the
diagnosis of TOA is 56–93%, with a specicity
results (inclusion of any adnexal mass vs. limiting it to those diagnosed explicitly as an
abscess) [139]. TAUS is excellent for the follow-up of percutaneous or conservative treatment [62].
Pyosalpinx is a thick-wall cystic “sausage”shaped structure with an incomplete septum.
Pelvic actinomycosis from IUD shows a spaceoccupying lesion in the lower abdomen, affecting
the bladder, lower uterine segment, and upper
segment of the cervix (Fig.13.5a).
of 86–98% [139]. The wide range is likely due
to variability in the technology used (TAUS vs.
TVUS), the person performing and interpreting
13.8.3 Abdominal CT
the US (radiologist vs. gynecologist), the study
population (patients with suspected PID and
patients with a palpable adnexal mass and suspected PID vs. only patients eventually requiring laparoscopy or surgery in the workup of
their PID), the study design (retrospective vs.
prospective), and interpretation of positive
For these indications, an abdominal CT scan is
avoided during pregnancy. However, if MRI is
unavailable or during the postpartum period, CT
is used for suspected TOA (Fig.13.6a, b) or associated pathologies such as ectopic pregnancy
(Fig.13.6c).

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13 Complicated Pelvic Inammatory Disease
a
Fig. 13.5 Diagnosis of pelvic actinomycosis. (a) A
space-occupying pelvic cavity lesion on US affected the
bladder and the lower uterine segment wall. (b) Penetrating
a
b
b
placental implantation with bleeding was suspected on
MRI. (Reproduced with permission from [28])
c
Fig. 13.6 Abdominal CT. (a, b) Pelvic abscess (asterisk)
and right tubo-ovarian abscess (arrow) at 19weeks of ges-
tation. (c) Coronal view of the fetal skeleton (yellow
13.8.4 Abdominal MRI
Abdominal MRI is indicated when US ndings
are equivocal (Fig. 13.7). Abdominal MRI is
more accurate than TAUS in diagnosing PID in
the general female population. The sensitivity is
95%, the specicity 89%, and the accuracy 93%.
For TVUS, the corresponding values are 81%,
78%, and 80% [142]. In pregnant patients,
abdominal MRI reveals or conrms cystic mass
with septations [107, 138]. Abscess or mass
around the lower pole of the uterus and cervix is
arrow), tubo-ovarian abscess (white arrow), and leiomyo-
matous uterus (red arrow) [140]. (Reproduced with per-
mission from [141])
suspicious of actinomycosis, especially with a
history of IUD (Fig.13.5b). The additional benet is an exclusion of acute appendicitis with
right-sided mass [107].
13.8.5 Bacterial Cultures
In the general female population with acute PID,
one-third of the cultures from culdocentesis and
fallopian tube exudates are sterile [143–145].
The explanation is recurrent salpingitis, which

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a
Fig. 13.7 (a, b) Pelvic MRI shows an 11.5×6.7×9.0cm right-sided ovarian cyst with internal loculation (white
arrow) and an intrauterine pregnancy. (Reproduced with permission from [107])
destroys the tubal architecture obstructing the
passage of the organisms into the peritoneum and
intracellular organisms (e.g., Chlamydia spp.),
not isolated from exudates. Improper culture
techniques for viruses, Chlamydia spp., etc.,
cause falsely sterile cultures.
The positive endocervical culture for N. gon-
orrhoeae stresses a relatively high frequency
(6%) of asymptomatic gonorrheal infection in
pregnancy [145].
On initial evaluation with suspected or
proven (pyo)salpingitis, routine endocervi-
cal cultures should be obtained in all preg-
nant patients.
13.9 Prevention
b
recovery, like the transabdominal approach, seem
preferable.
13.9.2 Procedural Vaginal Antisepsis
Traditionally, the vagina is not prepared with
antiseptic solutions (e.g., aqueous povidoneiodine) before TVOR since these agents are considered embryotoxic. Therefore, only normal
saline irrigation of the vagina is usually the norm
before TVOR.However, most believe that using
only normal saline rinsing and irrigating the
vagina canal can wash away the vaginal discharge
without destroying potentially harmful bacteria
preexisting in the vaginal ora. An additional
antiseptic solution followed by a normal saline
solution can eliminate most or entire vaginal
ora. This process would not jeopardize the
development of the oocyte because all the antiseptic solution has been completely ushed away
before TVOR [100].
13.9.1 Preprocedural Elimination
ofEndometriosis
Vaginal preparation with povidone- iodine
Endometriosis predisposes to TVOR-induced
PID (see Sect 13.4.2.1 and 13.4.2.2). Complete
evaluation and removal of endometrioma should
be considered [105]. With endometriosis and pelvic adhesions, non-vaginal methods of oocyte
or chlorhexidine solution compared to
saline or not cleansing immediately before
CS probably reduces the risk of post-cesar-
ean endometritis [Level of evidence
MODERATE] [146].

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13 Complicated Pelvic Inammatory Disease
13.9.3 Prophylactic Antibiotics/
Antifungal Agents
Older studies question prophylactic antibiotic
use, given the low incidence of pelvic infections
[86, 92, 123]. Others, however, do advocate using
prophylactic antibiotics [71, 89, 90]. Although
there is no consensus on the type and protocol for
antibiotic use, doxycycline and metronidazole
are most commonly used. First-generation cephalosporins, routinely used as prophylactic antibiotics preoperatively, are also used before TVOR
[87]. Due to several C. glabrata infections diagnosed in the second half of gestation following
IVF, some recommend uconazole, an antifungal
agent, as part of the protocol before TVOR [89,
147].
Another approach is antibiotic prophylactic in
high-risk patients, such as those with a history of
PID or endometriosis. Patients with OAs almost
always have a history of salpingitis, endometriosis, pelvic adhesions, hydrosalpinx, or pelvic surgery [70, 71]. Prophylactic antibiotics during
TVOR are recommended in these groups of
patients with increased risk [70, 93].
13.10 Treatment
13.10.1 Medical Treatment
The most frequently used antibiotic before 1970
was penicillin. After 1985, gentamicin and
clindamycin were most commonly used [54].
There are insufcient data from clinical trials to
recommend a specic regimen for pregnant
women with PID, and empirical therapy with
agents effective against N. gonorrhoeae, C. tra-
chomatis, and anaerobic infections should be
considered. Local antibiotic sensitivity patterns
should be taken into account (e.g., IV ceftriaxone
2g once daily plus IV erythromycin 50 mg/kg
once daily, with the addition of metronidazole
given orally [500 mg twice daily], per rectum
[1g three times daily], or IV [500mg three times
daily]) (Evidence level III, B) [148]. Prolonged
antibiotic therapy is probably necessary for
infected endometrioma. Therapy should be
guided not simply on clinical improvement but
on infected endometrioma culture and sensitivities and achievement of effective concentrations
of the drug at the site of infection [149].
13.10.1.1 Tubo-Ovarian Abscess
A minor pelvic infection (0.3% of cases) is
dened by pyrexia and pelvic tenderness with no
evidence of abscess formation on US. Early
infection can be treated with antibiotic therapy
[15, 70]. More severe infections leading to TOA
also occur in 0.3% [68, 70]. Unruptured pelvic
abscess or TOA may be given supportive care and
treated by preoperative broad-spectrum IV antibiotics effective against gram-positive, gramnegative, and anaerobic bacteria for at least 72h
before operative intervention. There are no guidelines addressing earlier operative intervention
after ART, and the possible worse outcome has
not been documented. Unsuccessful prolonged
antibiotic treatment could carry a high rate of
spontaneous abortion [62].
13.10.1.2 Ovarian Abscess
The optimal management of TVOR-related OA
during pregnancy is unclear. Ruptured OA with
peritonitis requires urgent surgical intervention.
Whether drainage should be delayed in more
stable clinical settings is uncertain. IV antibiotics
effective against gram-positive, gram-negative,
and anaerobic bacteria should be administered.
The easier spread of infection is present
in advanced pregnancy when ovaries are
out of the pelvis.
13.10.2 Nonsurgical Drainage
For unruptured TOA, under US or CT control,
percutaneous [56, 150] or transvaginal catheter
drainage combined with IV antibiotics is suggested as the rst-line treatment to prevent postoperative complications because that procedure
is minimally invasive and easy to perform [55,

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59, 60, 107]. Peristaltic bowel on US helps avoid
bowel puncture.
Percutaneous US-guided drainage during
pregnancy has a 40% failure rate [60]. This is due
to small-diameter catheters or multiloculated
abscesses, resulting in incomplete abscess drainage. Drainage failure could result if delivery
occurs before the complete drainage of the
abscess. The catheter might dislodge from the
abscess during delivery or postpartum uterine
involution when the ovary is drawn back into the
pelvis.
TOA after TVOR can be treated with TVUSguided drainage with posterior colpotomy and
T-drain replacement into the cul-de-sac. The
elimination of infection resulted in term delivery
[55].
13.10.3 Surgical Treatment
Two-thirds underwent exploratory laparotomies,
one-third underwent unilateral salpingooophorectomies, and a quarter underwent appendectomies [54].
13.10.3.1 Indications
Surgical treatment was performed in 88% of
pregnant patients with TOA [105], indicating that
surgical intervention is usually necessary. In the
general female population, US TOA morphology
cannot predict the necessity for operative treatment [151]. Indications for surgical therapy for
both TOA and OA include [67, 152] the
following:
• No response to antibiotics within 72h,
• Abscess rupture or adjacent organ
rupture,
• Surrounding organs affected by the
inamed mass,
• Unsuccessful drainage of the abscess,
• Uncooperative patient for percutaneous
drainage,
• Uncertain diagnosis.
349
Fig. 13.8 Laparoscopic image of ovarian cyst. A 10-cm
right-sided ovarian cyst with pus made severe adhesions
with surrounding pelvic organs and peritoneum. It also
contained an endometriotic lesion. (Reproduced with permission from [138])
13.10.3.2 Operative Principles
Most patients are young, and conservative surgery should be attempted if the pathology is limited to one adnexa [14].
Surgical drainage with postoperative antibiotics should be the rst-line therapy, albeit there is
no consensus on management [87, 153]. Apart
from nonoperative drainage (see Sect 13.10.2),
operative peritoneal lavage with drainage is common by laparoscopy [73, 81, 112, 138]. If severe
pelvic adhesions secondary to abscess formation
prevent completion of the laparoscopic procedure, the conversion to laparotomy is indicated.
For non-urgent conditions, the second trimester
of pregnancy has classically been considered the
safest period for surgical intervention.
An aspiration or abscess drainage (Fig.13.8)
has a failure rate of 37.5%, while resection of the
abscess (Fig.13.9) has only 4.3% [60]. In cases
with large unilateral adnexal masses, especially
when ruptured, isolated resection of the fallopian
tube [31], unilateral salpingo-oophorectomy [66,
110, 152, 153], or even hysterectomy with unilat-
eral or bilateral salpingo-oophorectomy, especially during postpartum could be done [120,
131]. Hysterectomies are more common among
multiparas [131, 154]. Pregnant women with unilateral involvement managed by preserving the
contralateral ovary and the tube have a favorable
outcome [13, 14, 75, 106, 132, 155].
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