http://hdl.handle.net/1956/952 Search the Channel search http://bora.uib.no/simple-search http://hdl.handle.net/1956/2392 Title: Portal and umbilical venous distribution in the human fetus : a longitudinal ultrasound study <br/> <br/>Authors: Kessler, Jörg <br/> <br/>Abstract: Knowledge of the venous perfusion of the human fetal liver is fragmentary and mainly limited to the umbilical circulation. Current ultrasound technology makes it possible to study blood flow noninvasively and to give new insights into the developmental changes during gestation. AIMS: The general aim of the study was to map the hemodynamics of the venous supply to the fetal liver in humans. In detail: to establish longitudinal reference ranges for ductus venosus flow velocities and waveform indices (paper I), to establish a technique for direct flow measurement in the main portal stem and study its development during the second half of pregnancy (paper II), to assess the flow velocity pattern in the left portal vein (paper III), and to determine the distribution of venous blood supply within the liver and explore the impact of maternal and fetal factors (paper IV). MATERIAL AND METHODS: After informed written consent, 160 women with low-risk pregnancies were recruited to a longitudinal study according to a protocol approved by the Regional Committee for Research Ethics (REK-Vest 04/3837). 4-5 ultrasound examinations, each lasting 60 minutes, were done at four weeks intervals between 20 and 40 weeks of gestation. At each session the inner diameter was measured in: 1. the intraabdominal portion of the umbilical vein, 2. the ductus venosus, 3. the main portal stem, and 4. the left portal vein. In the same vessels, time-averaged maximum flow velocties were measured by Doppler ultrasound. Volume blood flow was calculated and normalised for fetal weight. Mean and percentile curves were constructed using regression analysis and multi-level modelling. The impact of maternal and fetal factors on liver blood flow was investigated by deviance statistics. RESULTS: The established longitudinal reference ranges for ductus venosus flow velocities and waveform indices allow the calculation of conditional percentiles, which are narrower and commonly shifted compared to those of the entire population (Paper I). Blood flow in the main portal stem was pulsatile in 99%. Both diameter and flow velocities doubled during the observation period. Correspondingly, blood flow increased throughout gestation, and so did flow, normalised for fetal weight (Paper II). Flow velocities in the left portal branch increased throughout gestation. We found pulsatile flow in 69%, usually directed towards the right lobe. However, intermittent flow reversal occurred during respiratory movements, and continuous reversal in 8% of the observations close to term (Paper III). Total venous liver flow increased throughout gestation, while normalised flow decreased. Lobe specific flow distribution was stable during gestation directing 60% of the total venous liver flow to the left and 40% to the right lobe. The umbilical vein was the dominating venous blood source, but the portal fraction grew during the last trimester. Venous liver flow and its components were related to birthweight, while lobe specific flow and fractional flow distribution to the lobes were related to pregnancy weight gain (Paper IV). CONCLUSION: We have established longitudinal reference ranges for all components of venous liver supply and the ductus venosus in the human fetus. The reference ranges for ductus venosus velocimetry are appropriate for serial measurements, especially when conditional terms are applied (Paper I). The present established technique of assessing flow in the main portal stem had a high success rate and could be used to show an increasing hemodynamic importance of the main portal stem towards term (Paper II). The umbilico-portal watershed is usually situated in the right liver lobe, but may shift towards the left portal vein even in circulatory uncompromised fetuses. The time-averaged maximum flow velocity is suggested for the evaluation of the umbilico-portal watershed (Paper III). The relationship between venous liver flow and birth weight may indicate a link between liver perfusion and fetal growth. The growing portal fraction of the total venous blood flow signifies the high circulatory priority given to the splanchnic circulation close to term. The relationship between low pregnancy weight gain and the distributional shift in favour of left liver lobe perfusion may be part of an adaptation to various intrauterine environments (Paper IV). Mon, 25 Jun 2007 22:58:59 GMT http://hdl.handle.net/1956/1914 Title: The effects of smoking and hypertensive disorders on fetal growth <br/> <br/>Authors: Rasmussen, Svein; Irgens, Lorentz M. <br/> <br/>Abstract: Background: It is well known that smoking and pregnancy induced hypertension (PIH) are associated with decreased fetal growth. It has been reported that in preeclampsia the fetal growth deficit attributable to smoking is higher, which has been contradicted in other studies. We therefore evaluated the effects on fetal growth of early- and late onset PIH and chronic hypertension and how cigarette smoking modify these effects. We also quantified the proportion of small for gestational age (SGA) cases attributable to PIH, chronic hypertension, and smoking. Methods: Population-based study based on record of 215598 singleton pregnancies from the Medical Birth Registry of Norway. Results: In severe preeclampsia, mild preeclampsia, transient hypertension, and normotension in term birth, odds ratios (ORs) of SGA in smokers compared with non-smokers were 1.4 (95% confidence interval 0.9, 2.2), 1.6 (1.3, 1.9), 2.3 (1.8, 3.1), and 2.0 (1.9, 2.1), respectively. For preterm births, corresponding ORs were 1.3 (0.9, 2.0), 1.8 (1.1, 3.0), 4.1 (1.9, 9.0), and 1.7 (1.4, 2.0), respectively. The effect of early onset PIH was stronger than that in term births, while the effect of smoking was equal in preterm and term newborns. Only in non-smokers who delivered at term, the rates of SGA significantly increased with the severity of PIH (ORs = 1.3 (1.1, 1.5), 1.8 (1.7, 2.0), and 2.5 (2.2, 3.0) for transient hypertension, mild-, and severe preeclampsia, respectively). The combined effects of smoking and hypertension were generally not synergistic. The effect of smoking was not stronger in women who had chronic hypertension. Nor were the effects of chronic hypertension stronger in smokers. PIH explained 21.9 and 2.5% of preterm and term cases of SGA, respectively, while smoking explained 12% of SGA cases. Conclusion: The effects of hypertensive disorder and smoking were generally not synergistic, which suggest that they may exert their main actions on separate sites or work through separate mechanisms within or outside the placenta. If smoking were eliminated in pregnant women, the number of SGA cases would be reduced by 12%. Thu, 20 Apr 2006 22:58:59 GMT