Doppler ultrasonography in high-risk pregnancies: systematic review with meta analysis cholesterol levels yogurt tricor 160 mg sale. Abnormal velocity waveforms of the umbilical artery in growth-retarded fetuses: relationship to low cholesterol foods diet plan discount tricor 160mg free shipping antepartum late heart rate decelerations and outcome cholesterol eggs per week cheap 160 mg tricor fast delivery. The relationship of fetal hypoxia in growth retardation to cholesterol levels mg/dl purchase tricor 160 mg overnight delivery the mean blood velocity in the fetal aorta. Blood flow velocity waveforms in the descending fetal aorta: comparison between normal and growth retarded pregnancies. The blood flow velocity waveformin the fetal descending aorta: its relationship to behavioural states in growth retarded fetus at 37?38 weeks of gestation. Cerebral and umbilical arterial blood flow velocity waveforms in normal and growth retarded pregnancies. The blood flow velocity waveformin the internal carotid artery: its relationship to behavioural states in growth retarded fetus at 37 38 weeks of gestation. Simultaneous assessment of blood flow velocity waveforms in uteroplacental vessels, umbilical artery, fetal aorta and common carotid artery. Doppler studies in the growth retarded fetus and prediction of neonatal necrotising enterocolitis, haemorrhage, and neonatal morbidity. Mean blood velocities and impedance in the fetal descending thoracic aorta and common carotid artery in normal pregnancy. Doppler measurements of fetal and uteroplacental circulations: relationship with umbilical venous blood gases measured at cordocentesis. Changes of pulsatility index from fetal vessels preceding the onset of late decelerations in growth-retarded fetuses. The effect of carbon dioxide on Doppler flow velocity waveforms in the human fetus. Prediction of fetal outcome in small for gestational age fetuses: comparison of Doppler measurements obtained from different fetal vessels. Potential for diagnosing imminent risk to appropriateand small for-gestational-age fetuses by Doppler sonographic examination of umbilical and cerebral arterial blood flow. Accuracy of the middle-cerebral-to-umbilical-artery resistance index ratios in the prediction of neonatal outcome in patients at high risk for fetal and neonatal complications. Doppler dynamics and their complex interrelation with fetal oxygen pressure, carbon dioxide pressure, and pH in growth-retarded fetuses. Blood flow velocity waveforms from peripheral pulmonary arteries in normally grown and growth-retarded fetuses. Splenic artery velocity waveforms in small for gestational age fetuses: relationship with pH and blood gases measured in umbilical blood at cordocentesis. The Doppler cerebroplacental ratio and perinatal outcome in intrauterine growth restriction. In third trimester fetuses the ratio in pulsatility index between the fetal descending thoracic aorta and the middle cerebral artery may be more useful. Doppler fetal circulation in pregnancies complicated by pre-eclampsia or delivery of a small for gestational age baby. Doppler echocardiographic assessment of atrioventricular velocity waveforms in normal and small for gestational age fetuses. Relationship between fetal cardiac and extra-cardiac Doppler flow velocity waveforms and neonatal outcome in intrauterine growth retardation. Doppler echocardiographic evaluation of time to peak velocity in the aorta and pulmonary artery of small for gestational age fetuses. Distribution and recirculation of umbilical and systemic venous blood flow in fetal lambs during hypoxia. Doppler ultrasound evaluation of ductus venosus blood flow during acute hypoxemia in fetal lambs. Umbilical flow distribution to the liver and the ductus venosus: an in vitro investigation of the fluid dynamic mechanism in the fetal sheep. Phasic blood flow patterns in the superior and inferior venae cavae and umbilical vein of fetal sheep. Ductus venosus agenesis prevents transmission of central venous pulsations to the umbilical vein in fetal sheep. Inferior vena cava flow velocity waveforms in appropriate and small for gestational age fetuses. Cardiotocogram compared to Doppler investigation of the fetal circulation in the premature growth-retarded fetus: longitudinal observations. Umbilical vein pulsations and acid base status at cordocentesis in growth retarded fetuses with absent end diastolic velocity in umbilical artery. Atrial natriuretic peptide levels in fetal blood in relation to inferior vena cava velocity waveforms. Demonstration of fetal coronary blood flow by Doppler ultrasound in relation to arterial and venous flow velocity waveforms and perinatal outcome. The development of abnormal heart rate patterns after absent end-diastolic velocity in umbilical artery: analysis of risk factors. Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation. Ductus venosus blood velocity and the umbilical circulation in the seriously growth-retarded fetus. Blood flow through the ductus venosus in singleton and multifetal pregnancies and in fetuses with intrauterine growth retardation. Fetal venous, intracardiac, and arterial blood flow measurements in intrauterine growth retardation: relationship with fetal blood gases. Arterial and venous Doppler velocimetry in the severely growth-restricted fetus and association with adverse perinatal outcome. The fetal central venous pressure waveform in normal pregnancy and in umbilical placental insufficiency. Abnormal fetal aortic velocity waveform and minor neurological dysfunction at 7 years of age. Abnormal fetal aortic velocity waveform and intellectual function at 7 years of age. Fetal cerebral Doppler studies as a predictor of perinatal outcome and subsequent neurologic handicap. Clinical management of the fetus with markedly diminished umbilical artery end-diastolic flow. Obstetrical characteristics of a loss of end-diastolic velocities in the fetal aorta and/or umbilical artery using Doppler ultrasound. A series of screening studies involving assessment of impedance to flow in the uterine arteries have examined the potential value of Doppler in identifying pregnancies at risk of the complications of impaired placentation (Figures 1?3). They measured impedance to flow in the arcuate arteries at 18?20 weeks of gestation and defined as an abnormal result a resistance index of more than 0. They reported that this test identified 64% of pregnancies that subsequently developed pregnancy-induced hypertension (Table 1). Figure 1: Insonation of the uterine artery at the crossover with the iliac artery. Figure 2: Normal flow velocity waveform from the Figure 3: Flow velocity waveform from the uterine uterine artery at 24 weeks of gestation. They measured impedance to flow in the arcuate arteries at 24 weeks of gestation and defined as an abnormal result a resistance index of more than 0. Doppler signals could not be obtained in 8% of women and these pregnancies were considered to have abnormal test results. This study also examined prediction of intrauterine growth restriction (birth weight below the 10th centile for gestation), which was found in 18% of the cases and the sensitivity and positive predictive values were 71% and 33%, respectively. They measured impedance to flow in the uterine arteries at 21?24 weeks of gestation and defined an abnormal result by a resistance index of more than 0. The prevalence of pre-eclampsia and/or intrauterine growth restriction was 18% and the sensitivity of increased impedance in the prediction of this complication was 56% (Table 1). Table 1: Screening for pregnancy-induced hypertension in high-risk pregnancies by measurement of impedance to flow in the arcuate or uterine arteries Arduini et al. The early studies were limited by the use of continuous wave Doppler, which is a blind investigation. However, recent studies have used color Doppler ultrasound to assess flow in the uterine artery at the point where it crosses the external iliac artery, which is a more reproducible examination.
Disseminated retarded maturation of the placenta was found in 66% of the cases with pathological umbilical artery flow velocity waveforms cholesterol in shrimp meat tricor 160 mg without a prescription, whereas it occurred only in 6% of the cases with normal flow 10 cholesterol medication reactions generic tricor 160mg otc. It was suggested that these findings are compatible with physiological circulatory alterations enhancing continued fetal growth until the late post-term period food cholesterol chart uk tricor 160mg otc. In a subsequent study cholesterol in eggs organic 160mg tricor otc, these authors examined 44 pregnancies at 42?43 weeks of gestation. Another similarity between the growth-restricted and the post-term fetus was highlighted by the study of Arduini et al. During oxygen treatment, nine fetuses exhibited a temporary 20% increase in the impedance to flow in the internal carotid artery and, in this group, there was a higher incidence of emergency Cesarean delivery due to fetal distress and more neonatal complications than in the other 36 fetuses that did not respond to maternal hyperoxygenation. Some studies reported that the pregnancies which subsequently developed fetal distress in labor were associated with antepartum evidence of increased impedance in the umbilical artery, decreased impedance in the fetal middle cerebral artery, and decreased blood flow velocity in the fetal aorta. Rightmire and Campbell examined 35 pregnancies at more than 42 weeks of gestation and reported that impedance to flow in the uterine and umbilical arteries did not change with gestation, but impedance in the umbilical artery was higher in fetuses with a worse clinical outcome 16. Blood flow velocity in the fetal descending aorta decreased with gestation and velocity was lower in fetuses who passed meconium before delivery. It was suggested that fetal compromise in prolonged pregnancy is more a fetal?placental problem than a uteroplacental problem 16. Pregnancies that subsequently developed signs of fetal distress during labor had increased impedance in the umbilical artery, decreased impedance in the fetal middle cerebral artery, and decreased time averaged velocity in the fetal aorta. It was concluded that, in uncomplicated post-term pregnancies, those with abnormal Doppler results are prone to need intervention following fetal distress in labor 17. Further evidence for centralization of the fetal circulation was provided by the study of Devine et al. In contrast, the sensitivities of oligohydramnios (amniotic fluid index of less than 5 cm), non-reactive fetal heart rate pattern, and a biophysical profile score equal to or less than 6, had sensitivities equal to or less than 40%18. In this group, compared to those with normal amniotic fluid and reactive fetal heart rate pattern, there was no significant difference in impedance to flow in the umbilical and uterine arteries, but impedance in the fetal internal cerebral artery was significantly lower 19. Normal placental and fetal Doppler Some studies suggested that the pathophysiology of placental insufficiency in post-term pregnancies differs from that observed in cases of fetal growth restriction at earlier gestational ages, because, in post-term pregnancies, both placental and fetal Doppler indices are normal. The majority of Doppler measurements in pregnancies with subsequent asphyxia or otherwise complicated fetal outcome were within the 95% prediction interval for patients with normal fetal outcome. This study also reported that, in the prediction of asphyxia, the sensitivity for oligohydramnios and antepartum cardiotocography was less than 20%. They measured impedance to flow in the umbilical arteries and the fetal middle cerebral and renal arteries. In 15 pregnancies, there was oligohydramnios and, although in this group the mean birth weight was significantly lower than in the 42 pregnancies with normal amniotic fluid, there were no significant differences between the groups in the Doppler indices. It was concluded that, in post-term pregnancies, oligohydramnios is not associated with a major redistribution in the fetal circulation. Prolonged pregnancy: evaluating gestation-specific risks of fetal and infant mortality. The role of ultrasound assessment of amniotic fluid volume in the management of the postdate pregnancy. Central and peripheral haemodynamic changes in post-term fetuses: correlation with oligohydramnios and abnormal fetal heart rate pattern. Histologic placenta findings in prolonged pregnancy: correlation of placental retarded maturation, fetal outcome and Doppler sonographic findings in the umbilical artery. Fetal and uteroplacental circulatory changes in pregnancies proceeding beyond 43 weeks. Association between a low umbilical artery pulsatility index and fetal distress in labor in very prolonged pregnancies. Doppler assessment of fetal blood flow velocity waveforms during acute maternal oxygen administration as predictor of fetal outcome in post-term pregnancy. Doppler evaluation of umbilical and uterinearcuate arteries in the postdates pregnancy. Doppler sonography of the umbilical artery, mode of delivery and perinatal morbidity in prolonged pregnancy. Post-term pregnancies with normal cardiotocographs and amniotic fluid columns: the role of Doppler evaluation in predicting perinatal outcome. Cerebral, umbilical, and uterine resistance using Doppler velocimetry in postterm pregnancy. Doppler flow velocimetry of the umbilical artery, uteroplacental arteries and fetal middle cerebral artery in prolonged pregnancy. In monozygotic pregnancies, splitting of the single embryonic mass into two within 3 days of fertilization, which occurs in one-third of cases, results in dichorionic twins. When embryonic splitting occurs after the 3rd day following fertilization, there are vascular communications within the two placental circulations (monochorionic). Embryonic splitting after the 9th day following fertilization results in monoamniotic monochorionic twins, and splitting after the 12th day results in conjoined twins. Determination of chorionicity can be performed reliably by ultrasound examination at 11?14 weeks of gestation (Figure 1); in dichorionic twins, there is an extension of placental tissue into the base of the intertwin membrane (lambda sign) 1,2. Figure 1: Ultrasound appearance of monochorionic (left) and dichorionic (right) twin pregnancies at 12 weeks of gestation. In both types, there appears to be a single placental mass but, in the dichorionic type, there is an extension of placental tissue into the base of the intertwin membrane, forming the lambda sign. This increased loss in monochorionic pregnancies is likely to be the consequence of severe early-onset twin-to-twin transfusion syndrome. The perinatal mortality rate in twins is around six times higher than in singletons, and is about three to four times higher in monochorionic compared to dichorionic twins, regardless of zygosity 4,5. In monochorionic twins, the incidence is about 9% and in dichorionic twins it is about 5% 3. In monochorionic twins, an additional complication to prematurity is twin-to-twin transfusion syndrome. In twin pregnancies, the risk of delivering growth-restricted babies is about ten times higher than in singleton pregnancies 6. In a study of 467 twin pregnancies, the chance of growth restriction (birth weight below the 5th centile for gestation in singletons) of at least one of the fetuses was 34% for monochorionic and 23% for dichorionic twins 3. Furthermore, the chance of growth restriction of both twins was about four times as high in monochorionic (7. In monochorionic twins, a disparity in size between the fetuses may be a consequence of the degree of imbalance in fetal nutrition as a result of chronic twin-to-twin transfusion syndrome. In dichorionic twins, disparity in size may also be due to differences in fetal nutrition, but in this case such differences may be a consequence of discordancy in the effectiveness of trophoblastic invasion of the maternal spiral arteries and therefore placental function. Twin-to-twin transfusion syndrome In monochorionic twin pregnancies, there are placental vascular anastamoses which allow communication of the two fetoplacental circulations 7. In about 25% of pregnancies, imbalance in the net flow of blood across the placental vascular arteriovenous communications from one fetus, the donor, to the other, the recipient, results in twin-to-twin transfusion syndrome; in about half of these cases, there is severe twin-to-twin transfusion syndrome presenting as acute polyhydramnios in the second trimester. The pathognomonic features of severe twin-to-twin transfusion syndrome by ultrasonographic examination are the presence of a large bladder in the polyuric recipient fetus in the polyhydramniotic sac and absent bladder in the anuric donor, that is found to be stuck and immobile at the edge of the placenta or the uterine wall, where it is held fixed by the collapsed membranes of the anhydramniotic sac (Figure 2) 8. Other sonographic findings that may prove to be of prognostic significance include the presence of a hypertrophic, dilated and dyskinetic heart, with absence or reversal of flow in the ductus venosus during atrial contraction (Figure 3) 9. In the donor, the heart may be dilated, the bowel is hyperechogenic, and there is absent end-diastolic flow in the umbilical artery; these features are commonly seen in hypoxemic fetuses in pregnancies with severe uteroplacental insufficiency. In severe twin-to-twin transfusion syndrome, survival with expectant management is less than 10% 8. In the polyuric recipient, there is a large bladder and polyhydramnios (left) and the anuric donor is held fixed to the placenta by the collapsed membranes of the anhydramniotic sac (right). Figure 3: Abnormal waveform of the ductus venosus with reversal of flow during atrial contraction in the recipient fetus of a pregnancy with twin-to-twin transfusion syndrome. The precise underlying mechanisms by which a select population of those monochorionic pregnancies with vascular communications go on to develop twin-to-twin transfusion syndrome is not fully understood. However, it has been hypothesized that primary maldevelopment of the placenta of the donor twin may cause increased peripheral resistance in the placental circulation, which promotes shunting of blood to the recipient; the donor therefore suffers from both hypovolemia due to blood loss and hypoxia due to placental insufficiency8. The recipient fetus compensates for its expanded blood volume with polyuria 10, but, since protein and cellular components remain in its circulation, the consequent increase in colloid oncotic pressure draws water from the maternal compartment across the placenta. A vicious cycle of hypervolemia, polyuria, hyperosmolality is established, leading to high-output heart failure and polyhydramnios.
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