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Introduction Foetal macrosomia is associated with various obstetrical complications and is a common reason for inductions and primary or secondary Caesarean sections. The objective of this study is the generation of descriptive data on the mode of delivery and on maternal and foetal complications in the case of foetal macrosomia. The causes and consequences of foetal macrosomia as well as the rate of shoulder dystocia are examined in relation to the severity of the macrosomia. Patients The study investigated all singleton births ≥ 37 + 0 weeks of pregnancy with a birth weight ≥ 4000 g at the Charité University Medicine Berlin (Campus Mitte 2001 - 2017, Campus Virchow Klinikum 2014 - 2017). Results 2277 consecutive newborns (birth weight 4000 - 4499 g [88%], 4500 - 4999 g [11%], ≥ 5000 g [1%]) were included. Maternal obesity and gestational diabetes were more common in the case of newborns weighing ≥ 4500 g than newborns weighing 4000 - 4499 g (p = 0.001 and p < 0.001). Women with newborns ≥ 5000 g were more often ≥ 40 years of age (p = 0.020) and multipara (p = 0.025). The mode of delivery was spontaneous in 60% of cases, vaginal-surgical in 9%, per primary section in 14% and per secondary section in 17%. With a birth weight ≥ 4500 g, a vaginal delivery was more rare (p < 0.001) and the rate of secondary sections was increased (p = 0.011). Women with newborns ≥ 4500 g suffered increased blood loss more frequently (p = 0.029). There was no significant difference with regard to the rate of episiotomies or serious birth injuries. Shoulder dystocia occurred more frequently at a birth weight of ≥ 4500 g (5 vs. 0.9%, p = 0.000). Perinatal acidosis occurred in 2% of newborns without significant differences between the groups. Newborns ≥ 4500 g were transferred to neonatology more frequently (p < 0.001). Conclusion An increased birth weight is associated with an increased maternal risk and an increased rate of primary and secondary sections as well as shoulder dystocia; no differences in the perinatal outcome between newborns with a birth weight of 4000 - 4499 g and ≥ 4500 g were seen. In our collective, a comparably low incidence of shoulder dystocia was seen. In the literature, the frequency is indicated with a large range (1.9 - 10% at 4000 - 4499 g, 2.5 - 20% at 4500 - 5000 g and 10 - 20% at ≥ 5000 g). One possible cause for the low rate could be the equally low prevalence of gestational diabetes in our collective. A risk stratification of the pregnant women (e.g. avoidance of vacuum extraction, taking gestational diabetes into account during delivery planning) is crucial. If macrosomia is presumed, it is recommended that delivery take place at a perinatal centre in the presence of a specialist physician, due to the increased incidence of foetal and maternal complications.

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We tested the hypothesis that hypoxia-reoxygenation (H/R) augments vasoreactivity to angiotensin II (ANG II). In particular, we compared an in situ live kidney slice model with isolated afferent arterioles (C57Bl6 mice) to assess the impact of tubules on microvessel response. Hematoxylin and eosin staining was used to estimate slice viability. Arterioles in the slices were located by differential interference contrast microscopy, and responses to vasoactive substances were assessed. Cytosolic calcium transients and NADPH oxidase (NOX) mRNA expression were studied in isolated afferent arterioles. SOD activity was measured in live slices. Both experimental models were subjected to control and H/R treatment (60 min). Slices were further analyzed after 30-, 60-, and 90-min hypoxia followed by 10- or 20-min reoxygenation (H/R). H/R resulted in enhanced necrotic tissue damage compared with control conditions. To characterize the slice model, we applied ANG II (10-7 M), norepinephrine (NE; 10-5 M), endothelin-1 (ET-1; 10-7 M), and ATP (10-4 M), reducing the initial diameter to 44.5 ± 2.8, 50.0 ± 2.2, 45.3 ± 2.6, and 74.1 ± 1.8%, respectively. H/R significantly increased the ANG II response compared with control in live slices and in isolated afferent arterioles, although calcium transients remained similar. TEMPOL incubation prevented the H/R effect on ANG II responses. H/R significantly increased NOX2 mRNA expression in isolated arterioles. SOD activity was significantly decreased after H/R. Enhanced arteriolar responses after H/R occurred independently from the surrounding tissue, indicating no influence of tubules on vascular function in this model. The mechanism of increased ANG II response after H/R might be increased oxidative stress and increased calcium sensitivity of the contractile apparatus.

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BACKGROUND: Descending vasa recta (DVR) supply the inner part of outer renal medulla an area at risk for hypoxic damages. OBJECTIVE: We hypothesize increased vasoreactivity after hypoxia/re-oxygenation (H/R) in DVR, which might contribute to the reduced medullary perfusion after an ischemic event. METHODS: Live kidney slices (200µm) from SD rats were used for functional experiments. TUNEL assay and H&E staining were used to estimate slice viability. Kidney slices were treated with carbogen or hypoxia (1% O2) for 60 or 90 min and vasoreactivity to Ang II (10-7 M) was recorded by DIC microscopy after re-oxygenation with carbogen. Expression of NOS and NADPH enzymes mRNA were determined in iron-perfusion isolated VR. RESULTS: Percentage of apoptotic cells increased in control and H/R after 90 min in the medulla. Ang II- induced constriction of DVR was reduced after 90 min in control (compared to 60 min), but not after H/R. NOS enzymes mRNA expression levels decreased over 90 min hypoxia. CONCLUSIONS: Increased reactivity of DVR to Ang II after H/R compared to control (90 min) suggest a role of DVR in renal ischemia/reperfusion injury.

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This is a case report of fatal cardiomyopathy in a fetus following maternal intrauterine infection with herpes simplex virus (HSV), despite the mother having no symptoms of an infection. The fetus showed signs of a disseminated infection affecting the heart, brain, lungs, liver, adrenal glands, and skin. HSV cardiomyopathy, characterized by vast necrosis, extensive calcifications, and inflammatory infiltration, was found to be the cause of intrauterine fetal death. To our knowledge, this is a unique report of an asymptomatic maternal nonprimary or recurrent HSV infection that induced a transmission of HSV resulting in extensive and fatal changes in the fetal heart.

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