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Objective: The aim of the article was to investigate the changes in intra-amniotic pressure following transabdominal amnioinfusion during pregnancy. Design: This retrospective study included 19 pregnant women who underwent transabdominal amnioinfusion during pregnancy to relieve umbilical cord compression and improve the intrauterine environment or to increase the accuracy of ultrasonography. Materials and Methods: We measured and analyzed the changes in intra-amniotic pressure, single deepest pocket, and the amniotic fluid index before and after amnioinfusion. We also determined the incidence of maternal or fetal adverse events, such as preterm premature rupture of membranes, preterm delivery, fetal death within 48 h, placental abruption, infection, hemorrhage, and peripheral organ injury. Results: A total of 41 amnioinfusion procedures were performed for 19 patients. The median gestational age during the procedure was 24.3 weeks. The median volume of the injected amniotic fluid was 250 mL. The median single deepest pocket and amniotic fluid index after amnioinfusion were significantly higher than those before amnioinfusion (4.0 cm vs. 2.65 cm; p < 0.001 and 13.4 cm vs. 6.0 cm; p < 0.001). However, the median (range) intra-amniotic pressure after amnioinfusion was not significantly different compared to that before amnioinfusion (11 mm Hg vs. 11 mm Hg; p = 0.134). Maternal or fetal adverse events were not observed following amnioinfusion. Conclusion: Intra-amniotic pressure remained unchanged following amnioinfusion. The complications associated with increased intra-amniotic pressure are not likely to develop if the amniotic fluid index and/or single deepest pocket remains within the normal range after amnioinfusion. Studies of groups with and without complications are warranted to clarify the relationship between the intra-amniotic pressure and incidence of complications.

Objective: Necrotizing funisitis (NF) is defined as the presence of an arc (i.e., crescent/band/ring/halos) of infiltrated neutrophils and/or associated debris in Wharton's jelly (WJ) of umbilical-cord (UC). However, no information exists about the comparison in intra-amniotic inflammatory-response (IAIR) and inflammation in extra-placental membranes between the presence and absence of NF in the context of inflammation in WJ among spontaneous preterm births (PTBs). The objective of current study is to examine this issue. Materials and methods: We examined IAIR and the frequency of amnionitis according to the progression of inflammation in UC (i.e. stage-1, umbilical phlebitis [inflammation in umbilical-vein(UV)] only; stage-2, involvement of at least one umbilical-artery[UA] and either the other UA or UV without extension into WJ; stage-3, the extension of inflammation into WJ without NF; stage-4, the extension of inflammation into WJ with NF) in 120singleton spontaneous PTBs (

To assess the association between the birth weight of newborns and microbial invasion of the amniotic cavity (MIAC) and/or intra-amniotic inflammation in pregnancies with preterm prelabor rupture of membranes.A total of 528 pregnancies with preterm prelabor rupture of membranes were included in this retrospective cohort study. Transabdominal amniocentesis to determine the presence of MIAC (through culturing and molecular biology methods) and intra-amniotic inflammation (according to amniotic fluid interleukin-6 level) was performed as part of standard clinical management. Based on the presence of MIAC and/or intra-amniotic inflammation, the participants were divided into four subgroups: with intra-amniotic infection (presence of both), with sterile IAI (intra-amniotic inflammation alone), with colonization (MIAC alone), and with negative amniotic fluid (absence of both). Birth weights of newborns are expressed as percentiles derived from INTERGROWTH-21st standards for (i) newborn birth weight and (ii) estimated fetal weight.No differences in birth weights, expressed as percentiles derived from newborn weight standards (infection: median 52; sterile: median 54; colonization: median 50; negative amniotic fluid: median 51;No association was identified between the birth weight of newborns and the presence of intra-amniotic inflammatory and infection-related complications in pregnancies with preterm prelabor rupture of membranes.

To determine the prevalence of Ureaplasma spp. DNA and its load in the cervical fluid in women with preterm labor with intact membranes (PTL) complicated by intra-amniotic infection (the presence o...

Intrauterine growth restriction affects up to 10% of all pregnancies, leading to fetal programming with detrimental consequences for lifelong health. However, no therapeutic strategies have so far been effective to ameliorate these consequences. Our previous study has demonstrated that a single dose of nutrients administered into the amniotic cavity, bypassing the often dysfunctional placenta via intra-amniotic administration, improved survival at birth but not birthweight in an intrauterine growth restriction rabbit model. The aim of this study was to further develop an effective strategy for intra-amniotic fetal therapy in an animal model. Intrauterine growth restriction was induced by selective ligation of uteroplacental vessels on one uterine horn of pregnant rabbits at gestational day 25, and fetuses were delivered by cesarean section on GD30. During the five days of intrauterine growth restriction development, three different methods of intra-amniotic administration were used: continuous intra-amniotic infusion by osmotic pump, multiple intra-amniotic injections, and single fetal intraperitoneal injection. Technical feasibility, capability to systematically reach the fetus, and survival and birthweight of the derived offspring were evaluated for each technique. Continuous intra-amniotic infusion by osmotic pump was not feasible owing to the high occurrence of catheter displacement and amnion rupture, while methods using two intra-amniotic injections and one fetal intraperitoneal injection were technically feasible but compromised fetal survival. Taking into account all the numerous factors affecting intra-amniotic fetal therapy in the intrauterine growth restriction rabbit model, we conclude that an optimal therapeutic strategy with low technical failure and positive fetal impact on both survival and birthweight still needs to be found.

To determine the levels of granzyme A in amniotic fluid in pregnancies complicated by preterm prelabor rupture of membranes (PPROM), based on the presence of microbial invasion of the amniotic cavity (MIAC) and/or intra-amniotic inflammation (IAI).A total of 166 women with singleton pregnancies complicated by PPROM were included. Amniocentesis was performed at the time of admission and assessments of MIAC (using both cultivation and non-cultivation techniques) and IAI (interleukin-6 in amniotic fluid) were performed on all subjects. Based on the presence/absence of MIAC and IAI, the women were further divided into the following subgroups: intra-amniotic infection, sterile IAI, colonization, and absence of both MIAC and IAI. Amniotic fluid granzyme A levels were assessed using ELISA.Women with MIAC had lower levels of granzyme A in the amniotic fluid than women without this condition (with MIAC: median 15.9 pg/mL vs. without MIAC: median 19.9 pg/mL,The presence of sterile IAI was associated with elevated levels of granzyme A in amniotic fluid.

Fetal growth restriction (FGR) is associated with decreased insulin secretory capacity and decreased insulin sensitivity in muscle in adulthood. We investigated whether intra-amniotic IGF-I treatment in late gestation mitigated the adverse effects of FGR on the endocrine pancreas and skeletal muscle at 18 mo of age. Singleton-bearing ewes underwent uterine artery embolization between 103 and 107 days of gestational age, followed by 5 once-weekly intra-amniotic injections of 360-µg IGF-I (FGRI) or saline (FGRS) and were compared with an unmanipulated control group (CON). We measured offspring pancreatic endocrine cell mass and pancreatic and skeletal muscle mRNA expression at 18 mo of age (

Indications and administration of intra‐amniotic infusions of L‐thyroxine in the context of non‐immune fetal hypothyroidism with goiter lack of standardization. Systematic follow‐up of clinical features related to thyroid hormonal homeostasis may be useful to evaluate their efficiency and develop standardized management guidelines.

Introduction: The amniotic fluid nicotinamide phosphoribosyltransferase (NAMPT) levels have not been compared among women with preterm prelabor rupture of membranes (PPROM) comorbid with intra-amni...

Introduction: We aimed to compare the amniotic fluid interleukin (IL)-6 concentrations measured using the automated electrochemiluminescence immunoassay method and ELISA, and to establish an IL-6 c...

Macrophage inflammatory protein 1α is a chemokine produced by various immune, epithelial, mesothelial, and fibroblast cells after exposure to bacterial lipopolysaccharide or pro-inflammatory molecules. The primary aim of this study was to determine MIP-1α concentrations in amniotic and cervical fluids from pregnancy with spontaneous preterm labor with intact membranes (PTL) with respect to the presence of intra-amniotic infection (both microbial invasion of the amniotic cavity and intra-amniotic inflammation) and sterile intra-amniotic inflammation (intra-amniotic inflammation alone). The secondary aim was to assess the diagnostic indices of MIP-1α in predicting intra-amniotic infection.Seventy-four women with PTL were included in this study. Paired amniotic and cervical fluid samples were obtained using transabdominal amniocentesis and a Dacron polyester swab, respectively. Microbial invasion of the amniotic cavity was diagnosed based on a combination of culture and molecular biology methods. The concentration of IL-6 in the amniotic and cervical fluids was measured using an automated electrochemiluminescence immunoassay method. Intra-amniotic inflammation was defined as an amniotic fluid IL-6 concentration of ≥3000 pg/mL. The MIP-1α concentrations in the samples were assessed using an enzyme-linked immunosorbent assay.A difference in amniotic fluid MIP-1α was observed among women with intra-amniotic infection, sterile intra-amniotic inflammation, and negative amniotic fluid (infection: median 1779.0 pg/mL; sterile, median 102.7 pg/mL; negative, median 19.9 pg/mL;In PTL pregnancies with the presence of intra-amniotic infection, the concentration of MIP-1α is elevated in amniotic fluid but not in cervical fluid. Amniotic fluid MIP-1α may provide a useful marker for intra-amniotic infection in women with PTL.

Objectives Preterm birth remains the leading cause of perinatal morbidity and mortality worldwide. Preterm birth is preceded by spontaneous preterm labor, which is commonly associated with sterile intra-amniotic inflammation; yet, no approved treatment exists for this clinical condition. Corticosteroids are the standard of care to improve neonatal outcomes in women at risk of preterm birth. Herein, we first validated our model of alarmin-induced preterm birth. Next, we investigated whether treatment with betamethasone could prevent preterm birth resulting from sterile intra-amniotic inflammation in mice. Methods Under ultrasound guidance, the first cohort of dams received an intra-amniotic injection of the alarmin high-mobility group box-1 (HMGB1, n=10) or phosphate-buffered saline (PBS, n=9) as controls. A second cohort of dams received HMGB1 intra-amniotically and were subcutaneously treated with betamethasone (n=15) or vehicle (n=15). Dams were observed until delivery, and perinatal outcomes were observed. Results Intra-amniotic HMGB1 reduced gestational length (p=0.04), inducing preterm birth in 40% (4/10) of cases, of which 100% (4/4) were categorized as late preterm births. Importantly, treatment with betamethasone extended the gestational length (p=0.02), thereby reducing the rate of preterm birth by 26.6% (from 33.3% [5/15] to 6.7% [1/15]). Treatment with betamethasone did not worsen the rate of neonatal mortality induced by HMGB1 or alter weight gain in the first three weeks of life. Conclusions Treatment with betamethasone prevents preterm birth induced by the alarmin HMGB1. This study supports the potential utility of betamethasone for treating women with sterile intra-amniotic inflammation.

To perform a systematic review of the literature available on the association between the presence of microbial invasion of the amniotic cavity (MIAC) and/or intra-amniotic inflammation and long-term neurodevelopmental outcomes of infants from pregnancies complicated by preterm prelabor rupture of membranes (PPROM).A literature search, from their earliest entries to May 2020, was performed by employing three electronic databases (Web of Science, PubMed, and Scopus). The selection criteria were as follows: (1) singleton pregnancies with PPROM; (2) available information regarding MIAC and/or intra-amniotic inflammation; (3) long-term (at least one year of the corrected age) neurodevelopmental outcomes of respective infants.The initial search identified 10,953 articles, of which 8 were selected for full-text reading; however, none were included in the review owing to the following reasons: (i) spontaneous preterm labor with intact membranes and/or indicated (iatrogenic) preterm delivery were included in the studies without providing separate data for PPROM (The literature search provides evidence of a knowledge gap in the association between the presence of MIAC and/or intra-amniotic inflammation and long-term neurodevelopmental outcomes in infants with PPROM.

Background:Gardnerella vaginalis(GV) is most frequently associated with bacterial vaginosis and is the second most common etiology causing intrauterine infection afterUreaplasma urealyticum. Intrauterine GV infection adversely affects pregnancy outcomes, resulting in preterm birth, fetal growth restriction, and neonatal pneumonia. The knowledge of how GV exerts its effects is limited. We developed anin vivoanimal model to study its effects on fetal development.Materials and Methods:A survival mini-laparotomy was conducted on New Zealand rabbits on gestational day 21 (28 weeks of human pregnancy). In each dam, fetuses in the right uterine horn received intra-amniotic 0.5 × 102colony-forming units of GV injections each, while their littermate controls in the left horn received sterile saline injections. A second laparotomy was performed seven days later. Assessment of the fetal pups, histopathology of the placenta and histomorphometric examination of the fetal lung tissues was done.Results:Three dams with a combined total of 12 fetuses were exposed to intra-amniotic GV, and 9 fetuses were unexposed. The weights of fetuses, placenta, and fetal lung were significantly lower in the GV group than the saline-inoculated control group [mean gross weight, GV (19.8 ± 3.8 g) vs. control (27.9 ± 1.7 g),p< 0.001; mean placenta weight, GV (5.5 ± 1.0 g) vs. control (6.5 ± 0.7 g),p= 0.027; mean fetal lung weight, GV (0.59 ± 0.11 g) vs. control (0.91 ± 0.08 g),p= 0.002. There was a two-fold increase in the multinucleated syncytiotrophoblasts in the placenta of the GV group than their littermate controls (82.9 ± 14.9 vs. 41.6 ± 13.4,p< 0.001). The mean alveolar septae of GV fetuses was significantly thicker than the control (14.8 ± 2.8 μm vs. 12.4 ± 3.8 μm,p= 0.007). Correspondingly, the proliferative index in the interalveolar septum was 1.8-fold higher in the GV group than controls (24.9 ± 6.6% vs. 14.2 ± 2.9%,p= 0.011). The number of alveoli and alveolar surface area did not vary between groups.Discussion:Low-dose intra-amniotic GV injection induces fetal growth restriction, increased placental multinucleated syncytiotrophoblasts and fetal lung re-modeling characterized by alveolar septal hypertrophy with cellular proliferative changes.Conclusion:This intra-amniotic model could be utilized in future studies to elucidate the acute and chronic effects of GV intrauterine infections.

To determine the concentration of interleukin-6 (IL-6) in the cervical fluid in women with spontaneous preterm labor with intact fetal membranes (PTL) complicated by intra-amniotic infection (the presence of both microbial invasion of the amniotic cavity and intra-amniotic inflammation), or sterile intra-amniotic inflammation (the presence of intra-amniotic inflammation alone).Eighty women with singleton pregnancies complicated by PTL between gestational ages 22 + 0 and 34 + 6 weeks were included in this retrospective cohort study. Samples of amniotic and cervical fluids were collected at the time of admission. Amniotic fluid samples were obtained via transabdominal amniocentesis, and cervical fluid was obtained using a Dacron polyester swab. Microbial invasion of the amniotic cavity was diagnosed based on the combination of culture and molecular biology methods. The concentration of IL-6 in the amniotic and cervical fluids were measured using an automated electrochemiluminescence immunoassay method. Intra-amniotic inflammation was defined as an amniotic fluid IL-6 concentration ≥3000 pg/mL.The presence of intra-amniotic infection and sterile inflammation was identified in 15% (12/80) and 26% (21/80) of the women, respectively. Women with intra-amniotic infection (median: 587 pg/mL;In pregnancies with PTL, both forms of intra-amniotic inflammation are associated with elevated concentrations of IL-6 in the cervical fluid.

Background: Gardnerella vaginalis (GV) is most frequently associated with bacterial vaginosis and is the second most common etiology causing intrauterine infection after Ureaplasma urealyticum. Intrauterine GV infection adversely affects pregnancy outcomes, resulting in preterm birth, fetal growth restriction, and neonatal pneumonia. The knowledge of how GV exerts its effects is limited. We developed an in vivo animal model to study its effects on fetal development. Materials and Methods: A survival mini-laparotomy was conducted on New Zealand rabbits on gestational day 21 (28 weeks of human pregnancy). In each dam, fetuses in the right uterine horn received intra-amniotic 0.5 × 102 colony-forming units of GV injections each, while their littermate controls in the left horn received sterile saline injections. A second laparotomy was performed seven days later. Assessment of the fetal pups, histopathology of the placenta and histomorphometric examination of the fetal lung tissues was done. Results: Three dams with a combined total of 12 fetuses were exposed to intra-amniotic GV, and 9 fetuses were unexposed. The weights of fetuses, placenta, and fetal lung were significantly lower in the GV group than the saline-inoculated control group [mean gross weight, GV (19.8 ± 3.8 g) vs. control (27.9 ± 1.7 g), p < 0.001; mean placenta weight, GV (5.5 ± 1.0 g) vs. control (6.5 ± 0.7 g), p = 0.027; mean fetal lung weight, GV (0.59 ± 0.11 g) vs. control (0.91 ± 0.08 g), p = 0.002. There was a two-fold increase in the multinucleated syncytiotrophoblasts in the placenta of the GV group than their littermate controls (82.9 ± 14.9 vs. 41.6 ± 13.4, p < 0.001). The mean alveolar septae of GV fetuses was significantly thicker than the control (14.8 ± 2.8 μm vs. 12.4 ± 3.8 μm, p = 0.007). Correspondingly, the proliferative index in the interalveolar septum was 1.8-fold higher in the GV group than controls (24.9 ± 6.6% vs. 14.2 ± 2.9%, p = 0.011). The number of alveoli and alveolar surface area did not vary between groups. Discussion: Low-dose intra-amniotic GV injection induces fetal growth restriction, increased placental multinucleated syncytiotrophoblasts and fetal lung re-modeling characterized by alveolar septal hypertrophy with cellular proliferative changes. Conclusion: This intra-amniotic model could be utilized in future studies to elucidate the acute and chronic effects of GV intrauterine infections.

Objective This study aimed to determine the relationship between fetal exposure to intra-amniotic infection/inflammation (IAI) and fetal heart ventricular function as assessed by circulatory levels of N-terminal fragment brain natriuretic protein (NT-proBNP) and the Tei index. Study Design We analyzed 70 samples of paired amniotic fluid (AF) and cord blood retrieved from mothers who delivered preterm at Results IAI was characterized by significantly higher levels of AF (p 0.05, both). Conclusion Fetal myocardial left ventricular function does not seem to be significantly impaired in fetuses born alive due to IAI if delivery of the fetus occurs immediately following the diagnosis of IAI.

Our study aimed to analyze the differences in intra-amniotic pressures in patients with polyhydramnios with and without symptoms.We recruited patients with pregnancies in which amnioreduction was performed for polyhydramnios in the Department of Fetal-Maternal Medicine at Nagara Medical Center between April 2017 and August 2018. Amnioreduction was performed for severe polyhydramnios with maternal symptoms [symptomatic group] or polyhydramnios without maternal symptoms [asymptomatic group] such as abdominal distension, dyspnea, or threatened premature labor. We measured the intra-amniotic pressure after every 200 ml volume reduction during the amnioreduction.A total of 27 patients who underwent amnioreduction were classified into symptomatic (66.7%, 18/27) and asymptomatic (33.3%, 9/27) groups. Gestational age, amniotic fluid index at the time of amnioreduction, and the volume of amniotic fluid removed were not significantly different between the symptomatic and asymptomatic groups [median 32.4 weeks vs. 33.1 weeks, median 38.0 cm vs. 39.0 cm, and median 1500 ml vs. 2500 ml, respectively]. However; the intra-amniotic pressure before amnioreduction was significantly higher in the symptomatic group than in the asymptomatic group [median 15.0 mmHg (range, 10-27) vs. 10.0 mmHg (range, 6.0-13); p 0.005]. After amnioreduction, these pressures decreased significantly to median 9.0 mmHg (range, 5.0-13) (p 0.001) in the symptomatic and 7.0 mmHg (range, 4.0-11) (p 0.05) in the asymptomatic group. The median intra-amniotic pressure gradually decreased and reached a plateau during the amnioreductions in both groups.With polyhydramnios, the intra-amniotic pressure was significantly higher in the symptomatic group than in the asymptomatic group. Therefore, uterine pressure tolerance might vary according to the individual. In addition, intra-amniotic pressure monitoring might enhance the safety during amnioreduction procedures to avoid drastic and potentially harmful pressure changes.

Background: To investigate the blood glucose level response of diabetic pregnant women when administrating antenatal dexamethasone to accelerate fetal lung maturity in different routes. Methods: This prospective cohort study included 60 pregnant women with diabetes who required promotion of fetal lung maturity in Peking University First Hospital from January 2013 to April 2015. Dexamethasone was administered by IM (n = 29) or IAC (n = 31). Blood glucose level was monitored before injection, and 1 day, 2 days and 3 days after injection. Results: In the intramuscular injection group, the preprandial and postprandial blood glucose concentration was significantly elevated in the first two days (P < 0.001), and the postprandial blood glucose level was still higher than basal level (P = 0.034) on the third day. In the intra-amniotic injection group, the preprandial and postprandial blood glucose concentration was also significantly elevated on the first day (P < 0.001), but soon returned to the basal level on the second day. No significant difference was found in the magnitude of glucose increase between the two groups. Conclusion: Blood glucose level is significantly influenced by intramuscular injection of antenatal dexamethasone rather than amniotic cavity injection.

Introduction: Foetal hypothyroidism negatively impacts somatic and neurological child development and can be the cause of serious obstetric and perinatal complications. We present a rare case of a large foetal dyshormonogenetic goitre, causing foetal neck hyperexten­sion, oesophageal compression, and cardiac high-output failure. Material and methods: A foetal goitre complicated by cardiomegaly and polyhydramnios was diagnosed at 23 weeks of gestation (WG) on a routine ultrasonographic (US) assessment in a healthy nullipara. Foetal blood sampling was performed and a severe foetal hypothyroid­ism was diagnosed. Treatment was undertaken with an intra-amniotic followed by combined intra-amniotic and intravenous injections of L-thyroxine (L–T4). A total of 11 doses of L–T4 were administered between 24–37 WG to the foetus. Results: A complete regression of foetal goitre, cardiomegaly, and polyhydramnios was observed. At 38 WG the patient delivered vagi­nally a male infant with mild hypothyroidism and no signs of goitre or cardiomegaly on postnatal US. Neurological development of the one year old baby is normal. Conclusions: The effective diminishing of serum TSH concentration and goitre size was reached after combined intra-amniotic and in­travenous L–T4 injections were given. L–T4 requirement in the foetus is equal to or above 15 μg/kg daily and should be given in weekly intervals due to its rapid metabolism by the foetus and by placental type 3 deiodinase. Intra-amniotic L–T4 administration may be inef­fective when a large goitre indisposes amniotic fluid swallowing by the foetus, so then the combined L–T4 injections into the umbilical vein and intra-amniotically in experienced hands seems to be a reasonable and effective option.

Problem It is not known whether 17-alpha-hydroxyprogesterone caproate (17OHP-C) is effective for preventing preterm delivery with an episode of preterm labor (PTL) with or without intra-amniotic inflammation/infection. Methods of study This was a retrospective cohort study. One hundred and seven PTL patients were selected and divided into a 17OHP-C group (use of 17OHP-C: n = 53) and a no-treatment group (no use of 17OHP-C: n = 54). Moreover, the patients were divided into three subgroups (subgroup A: without intra-amniotic inflammation, B: with mild intra-amniotic inflammation, and C: with severe intra-amniotic inflammation) according to their level of amniotic interleukin (IL)-8, and perinatal prognosis was analyzed. Results Interval from admission to delivery (days) in the 17OHP-C group (76 [13-126], n = 34) was significantly longer than that in the no-treatment group (50 [8-104], n = 33; P = .012) in subgroup B. In cases without intra-amniotic microbes in subgroup B, a significant prolongation of gestational days was associated with the 17OHP-C group (79 [13-126], n = 25) compared with the no-treatment group (50 [8-104], n = 29; P = .029). However, there were no significant differences in subgroups A or C. Conclusion 17OHP-C could prolong gestational period in limited PTL cases with sterile mild intra-amniotic inflammation.

Intra-amniotic, fetal intrathoracic, and intraperitoneal pressures during pregnancy have been previously investigated. However, to our knowledge, changes in these pressures during uterine contractions have not been reported. Herein, we present three cases of polyhydramnios, fetal pleural effusion, and fetal ascites, in which intra-amniotic, fetal intrathoracic, intraperitoneal pressures increased with uterine contractions. These pressure increases may affect the fetal circulation. We suggest that managing potential premature delivery (e.g., with tocolysis) is important in cases with polyhydramnios and excess fluid in fetal body areas, such as the thorax, abdomen, and heart. The results of this preliminary study on intrafetal pressure measurements will be useful in performing fetal and neonatal surgeries in the future.

Objective We report a case of nonimmune hydrops fetalis caused by atrial flutter, which was successfully treated by intraperitoneal and intra-amniotic injections of amiodarone. Case Report A 27-year-old woman presented at 30 weeks of pregnancy with hydrops fetalis caused by a fetal atrial flutter. As the transplacental passage of antiarrhythmic agents is impaired in hydrops fetalis, we chose direct treatment using fetal intraperitoneal and intra-amniotic injections (75–300 mg) of amiodarone. We managed to successfully convert the fetal atrial flutter to normal sinus rhythm. The woman delivered a live female baby at 33 weeks of gestation with normal sinus rhythm and neurological development. Conclusion Intrauterine antiarrhythmic treatment can reduce perinatal morbidity and mortality. This report suggests that direct fetal therapy using intraperitoneal or intra-amniotic injections of amiodarone constitutes an effective treatment for atrial flutter in cases of hydrops fetalis.

The primary aim of this study was to identify the association between the local inflammatory response in gingival crevicular fluid measured by the levels of multiple proteins and maternal and intra-amniotic inflammatory responses measured by maternal serum C-reactive protein (CRP) and amniotic fluid interleukin (IL)-6 concentrations, respectively, in women with preterm prelabor rupture of membranes (PPROM).A prospective study was performed in which 78 women with singleton pregnancies complicated by PPROM between 24 + 0 and 36 + 6 weeks of gestation were included. Transabdominal amniocenteses were performed at the time of admission. A bedside assessment of amniotic fluid IL-6 was performed. Maternal serum CRP concentration was also measured at the time of admission. Gingival crevicular fluid was collected from the pocket of the selected tooth (the tooth with the deepest pocket) using standard sterile paper strips within 72 h after admission. Twenty-six proteins in the gingival crevicular fluid were assessed by multiplex the Meso-Scale technology.No correlations between the levels of proteins in the gingival crevicular fluid and maternal serum CRP and amniotic fluid IL-6 concentrations were found, except for a weak positive correlation between granulocyte macrophage colony-stimulating factor and CRP.The local inflammatory response in the gingival crevicular fluid is not related to the maternal and intra-amniotic inflammatory responses in women with PPROM.

Background: Preterm labor is defined as labor occurring prior to 37 weeks which .There are different factors which can lead to preterm labor including maternal causes, chorioamnionitis, cervical insufficiency and others. Because there is no satisfactory clinical method fop prediction of preterm labor, so it is important to look for some probable predicting markers by para clinical investigation. Objectives: The main goal of this study is evaluation of relationship of intra-amniotic sludge in ultrasound exam and preterm delivery. Methods: In a cohort study included 84 pregnant women in 18 - 32 weeks of gestational age referred to Islamic Azad university of mashhad hospitals in 2015. Cervical length measurement and intra-amniotic sludge were examined by transvaginal probe. Depending on sludge density the cases were divided to three groups: no amniotic sludge, light sludge and dense sludge. According to gestational age at delivery time the women were classified into two groups: term (delivery after 37 weeks) and preterm (delivery before 37 weeks). Results: The prevalence of preterm delivery was 14/3%. The frequencies of term delivery in mothers with dense, light and no sludge were 78/6%, 82/1% and 96/4 % respectively, and for preterm delivery they were 21/4%, 17/9% and 3/6% respectively. But there was no statistically significant relationship between term and preterm delivery and type of sludge. Neonatal weight in mothers with sludge, was significantly lower than mothers without sludge. Conclusions: There is no statistically significant relationship between preterm delivery and type of sludge.

Inflammation and infection play a major role in preterm birth. The purpose of this study was to (i) determine the prevalence and clinical significance of sterile intra-amniotic inflammation and (ii) examine the relationship between amniotic fluid (AF) concentrations of high mobility group box-1 (HMGB1) and the interval from amniocentesis to delivery in patients with sterile intra-amniotic inflammation.AF samples obtained from 135 women with preterm labor and intact membranes were analyzed using cultivation techniques as well as broad-range PCR and mass spectrometry (PCR/ESI-MS). Sterile intra-amniotic inflammation was defined when patients with negative AF cultures and without evidence of microbial footprints had intra-amniotic inflammation (AF interleukin-6 ≥ 2.6 ng/mL).(i) The frequency of sterile intra-amniotic inflammation was significantly greater than that of microbial-associated intra-amniotic inflammation [26% (35/135) versus 11% (15/135); (P = 0.005)], (ii) patients with sterile intra-amniotic inflammation delivered at comparable gestational ages had similar rates of acute placental inflammation and adverse neonatal outcomes as patients with microbial-associated intra-amniotic inflammation, and (iii) patients with sterile intra-amniotic inflammation and high AF concentrations of HMGB1 (≥8.55 ng/mL) delivered earlier than those with low AF concentrations of HMGB1 (P = 0.02).(i) Sterile intra-amniotic inflammation is more frequent than microbial-associated intra-amniotic inflammation, and (ii) we propose that danger signals participate in sterile intra-amniotic inflammation in the setting of preterm labor.

BACKGROUND: Intra-amniotic lipopolysaccharide (LPS) exposure may affect neonatal outcome by altering fetal lung and immune system development. We hypothesized that intra-amniotic LPS exposure would cause persistent fetal pulmonary responses as the lungs develop in utero. METHODS: Fetal lambs were exposed to intra-amniotic LPS at 118 or at 118 and 123 d of gestational age (GA) with delivery at 125, 133, or 140 d (term = 147 d). Immune responses, PU.1 expression, Toll-like receptor (TLR)-1,2,4,6 mRNA levels, mast cell levels, and pulmonary elastin deposition were evaluated. RESULTS: After a single dose of LPS, pulmonary inflammatory responses were observed with increases of (i) PU.1 and TLR1 at 125 d GA and (ii) monocytes, lymphocytes, TLR2, and TLR6 at 133 d GA. Repetitive LPS exposure resulted in (i) increases of neutrophils, monocytes, PU.1, and TLR1 at 125 d GA; (ii) increases of neutrophils, PU.1, and TLR2 at 133 d GA; and (Hi) decreases of mast cells, elastin foci, TLR4, and TLR6 at early gestation. At 140 d GA, only PU.1 was increased after repetitive LPS exposure. CONCLUSION: The preterm fetal lung can respond to a single exposure or repeated exposures from intra-amniotic LPS in multiple ways, but the absence of inflammatory and structural changes in LPS-exposed fetuses delivered near term suggest that the fetus can resolve an inflammatory stimulus in utero with time.