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Congenital heart defects are common and occur in approximately 0.9% of births. In France, the registries cover approximately 20% of the population but not the entirety of France; therefore, we aimed to update the incidence data for congenital heart defects in France from 2013 to 2022 using the medico-administrative database PMSI-MCO (French Medical Information System Program in Medicine, Surgery, and Obstetrics). We aimed to compare the frequency of risk factors in a population with congenital heart defects and a reference population. From 2013 to 2022, we included children aged < 3 years diagnosed with congenital heart defects according to the International Classification of Diseases, 10th Revision, in the PMSI-MCO database. We compared them with a population without congenital defects on several medical data items (e.g., parity, gemellarity, and mortality rate). Bivariate and multivariate analyses compared children with congenital heart defects and children without congenital malformation. We identified 83,879 children with congenital heart defects in France from 2013 to 2022 in the PMSI-MCO database and 7,739,840 children without such defects, including 7,218,952 without any congenital defects. We observed more deaths (7.49% vs. 0.68%, d = 0.59) and more twinning (8.67% vs. 1.23%, d = 0.35) among children with congenital heart defects. Multivariate analysis revealed an increased risk of congenital heart defects in male individuals (OR [odds ratio] 1.056, 95% CI [confidence interval] [1.039-1.076]) and cases of medically assisted reproduction (OR 1.115, 95% CI [1.045-1.189]) and a reduced risk in the case of multiparity (OR 0.921, 95% CI [0.905-0.938]). According to the PMSI-MCO database, the incidence of congenital heart defects in France from 2013 to 2022 is 1% of births. Congenital heart defects are more frequent in cases of prematurity, twinning, primiparity, male sex, and maternal age > 40 years.

Congenital diaphragmatic hernia (CDH) is associated with a high incidence of respiratory problems, even after initial hospital discharge. These problems are likely to lead to re-hospitalization during infancy, although actual frequency of readmissions is unknown. We aimed to determine the rate of hospitalization for wheezing in infants with CDH between the time of initial discharge and 24 months of age, and to identify factors associated with readmission. Data about infants with CDH born in three French reference tertiary centers between January 2009 and March 2013 who were alive at hospital discharge, were extracted from a prospective national database. Ninety-two children were identified, and 86 were included in the analysis. In total, 116 wheezing episodes requiring a doctor's visit occurred in 50 infants (58%) before 24 months of age. Twenty-two children (26%) were readmitted at least once for wheezing exacerbations. RSV was present in 6 of 15 (40%) of children with available nasal samples at first readmission, and 1 of 5 (20%) at second readmission. Thoracic herniation of the liver, low gestational age, longer initial hospitalization, need for oxygen therapy at home, and eczema were all significantly associated with readmission for wheezing exacerbations. Fifty-three infants (62%) received palivizumab prophylaxis, but there was no association with the overall rate of readmission for wheezing exacerbations or RSV-related hospitalization. The rate of readmission for wheezing among infants with CDH is high, and significantly influenced by several prenatal and neonatal factors. Palivizumab prophylaxis was not associated with the rate of readmission.

Perinatal anoxia remains an important public health problem as it can lead to hypoxic–ischaemic encephalopathy (HIE) and cause significant neonatal mortality and morbidity. The mechanisms of the fetal brain’s response to hypoxia are still unclear and current methods of in utero HIE prediction are not reliable. In this study, we directly analysed the brain response to hypoxia in fetal sheep using in utero EEG. Near-term fetal sheep were subjected to progressive hypoxia induced by repeated umbilical cord occlusions (UCO) at increasing frequency. EEG changes during and between UCO were analysed visually and quantitatively, and related with gasometric and haemodynamic data. EEG signal was suppressed during occlusions and progressively slowed between occlusions with the increasing severity of the occlusions. Per-occlusion EEG suppression correlated with per-occlusion bradycardia and increased blood pressure, whereas EEG slowing and amplitude decreases correlated with arterial hypotension and respiratory acidosis. The suppression of the EEG signal during cord occlusion, in parallel with cardiovascular adaptation could correspond to a rapid cerebral adaptation mechanism that may have a neuroprotective role. The progressive alteration of the signal with the severity of the occlusions would rather reflect the cerebral hypoperfusion due to the failure of the cardiovascular adaptation mechanisms.

Fetal infection during labor with fetal inflammatory response syndrome (FIRS) is associated with neurodevelopmental disabilities, cerebral palsy, neonatal sepsis, and mortality. Current methods to diagnose FIRS are inadequate. Thus, the study aim was to explore whether fetal heart rate variability (HRV) analysis can be used to detect FIRS. In chronically instrumented near-term fetal sheep, lipopolysaccharide (LPS) was injected intravenously to model FIRS. A control group received saline solution injection. Hemodynamic, blood gas analysis, interleukin-6 (IL-6), and 14 HRV indices were recorded for 6 h. In both groups, comparisons were made between the stability phase and the 6 h following injection (H1-H6, respectively) and between LPS and control groups. Fifteen lambs were instrumented. In the LPS group (n = 8), IL-6 increased significantly after LPS injection (p < 0.001), confirming the FIRS model. Fetal heart rate increased significantly after H5 (p < 0.01). In our FIRS model without shock or cardiovascular decompensation, five HRV measures changed significantly after H2 until H4 in comparison to baseline. Moreover, significant differences between LPS and control groups were observed in HRV measures between H2 and H4. These changes appear to be mediated by an increase of global variability and a loss of signal complexity. As significant HRV changes were detected before FHR increase, these indices may be valuable for early detection of acute FIRS.

Fetal heart rate (FHR) deceleration is the most common change seen during labor. The role of the autonomic nervous system in regulating the fetal cardiovascular response during multiple uterine contractions has been well-established. However, the mechanism underlying the hemodynamic response remains unclear and the specific reflex that mediates the cardiovascular modifications is still controversial. This study aimed to determine the role of the sympathetic and parasympathetic systems on fetal hemodynamics in complete cord occlusion. Chronically instrumented fetal sheep were randomized to receive an intravenous injection of atropine 2.5 mg (n = 8), propranolol 5 mg (n = 7), atropine and propranolol (n = 7), or a control protocol (n = 9), followed by three episodes of 1-minute umbilical cord occlusion repeated every 5 minutes. Cord compression induces a rapid decrease in the FHR and a rapid increase in MAP. The decrease in FHR is caused by an increase in parasympathetic activity, (atropine and atropine-propranolol abolish the FHR response to the occlusion). The change in FHR during occlusion was not modified by propranolol injection, showing no effect of sympathetic tone. The increase in MAP during occlusion was similar in the four protocols. After releasing occlusion, the FHR was still lower than that at baseline due to a sustained parasympathetic tone. Suppression of the parasympathetic output to the cardiovascular system unmasks an increase in the FHR above baseline values. The lower FHR with the propranolol protocol further supports an increase in myocardial β-adrenoceptor stimulation after cord release. The increase in MAP after cord release was similar in the four protocols, except after the early stage of interocclusion period in atropine protocol. Four minutes after cord release, the FHR returned to baseline irrespective of the drugs that were infused, thereby showing recovery of ANS control. Blood gases (pH, PaCO 2 , PaO 2 ) and plasma lactate concentrations was similar between the four protocols at the end of three applications of UCO. Complete cord compression-induced deceleration is likely due to acute activation of parasympathetic output. β-adrenoceptor activity is involved in the increase in FHR after cord release. Understanding the reflexes involved in FHR deceleration may help us understand the mechanisms underlying fetal autonomic adaptation during cord occlusion.

The effect on neonatal mortality of mode of delivery of a fetus in breech presentation at an extremely preterm gestational age remains controversial. To compare mortality associated with planned vaginal delivery (PVD) of fetuses in breech presentation with that of fetuses in breech presentation with a planned cesarean delivery (PCD). Retrospective study reviewing records over a 19-year period in a level 3 university referral center of singleton infants born between 25+0 and 27+6 weeks of gestation, alive on arrival in the delivery room, and weighing at least 500 grams at birth. Infants in the first group were in breech presentation with PVD and the second in breech presentation with PCD. The principal endpoint was neonatal death. During the study period, we observed 113 breech presentations with PVD, and 80 breech presentations with PCD. Although not significant after adjustment, neonatal mortality in the breech PVD group was more than twice that of the breech PCD group (19.5 vs 7.8%, P = 0.031, ORa = 2.6, 95% CI 0.8-9.3, NNT = 8). This higher neonatal mortality in the breech PVD group was exclusively associated with a higher risk of death in the delivery room (12.4 vs 0.0% P = 0.001, OR not calculable, NNT = 8). In these extremely preterm breech presentations with PVD, neonatal mortality in the delivery room was associated with entrapment of the aftercoming head, cord prolapse, and a short duration of labor. For deliveries between 25+0 and 27+6 weeks' gestation, vaginal delivery in breech presentation is associated with a higher risk of death in the delivery room.

Background The effect on neonatal mortality of mode of delivery of a fetus in breech presentation at an extremely preterm gestational age remains controversial. Objective To compare mortality associated with planned vaginal delivery (PVD) of fetuses in breech presentation with that of fetuses in breech presentation with a planned cesarean delivery (PCD). Material and methods Retrospective study reviewing records over a 19-year period in a level 3 university referral center of singleton infants born between 25+0 and 27+6 weeks of gestation, alive on arrival in the delivery room, and weighing at least 500 grams at birth. Infants in the first group were in breech presentation with PVD and the second in breech presentation with PCD. The principal endpoint was neonatal death. Results During the study period, we observed 113 breech presentations with PVD, and 80 breech presentations with PCD. Although not significant after adjustment, neonatal mortality in the breech PVD group was more than twice that of the breech PCD group (19.5 vs 7.8%, P = 0.031, ORa = 2.6, 95% CI 0.8–9.3, NNT = 8). This higher neonatal mortality in the breech PVD group was exclusively associated with a higher risk of death in the delivery room (12.4 vs 0.0% P = 0.001, OR not calculable, NNT = 8). In these extremely preterm breech presentations with PVD, neonatal mortality in the delivery room was associated with entrapment of the aftercoming head, cord prolapse, and a short duration of labor. Conclusion For deliveries between 25+0 and 27+6 weeks’ gestation, vaginal delivery in breech presentation is associated with a higher risk of death in the delivery room.

ObjectiveRecent evidence indicates that levels of breast milk (BM) hormones such as leptin can fluctuate with maternal adiposity, suggesting that BM hormones may signal maternal metabolic and nutritional environments to offspring during postnatal development. The hormone apelin is highly abundant in BM but its regulation during lactation is completely unknown. Here, we evaluated whether maternal obesity and overnutrition impacted BM apelin and leptin levels in clinical cohorts and lactating rats.MethodsBM and plasma samples were collected from normal-weight and obese breastfeeding women, and from lactating rats fed a control or a high fat (HF) diet during lactation. Apelin and leptin levels were assayed by ELISA. Mammary gland (MG) apelin expression and its cellular localization in lactating rats was measured by quantitative RT-PCR and immunofluorescence, respectively.ResultsBM apelin levels increased with maternal BMI, whereas plasma apelin levels decreased. BM apelin was also positively correlated with maternal insulin and C-peptide levels. In rats, maternal HF feeding exclusively during lactation was sufficient to increase BM apelin levels and decrease its plasma concentration without changing body weight. In contrast, BM leptin levels increased with maternal BMI in humans, but did not change with maternal HF feeding during lactation in rats. Apelin is highly expressed in the rat MG during lactation and was mainly localized to mammary myoepithelial cells. We found that MG apelin gene expression was up-regulated by maternal HF diet and positively correlated with BM apelin content and maternal insulinemia.ConclusionsOur study indicates that BM apelin levels increase with long- and short-term overnutrition, possibly via maternal hyperinsulinemia and transcriptional upregulation of MG apelin expression in myoepithelial cells. Apelin regulates many physiological processes, including energy metabolism, digestive function, and development. Further studies are needed to unravel the consequences of such changes in offspring development.

The large number of drugs administered simultaneously to neonates and children in hospital results in the formation of particles that are potentially infused. We have investigated the ability of IV in-line filters to eliminate particulate matter from multidrug infusion lines and so prevent contamination. The impact on particle occurrence of the internal volume of the IV line below the in-line filter was then evaluated. The multidrug therapy given to children was reproduced with and without in-line filtration. Three combinations with a filter were tested to vary the internal volume (V) between the filter and the catheter egress. The catheter was then connected to a dynamic particle count to evaluate the particulate matter potentially administered to children during infusion. The introduction of in-line filters led to a significant reduction in overall particulate matter, from 416,974 [208,479–880,229] to 7,551 [1,985–11,287] particles (p < 0.001). Larger particles of ≥10 and 25 µm were also significantly reduced. Adding an extension set to the egress of the in-line filter (V = 1.7 mL) caused a significant increase in particulate contamination for both. This study showed that in-line filtration is an effective tool in preventing particle administration to patients. Their position in the infusion in-line is therefore important because of its impact on internal volume and drug particle formation.

Purpose Opioid use during labour can interfere with cardiotocography patterns. Heart rate variability indirectly reflects a fluctuation in the autonomic nervous system and can be monitored through time and spectral analyses. This experimental study aimed to evaluate the impact of nalbuphine administration on the gasometric, cardiovascular, and autonomic nervous system responses in fetal sheep. Methods This was an experimental study on chronically instrumented sheep fetuses (surgery at 128 ± 2 days of gestational age, term = 145 days). The model was based on a maternal intravenous bolus injection of nalbuphine, a semisynthetic opioid used as an analgesic during delivery. Fetal gasometric parameters (pH, pO 2 , pCO 2 , and lactates), hemodynamic parameters (fetal heart rate and mean arterial pressure), and autonomic nervous system tone (short-term and long-term variation, low-frequency domain, high-frequency domain, and fetal stress index) were recorded. Data obtained at 30–60 min after nalbuphine injection were compared to those recorded at baseline. Results Eleven experiments were performed. Fetal heart rate, mean arterial pressure, and activities at low and high frequencies were stable after injection. Short-term variation decreased at T30 min ( P  = 0.02), and long-term variation decreased at T60 min ( P  = 0.02). Fetal stress index gradually increased and reached significance at T60 min ( P  = 0.02). Fetal gasometric parameters and lactate levels remained stable. Conclusion Maternal nalbuphine use during labour may lead to fetal heart changes that are caused by the effect of opioid on the autonomic nervous system; these fluctuations do not reflect acidosis.