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12 Symptomatic Uterine Myoma
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100. Sparic R, Malvasi A, Kadija S, Babovic I, Nejkovic
L, Tinelli A.Cesarean myomectomy trends and controversies: an appraisal. J Matern Fetal Neonatal
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101. Sparic R.Intraoperative hemorrhage as a complication of cesarean myomectomy: analysis of risk factors. Vojnosanitetski Pregl. 2016;73:415–21.
102. Vilos GA, Allaire C, Laberge PY, Leyland N. The
management of uterine leiomyomas. J Obstet
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103. Pergialiotis V, Sinanidis I, Louloudis IE, Vichos T,
Perrea DN, Doumouchtsis SK. Perioperative complications of cesarean delivery myomectomy: a
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Complicated Pelvic Inammatory
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Disease
13
Abstract
Pelvic inammatory disease is rare during
pregnancy. The most obvious reason is that
many pregnancies are more or less desired,
and one of the preparations is the prepregnancy treatment of any disease, especially of
reproductive organs. Pregnancy is said to protect against pelvic infections, and clinicians
are unlikely to suspect complicated pelvic
inammatory disease as a cause of an acute
abdomen in pregnancy. The modern factor of
pelvic inammatory disease during pregnancy is assisted reproductive technology
with the inoculation of infective pathogens to
the peritoneal cavity. Therefore, techniques
for preventing infection inoculation during
assisted reproductive technologies are mandatory and discussed in detail. Clinical presentation is the same as in the nonpregnant
population with the same differential diagnoses. Before the widespread use of abdominal
sonography, preoperative or prelabor diagnosis was rare. Abdominal CT or MRI accurately denes the type and severity of the
pelvic inammatory disease. Accurate staging enables the use of the different therapeutic modalities available.
13.1 General Female Population
For an easier understanding of pelvic inammatory disease (PID) characteristics in pregnancy,
considerations in the general female population
are presented.
13.1.1 Tubo-Ovarian Abscess
13.1.1.1 Incidence
Despite increasing the number of broad-spectrum
antibiotics, PID and its complications continued
to reach epidemic proportions into the 1990s.
Acute salpingitis and PID account for more than
350,000 hospital admissions and 150,000 surgical procedures per year [1]. Also, nearly onethird of patients hospitalized for PID develop
some degree of pelvic abscess [2]. Other sequels
such as ectopic pregnancy, salpingitis isthmica
nodosa, tubal infertility, chronic pelvic pain syndromes, and pelvic adhesions are other consequences of PID (Fig.13.1).
13.1.1.2 Pathophysiology
A tubo-ovarian abscess (TOA) is the most severe
manifestation of salpingitis. The intra-abdominal
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
G. Augustin, Acute Abdomen During Pregnancy, https://doi.org/10.1007/978-3-031-26021-6_13
331
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1000
Case rate, cases/100 000
Year
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13 Complicated Pelvic Inammatory Disease
Fig. 13.1 Case rates for
Chlamydia trachomatis
infection (age,
15–39years), pelvic
inammatory disease
(age, 15–44years), and
ectopic pregnancy (age,
15–44years), British
Columbia, Canada,
1992–2009. PID pelvic
inammatory disease,
EP ectopic pregnancy
[3]
rupture of a TOA is potentially life-threatening,
with mortality rates as high as 8.6% [4]. PID and
subsequent TOA may result whenever bacteria
access the upper female genital tract. Under normal circumstances, the fallopian tubes and related
pelvic structures are sterile. However, access to
the upper genital tract via sexually transmitted
diseases or through instrumentation of the uterus
may inoculate the uterus with bacteria from the
vagina, causing infection. Passive transport and
vectors, such as spermatozoa and Trichomonas,
assist in the ascending infection from the polymicrobial vagina and cervix [5]. Once in sufcient
numbers and virulence in the upper genital tract,
these bacteria initiate an inammatory reaction
(endometritis–salpingitis–peritonitis) that results
in the signs and symptoms of PID.The rate of a
TOA developing from a typical PID ranges from
1–4% [6].
13.1.1.3 Microbiology
TOA is usually polymicrobial, whereas general
pelvic infections may often be monomicrobial.
Chlamydia
PID
EP
200 400 600 800
1995 2000 2005
TOAs are usually a mixture of anaerobic, facultatively anaerobic, and aerobic organisms, with the
purest isolated being anaerobes. The most frequent isolates from TOAs include a variety of
Enterobacteriaceae, such as E. coli (37%), B.
fragilis (22%), and other Bacteroides spp. (26%),
Peptostreptococcus spp. (18%), and Peptococcus
spp. (11%) [4, 7]. Sexually transmitted organisms such as N. gonorrhoeae and C. trachomatis
are usually not present in the abscess but may be
recovered from the cervix in one-third of cases.
The emergence and recognition of Prevotella
bivia (formerly Bacteroides bivius) and Prevotella
disiens as major pathogens in upper female geni-
tal tract infection, combined with data suggesting
that increased concentration of anaerobic organisms in the vagina is a risk factor for PID, point
toward an anaerobic-predominant mixed infection as a cause of PID and TOA.These anaerobic
bacteria, such as Bacteroides spp. and
Peptostreptococcus spp., are commonly found in
high concentrations in the vagina of women with
bacterial vaginosis [5].
13.1 General Female Population
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13.1.1.4 Prevention
Prevention of PID or prepregnancy treatment
eliminates or minimized PID complications in
pregnancy.
• Delay in the treatment of PID is associated
with an increase in the risks of ectopic pregnancy and tubal factor infertility (LE3),
• Antibiotic therapy enables a cure in 80 to 90%
of cases (LE1),
• Antibiotic treatment is indicated once the clini-
cal diagnosis of PID is probable after microbiological samples are taken (grade A),
• Vaginal sampling for microbiological diagno-
sis is recommended before elective termination
of pregnancy. (Pelvic inammatory diseases:
Updated French guidelines, 2020 [8]).
13.1.1.5 Clinical Presentation
The clinical diagnosis of TOA has similar diagnostic difculties as PID. Women presenting
with PID and pelvic mass may have a TOA, or it
could be a hydrosalpinx, tubo-ovarian complex,
or other complex adnexal mass. Patients with
TOAs typically present with pelvic or abdominal
pain and fever. A history of PID may be present
in only 50% of patients. A signicant proportion
of women with TOA are afebrile (20–30%) (these
have normal WBC counts) [2].
Pelvic examination usually reveals extreme
pelvic tenderness (cervical motion tenderness),
and mass may be present. If rupture has occurred,
typical signs and symptoms of peritonitis are
present and may lead to septic shock.
13.1.1.6 Diagnosis
Leukocytosis is common, but afebrile patients
can have normal WBC levels [2]. CRP is a sensitive, specic inammatory marker for predicting
TOA in patients with complicated PID, and levels
>50mg/L suggest TOA [9].
Transvaginal ultrasound (US) is reliable for
diagnosing and following conservatively managed TOAs [7]. A typical appearance is a complex or cystic adnexal mass with multiple internal
echoes and septations. The “gold standard” for
the diagnosis is laparoscopy. However, laparos-
Table 13.1 Major and additive criteria for the diagnosis
of PID
Major criteria
The absence of these criteria tends to rule out a PID
diagnosis
Spontaneous pelvic pain (in the absence of another
disorder) and
Induced adnexal pain and/or
Pain on uterine mobilization
Additive criteria
Each of these criteria increases the probability of PID
History: Sexually transmitted infection; postpartum
or postabortion; recent endouterine maneuvers; rectal
syndrome (tenesmus, other anal spasms); vaginal
bleeding
Clinical examination: Temperature>38°C; purulent
leucorrhea
Laboratory tests: Elevated C-reactive protein; the
presence of chlamydia trachomatis, Neisseria
gonorrhoeae, or mycoplasma genitalium on
bacteriological examination; endometritis on
endometrial biopsy sample; salpingitis on the
mbrial biopsy sample
US: Thickening of the tubal wall (>5mm); cogwheel
sign (thickened tubal fringes resembling incomplete
septa); heterogeneous latero-uterine mass potentially
septated with ne echoes
Reproduced with permission from [10]
PID pelvic inammatory disease
copy may be reserved for uncertain diagnoses as
US technology improves.
Criteria for PID in the general female popula-
tion apply to the pregnant population (Table13.1).
13.1.1.7 Treatment andPrognosis
Indications for surgery in the treatment of TOA
are the same as in the nonpregnant population
(see Sect. 13.9). CRP level trends correlate with
the success or failure of conservative TOA management. Increasing CRP levels during treatment
may be used as an indicator of the need for invasive intervention [9].
Intraperitoneal rupture of a TOA represents a
true surgical emergency, but the extent of the surgery required to achieve a cure is controversial
[7, 11]. Traditionally, aggressive surgery, usually
total abdominal hysterectomy with bilateral
salpingo- oophorectomy and drainage of all pockets of infection, was the treatment of choice. This
radical approach was common because of the
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13 Complicated Pelvic Inammatory Disease
Table 13.2 Protocols for antibiotic therapy of uncomplicated PID in the general population
Antibiotics Dose and route Duration Comments
First-line treatment
Ooxacin 400mg twice a day, oral 14days –
Metronidazole 500mg twice a day, oral 14days –
Ceftriaxone
a
500mg im. Injection – –
Possible alternatives
Ceftriaxone
Azithromycin
b
b
500mg im. Injection – –
1g per week 14days Limited efcacy against anaerobes
Moxioxacin 400mg/day 14days Higher cost; precautions for hepatic disorders
Ceftriaxone
Metronidazole
Doxycycline
Reproduced with permission from [10]
a
Can be used if necessary
b
Used together
c
Used together
c
c
c
500mg im. Injection – –
500mg twice a day, oral 14days –
100mg twice a day, oral 14days –
inadequacies of antibiotics at that time. This
procedure dropped the mortality rate from 100%
to 12% [12] and could be the procedure of choice
for a patient who has completed childbearing. In
patients with severe complicated disease, total
abdominal hysterectomy with bilateral adnexectomy may be necessary despite the patient’s
reproductive status. Patients without adnexa can
still conceive via invitro fertilization and embryo
transfer (IVF-ET). Subtotal hysterectomy is
another option [13]. Antibiotic therapy should
include a broad-spectrum cephalosporin such as
cefoxitin or cefotetan. Anaerobic coverage with
clindamycin or metronidazole is mandatory, with
their excellent ability to penetrate an abscess [7].
However, most women with a TOA are at the
peak of their reproductive years, and fertility is a
major issue. Conservative surgery should be
attempted if the pathology is limited to one side
and further reproduction is desired [14].
Conservative therapy of PID (Table13.2) or an
unruptured TOA (Table 13.3) consists of appropriate IV antibiotics [15], close monitoring of the
patient, and possible drainage of the abscess via
posterior colpotomy [15–17], CT- or US-guided
percutaneous drainage, or drainage via laparoscopy. The posterior colpotomy approach has
largely been abandoned because of a high complication rate. CT-guided percutaneous drainage
success rates are in the range of 77–94% [18].
Early laparoscopic drainage with irrigation and
antibiotics has a success rate of 95% [19].
Table 13.3 Proposed IV antibiotic therapies of tuboovarian abscess in the general population
Substance
b
Dosage
a
Duration
c
(days)
First-line treatment
Ceftriaxone 1–2g once a day 14–21
Metronidazoled500mg three times a
14–21
day
+ doxycyclined100mg twice a day
Alternatives
Ooxacin
+
metronidazole
c
d
400mg twice a day 14–21
500mg three times a
d
day
Cefoxitin 1–2g three times a day 14–21
+ doxycyclined100mg twice a day
Reproduced with permission from [10]
a
In cases of septic shock, severe sepsis, or immunode-
pression, 3–8mg/kg/d IV gentamicin can be added for no
more than 5days
b
Reassessment of the antibiotic therapy at 72h based on
the clinical and microbiological results is essential. In the
case of a de-escalation of the antibiotic spectrum, it is recommended that treatment against anaerobic microbes and
C. trachomatis continue until the therapy is completed
c
These protocols do not cover all bacteriological situa-
tions (e.g., the resistance of some gonococcal species to
uoroquinolones and the resistance of some enterobacteria species)
d
Because oral bioavailability is good for ooxacin, metro-
nidazole, and doxycycline, it is possible to administer
them orally as soon as the patient is no longer running a
fever, has no gastrointestinal disorders, and has shown
some clinical improvement
Drainage of a TOA in combination with antibiotic therapy is much more successful than conservative management. Patients treated with
13.2 Historical Considerations
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335
antibiotics alone have a 50–70% success rate.
The remaining patients eventually require surgical treatment [2, 5, 20]. Approximately 19% of
conservatively treated patients require reoperation later [2, 20, 21]. Some advocate early surgical intervention for TOA, with the highest success
rate (96.8%) and the lowest risk of readmission
within 12 months (16.1%) [22]. Others recommend for patients above 40 years, febrile, and
have a larger TOA, primary drainage at presentation [23]. In cases of grossly apparent bilateral
disease, a somewhat conservative approach of
bilateral partial adnexectomy without hysterectomy may be performed.
13.1.2 Ovarian Abscess
13.1.2.1 Historical Perspective
William T. Black presented the rst major series
of 105 cases in 1936 [24]. Streptococcus spp. was
found in 95%. The incidence of OA from all
cases of PID was 6%, while other cited authors in
that study claimed 12.4–15.45%. Wetchler and
Dunn collected 120 cases in females until 1985
[25], and Stubbleeld added ve cases in 1991
[26].
13.1.2.2 Pathophysiology
OA is a primary infection of the parenchyma of the
ovary, an entity distinctly different from
TOA.TOA, by contrast, involves the ovary by secondary spread from the infected fallopian tube
[25]. Ascending infection is the most important
mode of infection in nonpregnant women. OA has
also been reported due to non-gynecologic conditions such as acute perforated appendicitis, colonic
diverticulitis, distant infection from tonsillitis,
typhoid, parotitis, and tuberculosis. Association of
OA with an intrauterine device (IUD) has been
noted, and some may be secondary to Actinomyces
spp. [27, 28]. It may also occur due to a secondary
infection in a dermoid cyst, serous cystadenoma,
or a simple ovarian cyst.
13.2 Historical Considerations
In the sixth edition of Antenatal and Postnatal
Care, Francis J.Browne, in 1946 [29], stated that
salpingitis does not occur during pregnancy.
Even in that era, and decades before this sixth
edition, cases of PID during pregnancy were published [30–40]. Auguste (Marie Joseph Victor)
Brindeau (Fig.13.2) published the rst cases in
1917. He reported a case of fatal peritonitis from
OA rupture immediately after a term delivery
[42]. In addition to 12 personal cases of salpingooophoritis during pregnancy, Brindeau collected
81 more cases. Of these, 44 were operated on
[35]. Up to 1939, he added 23 personal cases
[35]. These cases, not described in detail, were
reported as being of an “unprecise nature.” In
many, if not all, the etiology was implied to be
criminal interference. Aleck W.Bourne, in 1921,
made detailed pathophysiology and progression
of acute puerperal salpingitis [43]. French gynecologists also added to this subject at that time—
Auvray in 1925 [39], Fruhinsholz, Hamant, and
Mosinger in 1929 [44], Devraigne and Ravina in
1937 [45], Bidoire in 1939 [34], and Metzger in
1939 [46]. Their cases occurred about the second
month of pregnancy, sometimes earlier, and were
almost invariably diagnosed as ectopic pregnancy
or acute appendicitis.
Lauchlan Aitken, in 1870, made the rst
description of a ruptured primary ovarian abscess
(OA) during premature labor in the seventh
month of pregnancy, with fetal and maternal
death [47]. Then HC Coe, in 1891, described
three cases. One had an OA rupture into the urinary bladder and later delivered a viable infant
[48]. KH Öhman, in 1913, operated on 7 days
after an uneventful delivery due to acute pelvic
symptoms with a mass to one side, which proved
to be a streptococci pyo-ovarium [40]. Tenani, in
1921, reported the rupture of a pyo-ovarium during the second stage of labor [49]. Pomini, in
1939, described a ruptured OA on the fth day
following a rapid, uneventful delivery [50].
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13 Complicated Pelvic Inammatory Disease
Fig. 13.2 Auguste (Marie Joseph Victor) Brindeau, a
French gynecologist (1867–1955), worked in Paris, nally
at the Clinique Tarnier, where he retired. One of the
13.3 Incidence
13.3.1 Acute Salpingitis
Acute salpingitis in pregnancy is rare. Metzger,
in 1939, made a 15-year review of French literature and found only seven references [46]. Up to
1959, all reported cases (12 cases) occurred in
the rst half of pregnancy [51]. Recent cases conrmed salpingitis as early as the peri- implantation
period [52]. Acute salpingitis is more common
during the rst trimester [53]. The average mean
gestational age for PID is 19weeks [54]. It probably occurs earlier but is diagnosed during the
second trimester.
13.3.2 Tubo-Ovarian Abscess
PID, in the form of a pelvic and peritoneal
abscess, rarely complicates pregnancy for several
reasons. First, in cases of a wanted pregnancy,
future mothers live healthy life avoiding any
risks, including sexually transmitted diseases.
founding members of the journal Gynécologie et
Obstétrique in 1919. (Reproduced with permission from
[41]; webpage Biusanté Paris)
Second, women with “gynecological problems”
visit gynecologists more often to eliminate any
possibility of interfering with a future pregnancy.
Diseases during the prepregnancy period are
cured, minimizing the possibility of disease are
during pregnancy. Third, women during gestation
use protection more often. Fourth, the cervical
mucus plug and intact amniotic membrane protect against ascending infection.
Acute salpingo-oophoritis or pelvic abscess
mainly occur early after transvaginal oocyte
retrieval (TVOR) [55] or in the rst trimester [56,
57] and is almost always on the right side [58,
59]. There is no side predilection in IVF-ET
because TOA starts on the side of TVOR.Up to
2021, at least 44 cases of TOA were published
[60–67]. Pelvic infection readily occurs or presents in the puerperium if there is an infection of
the birth canal during or following parturition
[61]. Pelvic infection after TVOR for IVF-ET is
<0.6% [68–71]. A pelvic abscess develops in
<50% of these cases [69]. Up to 1959, 20 cases
were collected, with bilateral TOA present in
50% of cases [51].
13.4 Etiopathogenesis
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13.3.3 Ovarian Abscess
Although the true incidence of OA in pregnancy
is unknown, it seems it is extremely rare [25, 27,
40, 47–49, 51, 72–81]. According to Dudley
etal., the ratio of OA to TOA is increased in pregnancy [58].
13.3.4 Intramyometrial andUterine
Horn Abscess
These entities are not described as part of PID,
but it is mentioned here due to the same possible
etiological factors. These are the rarest entities,
with only one report for both intramyometrial
(two cases) [82] and uterine horn abscess [83]
found.
13.4 Etiopathogenesis
The extension of the inammation by simple contiguity from the pelvic to the abdominal peritoneum
is especially liable to occur in cases of puerperal
pelvi-peritonitis at about the end of the second
week when the patient has not taken sufcient care
of herself.
(Gustave Bernutz)
Sometimes a pus tube forms after conception has
occurred, the woman having been infected and
impregnated at the same time.
(Joseph Bolivar Delee, 1938 [84])
13.4.1 Suppurative Salpingitis
13.4.1.1 Acute Suppurative Puerperal
Salpingitis
Aleck W. Bourne, in 1921 described acute puerperal salpingitis, which differs in many aspects
from that of non-puerperal origin [43]. By the end
of the rst week, when symptoms manifest, the fallopian tubes lie at or just above the pelvic brim near
the iliac vessels. At the same time, the ovaries are
placed below, just within the pelvis, and applied to
its lateral walls. The former is, therefore, outside
the limitation of the pelvic basin, surrounded by
coils of the small intestine; this considerably alters
the results which will follow the escape of pus from
the abdominal ostia, as compared with a similar
tubal condition in which the tubes are lodged
within the pelvic cavity. In the latter case, the
resulting abscesses are strictly circumscribed in the
pouch of Douglas, and the whole inammatory
area tends to be roofed in and delimited by the
omentum or small intestine. The general extension
of the infection into the abdominal peritoneum is
unusual, and the symptoms and signs are correspondingly localized. Resolution is a frequent
result; the patient recovers without operation and
may regain a fair state of health. However, conditions differ in puerperal salpingitis. The abdominal
location of the tubes is the cause of abdominal, not
pelvic peritonitis, since it allows the outpouring of
pus among the coils of the small intestine at or just
above the level of the sacroiliac joint, and herein
lies the essential difference between the two varieties of salpingitis. This difference manifests as
much in the physical signs exhibited as in the treatment required. Further, the hyperthermic condition
of the uterus and appendages during the puerperium will also modify the gravity of the symptoms
and the rapidity of their course.
The involution of the uterus appears to be
arrested at a point at which the fundus extends
about halfway between the symphysis and the
umbilicus. This may be due to infection within its
cavity or possibly to a neighboring active suppuration in the tubes. However, the important result is
that the tubes are maintained at their high level at or
above the pelvic brim for a considerable time after
the inception of the disease. Moreover, the large
uterus nearly lls the pelvic cavity and affords a
xed point comparatively high up in the abdomen,
proper for developing adhesions with other parts.
In the acute stage, the tubes are greatly congested and edematous, especially the ampullary
portion, while the mbriae are protruding, and
the ostium is discharging pus. The isthmus may
appear quite normal or swollen to a lesser extent.
Any adhesions at rst are light and easily separated, often due to akes of recent lymph and
chiey involving adjacent coils of the small
intestine and part of the cecum or sigmoid colon.
The abdominal ostium frequently opens into a
small abscess cavity walled in by the adherent coils
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13 Complicated Pelvic Inammatory Disease
and situated at rst just in front of and above the
sacroiliac joint. Later, when suppuration has
extended, it tends to pass forward along the brim of
the pelvis toward the uterine corn and is shut in
from above by the greater omentum, or the pus may
even come into relation with the abdominal wall.
13.4.1.2 Acute Salpingitis
A risk factor for acute salpingitis is an ectopic
pregnancy or vice versa. Coues of Boston, in
1911, reported 214 ectopic pregnancies with 16%
of mild catarrhal salpingitis in the opposite fallopian tube. Other etiopathogenetic factors are
the same as in TOA (see Sect. 13.4.2).
13.4.2 Tubo-Ovarian Abscess
During pregnancy, pelvic infection occurs independently of the gravid state, or the infection may
exist before the pregnancy. Friedman and Bobrow
have proposed four mechanisms for OA or TOA
during pregnancy [51] as follows:
• Hematogenous spread as in pelvic
tuberculosis,
• Lymphatic spread, especially from the vagina
and cervix,
• Infection of a (previously) existing ovarian
cyst,
• A are-up of an old infection.
Metzeger described similar mechanisms in
1939 [36] as follows:
When infection occurs during fertilization,
attachment and detachment of gonococci to
human sperm occur. The gonococcus acts as a
“hitchhiker” on the traveling sperm until a favorable environment for detachment is encountered,
such as in the uterus or fallopian tube [85].
Different pathogens have susceptibility to specic routes of infection and its spread. Gonorrheal
PID is often bilateral by ascending infection,
while tuberculosis PID results from hematogenous infection [51].
13.4.2.1 In Vitro Fertilization–Embryo
Transfer
TOA is a rare complication of TVOR, which usually fails. It occurs in 0.2–0.5% of TVOR [68,
86], but 32% of all OA were after TVOR [60].
Three different pathways for inoculation are
described [70, 87, 88] as follows:
• Inoculation of vaginal microorganisms
and anaerobe opportunists by puncture
through the non-sterile vagina,
• Reinfection through puncture of chronically infected ovaries,
• Infection through direct bowel puncture
with an inammatory or infectious
spillage.
Techniques to decrease the risk of pelvic
infection include [86, 89–92] the following:
• Infection at the time of fertilization,
• Infection soon after fertilization before
the uterine cavity has become closed by
conception (12weeks),
• Vascular or lymphatic spread (from a
septic focus in the vagina or cervix),
• A are-up of preexisting infection,
• Instrumentation sufcient to overcome
natural barriers,
• Ascending infection associated with
threatened abortion and intrauterine
bleeding.
• The fewest possible vaginal punctures
(2 max.),
• Vaginal preparation (0.5% saline or
10% povidone-iodine),
• Prophylactic antibiotics (IV cefazolin).
Prophylactic antibiotics following TVOR
are controversial as pelvic inammation is
uncommon, and these medications may not prevent all associated infections. Antibiotic prophylaxis is recommended in groups with a
higher risk for infection (see Sects. 13.4.2.2
and 13.4.2.3).
13.4 Etiopathogenesis
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13.4.2.2 In Vitro Fertilization–Embryo
Transfer andEndometriosis
Endometriosis/endometrioma is a risk factor for
PID and TOA/OA development following TVOR
[64, 66, 93–95]. Up to 80% of PID following
TVOR had underlying endometriosis [69].
Among its risk factors, incidental aspiration of an
ovarian endometrioma during TVOR activates
the pelvic infection [93, 96, 97]. Old blood in
endometrioma provides a culture medium for
bacteria to grow slowly after transvaginal inoculation. This explains the role of endometriosis in
predisposing patients to PID [93]. Endometriotic
pseudocapsule and old blood inside may prevent
antibiotic prophylaxis from overcoming the
transvaginal bacterial inoculation [93].
Furthermore, the altered immune system of a
patient with endometriosis might fail to overcome the inoculated bacteria [69].
Previous reports had indicated that aspiration
of endometriotic cysts before ovulation induction
for ART resulted in a better clinical outcome
[98]. To prevent infection in patients with endometrioma undergoing TVOR, the endometrioma
should be aspirated before TVOR [99]. However,
these endometriotic cysts reexpand quickly after
aspiration, and it is difcult to harvest some
oocytes without puncturing through these chocolate cysts. In addition, the chocolate content of
the follicular uid is sometimes found incidentally after aspiration [100]. Endometriosis surgery does not affect ART outcomes and does not
increase unresponsiveness to ovarian stimulation
[101]. Moreover, the ovarian reserve may be
adversely affected by the surgical excision of
endometrioma [102].
Endometriosis is a risk factor for develop-
ing a TOA or an OA [95]. Infection-
preventing measures should be applied not
only before and immediately after
TVOR.The excision of endometrioma less
than <4 cm in diameter is discouraged
before ART [103, 104].
13.4.2.3 Previous Pelvic
Inammatory Disease
The risk of infection is higher in cases of previous PID [70, 88, 105–107]. Unilateral TOA may
be explained by a “are-up” of preexisting but
latent salpingitis [108]. This possibility would
seem to necessitate a low-grade infection of the
fallopian tube in the rst instance leaving sufcient patency to permit the passage of a fertilized
ovum. After nidation, the infection may become
acute, probably because of the congestion produced by the gestation or unilateral salpingitis,
the other fallopian tube being patent and functioning [109]. Another proof of a “are-up” of
the previous infection is an intraoperative nding
of adhesions between the loops of the intestine,
the uterus, and the tubo-ovarian tissue indicating
the chronic nature of the disease [110].
Pelvic actinomycosis is considered a genuine,
albeit exceedingly rare, hazard of IUD. In one
study from the general female population, all 12
cases of OA were associated with IUD use, and
some were of actinomycotic origin [25]. As an
IUD-related pregnancy complication, ovarian
actinomycosis is even more exceptional, and a
history of IUD is common [27, 28]. The IUD
colonizes the endometrium, from where the bacteria proceed through the tube and into the peritoneal cavity, eventually gaining access to the
ovarian substance at ovulation. Why actinomycotic involvement of the fallopian tube sometimes does not occur is unclear unless the
dissemination of A. israelii is blood-borne or
lymphatic rather than the result of ascending
infection.
During the rst half of the twentieth century,
tuberculous salpingitis with intrauterine pregnancy was more frequent [111]. The frequency
with which pregnancy occurs in the presence of
pelvic tuberculosis is difcult to assess for the
following reasons: (1) The incidence of unsuspected pelvic tuberculosis in apparently healthy
females is unknown; (2) pelvic tuberculosis may
be discovered after pregnancy has occurred; (3)
in proved cases of pelvic tuberculosis, pregnancy
has rarely been reported.
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