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13 Complicated Pelvic Inammatory 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 inam­mation – 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 36h to 12years [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 (Table13.4). It is specied 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 inamma­tory 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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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, 120122].
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 classications and mechanisms [51, 126] are proposed for infection of ovaries during pregnancy (see Sect. 13.4.2). Data con­rming 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 conrmation 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 Inammatory 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 2in. below and external to the umbilicus, i.e., over the posterior part of the lateral brim of the pelvis. The uterine fundus rises about 5cm 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 difcult 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 indenite 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 specic, and the ndings may be altered signicantly by the size of the gravid uterus [56,
93]. The time of symptom onset is highly vari-
able, ranging from 5days to 287days 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 signicant 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 orices 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 [6870, 93] and in <25days 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 4weeks in 50% of patients and the remaining 50% from 4weeks 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 Inammatory Disease
13.7 Dierential Diagnosis
Table 13.4 summarizes gynecologic and non­gynecologic causes of inammatory 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 difcult 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 difcult for a loculated disease on imaging, and CA 125 is not tumor-specic (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 postinammatory 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 (6.7cm×5.6cm×5.1cm) with an irregular contour in the left adnexal region at 31weeks of IVF preg­nancy. (Reproduced with permission from [60])
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Fig. 13.4 Transabdominal sonography of a 12.5cm 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 specicity
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 Inammatory 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 19weeks 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 specicity 89%, and the accuracy 93%. For TVUS, the corresponding values are 81%, 78%, and 80% [142]. In pregnant patients, abdominal MRI reveals or conrms 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 ben­et 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 [143145]. The explanation is recurrent salpingitis, which
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a
Fig. 13.7 (a, b) Pelvic MRI shows an 11.5×6.7×9.0cm 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
ofEndometriosis
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 Inammatory 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 insufcient data from clinical trials to recommend a specic 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 2g once daily plus IV erythromycin 50 mg/kg once daily, with the addition of metronidazole given orally [500 mg twice daily], per rectum [1g three times daily], or IV [500mg 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 dened 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 72h 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 72h,
• Abscess rupture or adjacent organ rupture,
• Surrounding organs affected by the inamed mass,
• Unsuccessful drainage of the abscess,
• Uncooperative patient for percutaneous drainage,
• Uncertain diagnosis.
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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].