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13 Complicated Pelvic Inammatory Disease
a
Fig. 13.9 (a) Laparoscopic image of a left ovarian mass consistent with abscess and disseminated purulent uid. (b) Appearance after excision of the mass and irrigation of the pelvis. (Reproduced with permission from [73] under the CC BY 2.5)
13.10.4 Obstetric Management
CS is the most common mode of delivery [54]. With late decelerations, fetal bradycardia, or an increase in uterine contractions of a viable fetus, CS is performed during operative treatment of ruptured PID [60]. In near-term pregnancy, induction of labor is recommended. When the fetus is removed from the source of infection, any antibiotic can be administered to the mother. Also, if conservative therapy fails, laparoscopy is technically easier with the smaller uterus in the postpartum period [156].
13.11 Prognosis
13.11.1 Maternal Outcome
13.11.1.1 Tubo-Ovarian Abscess
At the beginning of the twentieth century, mater­nal survival was excellent, with more cases of pelvic tuberculosis during pregnancy [157]. With completely changed underlying microbial ora causing complicated PID in pregnancy, the maternal outcome is still excellent, with survival approaching 100% [73, 158]. Delay in diagnosis and treatment, especially with ruptured TOA causing peritonitis, increases the possibility of maternal mortality and morbidity [56]. Fertility impairment following TOA results from postin­ammatory tubal obstruction [159].
b
Compared to non-PID patients, PID patients have approximately 2× higher risk of preterm labor and ectopic pregnancy [160].
Due to a small number of patients and vari­ous PID stages, firm conclusions cannot be made. Surgical and percutaneous intervention carries 50% of the spontaneous abortion rate in first- trimester pregnancies. The TOA caused by TVOR seems to be better maintained dur­ing pregnancy, and the perinatal outcome is better than the naturally occurring TOA [67]. Surgical and percutaneous intervention could have a similar 50% abortion rate during the first trimester. During 14–20 weeks of preg­nancy, the cases are exceptionally rare, and conclusions cannot be made. After 20weeks of gestation, surgical treatment has a high delivery rate but cannot be compared to other methods performed in 1–3 patients [67]. Spontaneous TOA and TOA after TVOR have similar ratios (3:1) of delivery and abortion after 20 weeks of gestation. Through all tri­mesters, TOA without therapy has a 100% abortion rate [67].
13.11.1.2 Ovarian Abscess
Tenani, in 1921, reported the rupture of a pyo­ovarium during the second stage of labor, fol­lowed by maternal streptococci peritonitis and death [49]. Currently, maternal survival is 100% [27, 72]. Pelvic actinomycosis has low virulence, which is probably why spontaneous abortion
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does not occur. The preterm labor rate could be increased, but the number of cases is too small for denitive conclusions [27, 28].
13.11.1.3 Surgical Complications
Surgical complications inuence further preg­nancy and delivery, including surgical site infections, increased intra-abdominal pressure, and burst abdomen (see Chap. 22) [152].
13.11.2 Fetal Outcome
Fetal and neonatal mortality combined is 10.3– 50% [54, 161, 162]. The majority of births are at term [54]. Term delivery results from surgical [133, 163] or antibiotic [164] treatment during pregnancy. Live births have a high incidence of associated morbidities, such as neurological sequelae [161, 162]. Neonates can develop early­or late-onset sepsis and often have no apparent perinatal risk factor [162]. Reasons for the increase of pneumococcal neonatal sepsis recently may be the following: (1) increased rates of genital S. pneumoniae colonization due to changes in sexual practice (i.e., increased oro­genital sex); (2) improved laboratory isolation techniques; (3) the increased use of antimicrobi­als for prevention of group B streptococcal dis­ease selecting for more resistant pathogens such as S. pneumoniae [165]; and (4) publication bias with positive cases being published more fre­quently [161]. Possibly the type of bacteria dic­tates the rate of fetal loss (spontaneous abortion). The most common is type II atrial septal defect (Or 4.2) [166].
Acute PID in pregnancy results in an increased
rate of congenital cardiovascular anomalies (OR
2.6). Up to 1971, gonorrheal salpingitis/TOA had
50% fetal loss [126].
Fruhinsholz and Feuillade, in 1924, in their
classical paper dealing with utero-adnexal tuber­culosis and pregnancy, referred to cases reported by various observers of normal pregnancy fol­lowing conservative surgery for pelvic tuberculo­sis [157]. Today, pelvic tuberculosis in pregnancy is extremely rare.
13.11.2.1 Acute Salpingitis
Previously, the fetal outcome was poor. Up to 1993, the average gestational age at diagnosis was 12 weeks; 27% of patients reached term pregnancy and delivered; 40% resulted in sponta­neous abortions, 13% in stillbirth, and 7% in pre­mature delivery with fetal death [167].
13.11.2.2 Tubo-Ovarian Abscess
Several possible explanations for the role of infection in reducing pregnancy success have been suggested, especially during IVF-ET preg­nancy with PID. Introducing endotoxin-releas­ing bacteria into the peritoneal cavity during TVOR may induce abortion by promoting the release of prostaglandins, catecholamines, and cortisol, which play a role in the termination of pregnancy. Moreover, local inammatory reac­tions and fever may also affect pregnancy suc­cess rates [168].
Overall fetal loss was 36.8%, and surgically treated patients included 92.9% of overall fetal loss [60]. Pregnancy loss occurred in 90%, with TOA developing before 24 weeks of gestation [105]. The fetal survival rate of those pregnancies complicated by a TOA late in the second trimes­ter was 33% [106, 169]. The fetal mortality rate after PID from IVF-ET depends on the gesta­tional age and reaches 40–50% overall [107,
138]. A full-term pregnancy is reached in 1/3 of
cases [107].
13.11.2.3 Ovarian Abscess
Fetal mortality from OA depends on many fac­tors. Different authors claim different survival. Some claim extremely low fetal survival, with live cases delivered prematurely with severe fetal complications [56, 73, 87]. Others claim excel­lent survival of healthy newborns [27, 72].
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Vernix Caseosa Peritonitis
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Abstract
Vernix caseosa (VC) peritonitis is an extremely rare, poorly recognized complica­tion caused by an inammatory response to amniotic uid spilled into the maternal peri­toneal cavity. Two classic forms are recog­nized: VC peritonitis and VC granuloma. The third form is meconium peritonitis/granu­loma. Meconium, apart from detritus and digestive tract secretions, also contains ingested amnion with lanugo hair. With fetal distress, the fetal intestine empties. VC com­plications present during the rst postpartum days with abdominal pain and pyrexia. Nausea, vomiting, and dyspnea due to dia­phragmatic irritation are common. Contrast­enhanced abdominal CT reveals multiple oval rim-enhancing peritoneal lesions commonly misinterpreted. Nonoperative treatment includes antibiotics and steroids with a low success rate. Surgical treatment includes
lavage with the removal of all masses. Incorrect preoperative diagnosis results in removing many intra-abdominal organs commonly attributed to malignancy. Maternal survival is excellent, but the sequel is com­mon with operative and nonoperative treatment.
14.1 Denition andHistorical
Perspective
Vernix caseosa peritonitis (VCP) is an extremely rare, poorly recognized complication caused by an inammatory response to amniotic uid spilled into the maternal peritoneal cavity. The term ver- nix caseosa (VC) rst appeared in 1846 in the Dunglison Dictionary of Medical Sciences. The rst description of the term VCP was by Martin S.Krumerman and Gerald J.Pouliot in 1976 after the Cesarean section (CS) [1]. It was an unre­ported complication before the era of CS.
© 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_14
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14.2 Incidence
Less than 40 cases of VCP have been reported to date [26]. However, the incidence of VCP is undoubtedly underestimated because many cases with mild symptoms likely go unnoticed.
14.3 Pathology
14.3.1 Physiology ofVernix Caseosa
Birth is a state of rapid transition from the high­humidity aqueous intrauterine environment to the characteristically low-humidity (typically 20–40%) extrauterine environment. VC is the cheese-like substance covering the skin of the newborn, unique to humans during the last trimester of pregnancy, unique to humans. This material in the amniotic uid consists of an admixture of (1) fetal desqua­mated, anucleate, squamous, epithelial cells, (2) lanugo hair shafts, and (3) sebaceous glandular secretion. Biochemical studies have revealed the presence of lipids (62.5%), proteins (36%), and carbohydrates (1.5%) [7]. After delivery, VC dries spontaneously on the skin. VC has multiple protec­tive functions such as moisturizer, anti-infective, antioxidant, and enhancer of the acid mantle devel­opment after birth [8]. VC undergoes a substantial change during birth and is transferred from an aqueous, warm, and sterile environment to a gas­eous, colder, and xenobiotic-containing environ­ment postnatally [9]. Differences exist in VC composition between newborn boys and girls. Higher proportions of wax esters and triacylglycer­ols with longer hydrocarbon chains were observed in newborn girls [10]. The gestational age was likely to affect branched-chain fatty acids concen­trations, with the VC and meconium branched­chain fatty acids content being signicantly higher in full-term infants than in preterm infants [11]. VC is more prominent following CS than after vaginal births [12]. VC is absent in very low birth weight premature infants [8].
14.3.2 Vernix Caseosa Peritonitis/
Granuloma
(Unawareness of) VC commonly results in appendectomy. Only microscopic examination demonstrates multiple brinocellular exudates on the appendiceal serosa (Fig. 14.1a). The inammatory cells include an admixture of neu­trophils, eosinophils, lymphocytes, and macro­phages aggregated about anucleate squamous cells having wrinkled borders (Fig. 14.1b). Occasionally, a foreign body giant cell reaction is present (Fig.14.1c). Besides, a lanugo hair shaft surrounded by inammatory cells can be identi­ed (Fig. 14.1d). There are intense hyperemia and hemorrhagic foci. The anucleate squamous cells show strong positivity for AE1/AE3 cyto­keratin (Fig. 14.1e). Proliferating (reactive) submesothelial spindle cells also display strong positivity for AE1/AE3 cytokeratin. The squa­mous cells are arranged as single or in groups, and the cheesy exudate is brinous.
The predominant type of inammatory cells depends on the duration of VCP.Neutrophils are predominant soon after delivery. After several days, an acute and foreign body inammatory reaction will usually be evident. Weeks after delivery, granulomatous foreign body reactions predominate [13, 14].
14.3.3 Intraperitoneal Meconium
Peritonitis/Granuloma
Differential diagnosis from maternal meconium peritonitis could be difcult due to many simi­larities. Meconium peritonitis/granuloma char­acterizes numerous eosinophils scattered irregularly throughout the process. There are many giant cells with organized epithelioid tubercles. Within these cells, vacuoles contain a yellow-brown pigmented material arranged in cords and sheets; the latter stained positive for bile [15].
14.4 Pathophysiology
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a
b
de
c
Fig. 14.1 (a) Appendiceal biopsy shows normal mucosa, underlying muscularis propria (black arrow), and a sero­sal inammatory inltrate (blue arrows) centered around fetal squamous cells (purple arrow) (H&E; ×20) [16]; (b) Scattered anucleate squamous cells are surrounded by a mixed inammatory inltrate. The arrow indicates an anucleate squamous cell (H&E; ×200); (c) Mixed inam­matory inltrates with the presence of a multinucleated
14.4 Pathophysiology
14.4.1 Vernix Caseosa Peritonitis/ Granuloma
Spillage of VC into the peritoneal cavity incites an inammatory reaction causing symptoms resembling an acute abdomen. The leakage of amniotic uid results from the following:
• Antenatal or intrapartum tubal reux [2, 13],
• Premature rupture of membranes [17],
• Uterine perforation/rupture,
• Rupture of ovarian mature cystic teratoma,
• CS [14].
giant cell. This cell shows rests of squamous cells engulfed in its cytoplasm (H&E; ×200); (d) Lanugo hair shaft amidst inammatory cells (H&E; ×400); (e) Anucleate squamous cells and proliferating submesothelial cells show strong positivity for AE1/AE3 cytokeratin. The arrow points to an aggregate of anucleate squamous cells (Cytokeratin; ×200) [3]
Tubal reux of amniotic uid will not occur unless some disruption of the natural decidual– tubal barrier occurs or intrauterine pressure dif­ferences facilitate ow in this direction rather than through the cervix. In the normal gravid uterus of four or more months’ gestation, intact membranes, decidual hypertrophy, stromal edema, placentation, and the cervical mucus plug usually occlude the cavity [17].
Most cases were diagnosed in the postpartum period after uneventful CS.The spillage of amni­otic uid into the peritoneal cavity at CS is almost inevitable and usually insignicant. However, in some cases, it can be the trigger for a peritoneal reaction. The exact mechanism leading to the