RESUMO
BACKGROUND: The classic mid-trimester preterm premature rupture of membranes (PPROM) is defined as a rupture of the fetal membranes prior to 28 weeks of gestation (WG) with oligo/anhydramnion; it complicates approximately 0.4-0.7% of all pregnancies and is associated with very high neonatal mortality and morbidity. Antibiotics have limited success to prevent bacterial growth, chorioamnionitis and fetal inflammation. The repetitive amnioinfusion does not work because fluid is lost immediately after the intervention. The continuous amnioinfusion through the transabdominal port system or catheter in patients with classic PPROM shows promise by flushing out the bacteria and inflammatory components from the amniotic cavity, replacing amniotic fluid and thus prolonging the PPROM-to-delivery interval. OBJECTIVE: This multicenter trial aims to test the effect of continuous amnioinfusion on the neonatal survival without the typical major morbidities, such as severe bronchopulmonary dysplasia, intraventricular hemorrhage, cystic periventricular leukomalacia and necrotizing enterocolitis one year after the delivery. STUDY DESIGN: We plan to conduct a randomized multicenter trial with a two-arm parallel design. Randomization will be between 22/0 and 26/0 SSW. The control group: PPROM patients between 20/0 and 26/0 WG who will be treated with antibiotics and corticosteroids (from 22/0 SSW) in accordance with the guidelines of German Society of Obstetrics and Gynecology (standard PPROM therapy). In the interventional group, the standard PPROM therapy will be complemented with the Amnion Flush Method, with the amnioinfusion of Amnion Flush Solution through the intra-amnial catheter (up to 100 mL/h, 2400 mL/day). SUBJECTS: The study will include 68 patients with classic PPROM between 20/0 and 26/0 WG. TRIAL-REGISTRATION: ClinicalTrials.gov ID: NCT04696003. GERMAN CLINICAL TRIALS REGISTER: DRKS00024503, January 2021.
RESUMO
AIM: We used positron emission tomography (PET) with radioactive glucose (F-18-Fluor-Deoxglucose [FDG]) to investigate whether acute maternal hypoxemia causes alterations of glucose uptake of fetal organs and the placenta. MATERIAL AND METHODS: Investigation was performed under normal conditions and acute hypoxemia in 16 fetal sheep between 108 and 130 days of gestation. Maternal sheep were ventilated with 1.0-1.5% isoflurane/O(2) /N(2) O during whole scanning procedure. Acute hypoxia was induced by reducing O(2) in a ventilated gas mixture to achieve maternal arterial O(2) saturation at a constant level of about 75% baseline. Doppler ultrasound blood flow measurements were performed in the ductus venosus (DV), umbilical artery (UA) and vein (UV). Fetal blood samples were taken by cordocentesis of UV. Dynamic positron emission tomography combined with computed tomography (PET-CT) scans of fetuses were acquired over 60 min after intravenous injection of 300 MBq FDG in the mother. Relative FDG uptake in the fetal brain, heart, and liver was determined on summed images from 40-60 min using manually defined volumes of interest (VOI) normalized to mean FDG uptake in placentomes. RESULTS: Placental blood perfusion reduced significantly from 416.5 ± 116.4 mL/min to 253.5 ± 170.5 mL/min (mean ± SD) during hypoxia. Placental blood supply to the liver decreased from 79.5 ± 14% to 41.1% (P = 0.0001), while DV/UV ratio increased. FDG uptake of the placenta was not changed during hypoxia. Relative FDG uptake in the fetal heart was strongly increased under hypoxia (P = 0.019), whereas it did not differ in the fetal brain and liver. CONCLUSION: Fetal hypoxia is associated with decreased placental perfusion and liver blood supply. However, glucose uptake was not significantly decreased in the placenta and liver.
