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3.5 Treatment
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67
Burst abdomen in pregnancy (post laparotomy; post incisional hernia etc)
<24 weeks
Intra-abdominal sepsis
Ye s
Fetus alive
Ye s
SM NPWT/BB SVD/CS when possible EHR
NPWT/BB + EHR
Fetus aliveFetus aliv
No
SM
TOP
Ye s
NPWT/BB CS/SVD Mesh repair
TOP + 1º mesh repair
No
Fig. 3.10 Management algorithm for burst abdomen in pregnancy. SVD spontaneous vaginal delivery, NPWT negative pressure wound therapy, CS cesarean section, TOP termination of pregnancy, SM surgical management
Fig. 3.11 Intra­abdominal pressure before Cesarean section
403020
(preoperative) and postoperative (every 30min during 2h). (Reproduced with permission from [30] under the CC Attribution Licence)
>24 weeks
Intra-abdominal sepsis
Ye sNo
SVD/CS when possible
NPWT/BB
Ye s
NPWT/BB CS/SVD with Mesh repair
No
e etus alive
No
C/S 1º mesh repair
No
SM
C/S
NPWT/BB
EHR
involves laparotomy and peritoneal lavage if required, BB bogota bag, EHR elective hernia repair. (Reproduced with permission from [118])
Ye s
SM
EHR
100
Intra-abdominal pressure (mmHg)
IAP preoperative IAP M30 IAP M90
IAP M0 IAP M60 IAP M120
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3 Increased Intra-abdominal Pressure
3.6 Prognosis
3.6.1 Maternal Outcome
The maternal outcome depends on:
• the severity and duration of IAH/ACS,
• the cause of increased IAP,
• normalization of IAP after delivery.
Despite the presence of risk factors for IAH in ICU obstetric patients, the prevalence of IAH (IAP >12 mmHg) was only 6%, while 66% of patients had IAP 8–11mmHg. Interestingly, this is much lower than for mixed, nonpregnant populations of critically ill patients in the ICU (19–80%) [9].
The usual IAP may be slightly higher in criti­cally ill obstetric patients than in mixed popula­tions of critically ill patients. Nevertheless, IAP does not affect organ function depicted by the SOFA score, and the low prevalence of IAH pre­vented the evaluation of affected organ dysfunc­tion [9]. The prevalence of IAH was 75% in pregnant and 0% in postpartum patients.
and a mean IAP of 21.7mmHg. Maternal mortal­ity was 0% [121, 150].
3.6.2 Fetal Outcome
3.6.2.1 Burst Abdomen
Fetal mortality depends on (1) the gravid uterus incarceration at presentation and (2) gestation of less than 24weeks [114, 117, 118, 153].
3.6.2.2 Acute Pancreatitis
A study of 17 pregnant women with acute pan­creatitis in the third trimester (with 47% due to hyperlipidemia) found a high prevalence of IAH, with a mean IAP of 16.7 mmHg [121]. Two (12%) developed ACS, with organ dysfunction and a mean IAP of 21.7mmHg. Fetal mortality was 31.2%, and higher maternal IAP correlated with higher fetal mortality.
3.6.2.3 Acute Appendicitis
Both patients were in the second trimester. Neither received tocolysis, and neither went to preterm labor [122, 123]. Deliveries were uneventful, and both children had normal development.
Following delivery, a fall in IAP is associ-
ated with better survival [9].
3.6.1.1 Burst Abdomen
Various methods for (temporary) closure of burst abdomen in pregnancy were used: two cases with negative pressure wound therapy [117, 153], one with the mesh [114] and one with Bogota beg [118]. Maternal mortality was 0%.
3.6.1.2 Acute Pancreatitis
The development of IAH/ACS among patients with severe acute pancreatitis in the general pop­ulation is a strong predictor of mortality up to 49% [156]. A study of 17 pregnant women with acute pancreatitis in the third trimester (47% due to hyperlipidemia) found a high prevalence of IAH, with a mean IAP of 16.7mmHg [121]. Two (12%) developed ACS, with organ dysfunction
3.6.2.4 Obesity
High IAP may compress the maternal aorta and uterine arteries, reducing uterine perfusion pres­sure and fetoplacental insufciency. The higher predelivery IAP was associated with lower new­born NACS (Neurologic and Adaptive Capacity) scores. This association was found most often among women with Class III obesity (BMI ≥40kg/m2) who received spinal anesthesia [157].
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Acute Abdomen-Induced Preterm
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Labor
4
Abstract
The specic issue with acute abdomen during pregnancy is that many underlying conditions result in inammation and infection, which raise prostaglandin levels, which are crucial for normal labor progress. Therefore it is mandatory to stop the increased preterm pro­duction of prostaglandins. The only solution is early diagnosis and treatment of acute abdominal conditions during pregnancy. In addition to inammation, abdominal trauma is also an issue. It can cause placental abrup­tion and preterm labor. In addition to these two most common groups of the acute abdo­men during pregnancy, other important topics are discussed. These include maternal and fetal stress as a result of any cause of acute abdomen during pregnancy and the problem of adequate perioperative nutrition. Inadequate maternal nutrition results in dis­eases with a prolonged course before thera­peutic interventions such as conservatively treated acute cholecystitis or acute pancreati­tis. Prolonged inadequate postoperative nutri­tion is seen after many surgical procedures, especially those requiring bowel resections or reoperations. Therefore underlying pathology should be diagnosed and treated early in the course of the disease. Additional measures for detecting and preventing preterm labor should be instituted as early as possible.
4.1 Denitions
Preterm labor (PTL) is a process of regular con­tractions accompanied by the cervical change before 37 completed weeks of gestation. PTL can be:
• Induced for maternal or fetal indications
(drug-induced or delivery by elective or emer­gent Cesarean section (CS)),
• Spontaneous PTL:
– cervical dilation and intact membranes, – preterm premature rupture of the mem-
branes (PPROM).
PPROM is dened as the spontaneous rupture of the membranes at less than 37weeks’ gesta­tion at least 1h before the onset of contractions. About 30–35% of PTLs are indicated, 40–45% follow spontaneous PTL, and 25–30% follow PPROM [1, 2].
Preterm birth (PTB) is subdivided into extremely preterm (<28 weeks), very preterm (28–32 weeks), and moderate to late PTB (32– 36weeks) [3]. Today, births can occur as early as 16weeks of gestation, making the line between spontaneous abortion and spontaneous PTB more challenging.
PTL can be initiated by multiple mecha­nisms—infection/inammation, uteroplacental ischemia or bleeding, uterine trauma, uterine overdistension, or stress [4].
© 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_4
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4 Acute Abdomen-Induced Preterm Labor
4.2 Physiology ofLabor
Human labor is an inammatory, three-step pro­cess characterized by uterine contractility, cervi­cal ripening, and membrane activation/rupture [5]. The fundamental difference between the term labor and PTL is that the former results from the “physiologic activation” of this com­mon pathway. In contrast, PTL results from either early idiopathic activation of the normal labor or disease process (“pathologic activation”) that activates one or more of the components of the common pathway [5]. Monocytes and neutro­phils are primed in the peripheral blood associ­ated with term and PTL [6]. These cells inltrate the human myometrium and cervix during spon­taneous term labor, which is associated with a signicant increase in interleukin (IL -1β, IL-6, and IL-8) gene expression [7].
The common pathway of parturition includes the anatomic, biochemical, immunologic, endocri­nologic, and clinical events in the mother and fetus at term or PTL. Fetal cortisol is central to labor initiation [8]. As parturition nears, the fetal- adrenal axis becomes more sensitive to the adrenocortico­tropic hormone, increasing cortisol secretion. Fetal cortisol stimulates placental 17α-hydroxylase activity, decreasing progesterone secretion and increasing estrogen production. The reversal in the estrogen/progesterone ratio results in increased prostaglandin formation, initiating a cascade of events resulting in labor (see Sect. 4.2.4). During pregnancy, the uterus is maintained in a relatively quiescent state through the separate or combined autocrine–paracrine actions of inhibitors such as progesterone, prostacyclin (PGI2), relaxin, para­thyroid hormone-related peptide, calcitonin gene­related peptide, adrenomedullin, vasoactive intestinal peptide, nitric oxide, and corticotrophin­releasing hormone, which may inhibit and stimu­late uterine contractility [9].
Activation of the uterine components of the common pathway of parturition may be synchro­nous or asynchronous. Synchronous activation results in clinical spontaneous PTL. Asynchronous activation results in (1) predominant activation of the membranes that leads to PPROM, (2) of the cervix to cervical insufciency, and (3) that of the
myometrium to preterm uterine contractions without cervical change or rupture of membranes.
4.2.1 Myometrial Contractility
Increased cell-to-cell communication is respon­sible for the effectiveness of myometrial contrac­tility during labor. Gap junctions develop in the myometrium just before labor and disappear shortly after delivery [10, 11]. Gap junction for­mation and the expression of the gap junction protein, connexin-43, in human myometrium are similar in both term labor and PTL [12–14]. The appearance of gap junctions and increased expression of connexin-43 are part of the molec­ular and cellular events responsible for switching from contractures to contractions before the onset of parturition. Estrogen, progesterone, and pros­taglandins regulate gap junction formation and inuence the expression of connexin-43 [15–17]. Connexin-43 and other distinct contraction­associated proteins are characteristic of this phase of parturition [18–20]. α-actin was expressed in the myometrium in early pregnancy, whereas γ-actin was highly expressed by the myometrium with a contractile phenotype.
Myometrial phenotype programming [21] and sequential phenotypic changes start from an early proliferative phase. It is characterized by bromo­deoxyuridine incorporation, the proliferating cell nuclear antigen expression level, increased IGF-I signaling, and the expression of anti-apoptosis factors such as Bcl-2 [21]. An intermediate syn­thetic phase is characterized by increased cell size and synthesis/deposition of the interstitial matrix that forms the ground substance of the myometrium [22–24]. A late contractile phase is characterized by the upregulation of contraction­associated proteins, oxytocin, and prostaglandin receptors in which the cells are committed to labor [14, 25, 26]. This phenotypic program­ming is accomplished through two separate but integrated pathways: an endocrine cascade com­prising the fetal hypothalamic-pituitary-adre­nal-placental axis and a mechanical pathway in which fetal growth imposes tension on the uter-
4.2 Physiology ofLabor
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ine wall [9]. Abnormal myometrial stretch (i.e., polyhydramnios, multiple gestations) promotes the expression of gap junction proteins, oxytocin receptors, and prostaglandins in the amnion myo­metrium and cervical cells [27]. These alterations promote uterine activity and the degradation of the extracellular matrix, thereby facilitating cer­vical ripening and ROM.
4.2.2 Cervical Remodeling
The changes in the cervix include: (1) softening, (2) ripening, (3) dilatation, and (4) postpartum repair [28]. The molecular and cellular basis for cervical remodeling during pregnancy and partu­rition primarily depends on regulating extracel­lular matrix components [28, 29]. Leukocytosis in the cervix responds to increasing local levels of estrogens derived from fetal adrenal precur­sors. This results in the release of metalloprote­ases/collagenases, driving cervical ripening and dilatation. It facilitates access by cervicovaginal microora to the surface of the membranes cov­ering the cervical os, furthering the inammatory response in the amniotic cavity. Hyaluronidase activity increases in the cervix due to functional progesterone withdrawal, degrading hyaluronan leading to disaggregation of polymers, inamma­tory activation, and cervical ripening [30]. The softening of the cervix begins in early pregnancy. The tensile strength of the softened cervix appears to be maintained by an increase in colla­gen synthesis and growth of the cervix. Cervical ripening is characterized by a decreased concen­tration of collagen and the dispersion of collagen brils. The latter has been attributed to glycos­aminoglycans, such as decorin and hyaluronan, which promote the hydration of cervical tissue and dispersion of collagen bers [29]. Dilation of the cervix is an inammatory phenomenon with an inux of macrophages, neutrophils, and matrix degradation [31, 32]. Chemokines such as IL-8 [33, 34] and S100 proteins [35, 36] attract inam- matory cells, which, in turn, release pro­inammatory cytokines, including IL-1β [37, 38] and tumor necrosis factor-α (TNF-α) [36], which can activate the nuclear factor (NF)-κB signaling
pathway. NF-κB can block progesterone receptor­mediated actions [39]. Progesterone has been implicated in regulating cervical remodeling because the administration of antiprogestins in the mid-trimester and, at term, induces cervical ripening [28, 40, 41].
4.2.3 Decidual/Membrane
Activation
During pregnancy, the chorioamnionic mem­branes fuse with the decidua. In preparation for delivery, biochemical events lead to separation and postpartum expulsion of the membranes. Fibronectins are a family of essential extracellu­lar matrix proteins. The degradation of a heavily glycosylated form of cellular bronectin—fetal bronectin—present at the chorionic-decidual interface leads to its release into cervical and vaginal secretions immediately before term or PTL [42–44].
Enzymatic activity of matrix metalloprotein­ases (MMPs) and other proteases has been impli­cated in the process of rupture of membranes and parturition with intact membranes (with and without infection) [45, 46]. The precise decidual/ membrane activation mechanism remains unknown, but extracellular matrix-degrading enzymes, such as the MMPs and elastase, have a role. There is increased availability of MMP-1 (interstitial collagenase) [47], MMP-8 (neutro­phil collagenase) [47], MMP-9 (gelatinase-B) [48], and neutrophil elastase [49] in the amniotic uid of women with PPROM, compared with women in PTL with intact membranes. Plasmin has also been implicated [44] because it can degrade type III collagen, bronectin, and lam­inin [50]. A role for tissue inhibitors of MMPs (TIMPs) has also been postulated.
4.2.4 Prostaglandins
andParturition
Prostaglandins are the key mediators for the onset of labor [51]. They induce myometrial contractil­ity [51, 52], changes in extracellular matrix
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