Abnormal fetal pulmonary venous blood flow velocity waveforms in the presence of complete transposition of the great arteries.
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Biomedical subjects
Publications and source records attributed to G Rizzo.
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The objective of this study was to assess the value of Doppler indices calculated from the inferior vena cava and ductus venosus in the identification of acidemia and hypoxemia as determined by pH and gas analysis of fetal blood obtained by cordocentesis in growth-retarded fetuses. Doppler measurements were performed in the inferior vena cava and ductus venosus in 209 normally grown fetuses and in 89 growth-retarded fetuses. All growth-retarded fetuses were free from structural and chromosomal abnormalities, and uteroplacental insufficiency characterized by Doppler changes in the umbilical and middle cerebral arteries was the most likely etiology of the growth defect. In this group of fetuses, Doppler recordings were performed immediately before cordocentesis. Ten different indices were calculated from venous velocity waveforms, and reference limits for gestation were constructed by the cross-sectional analysis of data from normally grown fetuses. Logistic regression and receiver operator characteristic curve analysis were performed to examine the relationship between Doppler indices and acid-base status. The pre-load index (peak velocity during atrial contraction/peak velocity during systole) in the inferior vena cava was the best explanatory variable for acidemia (chi 2 = 48.33; p < or = 0.001). Hypoxemia was predicted less well by venous indices and the best results were achieved by the S/A ratio in the ductus venosus (chi 2 = 9.46; p < or = 0.005). In conclusion, our data suggest that acidosis in growth-retarded fetuses may be non-invasively identified by Doppler measurements of the inferior vena cava and that a higher efficiency can be achieved by the use of the pre-load index.
The objective of this study was to describe blood flow velocity waveforms of fetal peripheral pulmonary arteries in normally grown and growth-retarded fetuses. Doppler studies were performed in 182 normally grown fetuses (gestational age 18-40 weeks) and in 61 growth-retarded fetuses (gestational age 24-36 weeks) that were free from structural and chromosomal abnormalities and whose umbilical and middle cerebral artery Doppler findings suggested uteroplacental insufficiency as the most likely etiology of the growth defect. The pulsatility index was used to quantify the velocity waveforms. Successful recordings were obtained in 90.1% of the normally grown and 93.4% of the growth-retarded fetuses. In normally grown fetuses the pulsatility index values significantly decreased with advancing gestation. In growth-retarded fetuses the pulsatility index values were significantly elevated compared to those of normal fetuses. A significant relationship was observed between the severity of hypoxia and pulsatility index values from the peripheral pulmonary arteries in 29 fetuses in which Doppler recordings were obtained immediately before cordocentesis. In conclusion, these data show that in normal fetuses the Doppler-measured impedance to flow in the peripheral pulmonary circulation decreases with advancing gestation. Impedance to flow in the lungs is elevated in the presence of growth retardation and this increase is related to the severity of fetal hypoxia.
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OBJECTIVE: The purpose of this study was to evaluate whether cordocentesis is associated with the release of vasoactive substances and whether there are differences between normally grown and growth-restricted fetuses. STUDY DESIGN: 6-Keto-prostaglandin F1 alpha (the stable metabolite of prostacyclin), endothelin-1, and cyclic guanosine monophosphate were measured in fetal blood at the beginning and closing of cordocentesis in 30 normally grown fetuses and 25 growth-restricted fetuses. This latter group was characterized by abnormal Doppler index values in umbilical artery and middle cerebral artery, suggestive of chronic hypoxemia as the causative factor of the impaired growth. In six growth-restricted fetuses bradycardia occurred at the end of the procedure. Umbilical artery pulsatility index was measured by Doppler ultrasonography immediately before and after the procedure. RESULTS: The median interval between the two blood samples obtained by cordocentesis was 90 seconds (range 60 to 320 seconds). During this interval a significant rise of 6-keto-prostaglandin F1 alpha (p < or = 0.0001) and endothelin-1 (p = 0.03) was evidenced in normally grown fetuses. The increase in 6-keto-prostaglandin F1 alpha was significantly related (r = 0.52, p = 0.002) to the fall of umbilical artery pulsatility index occurring after the procedure. In growth-restricted fetuses cordocentesis induced a marked increase of endothelin-1 (p = 0.0002), which was significantly related to the severity of acidosis (r = 0.52, p = 0.018), whereas no modifications were evidenced for the other agents tested. The increase of endothelin-1 was higher in those growth-restricted fetuses showing bradycardia at the end of the procedure than in growth-restricted fetuses that did not (p = 0.04). The variations of the vasoactive substances assayed were not significantly related to the type of procedure (transamniotic or transplacental), the amount of blood aspirated during the procedure, the interval elapsing between the first and second samples, the gestational age at which the procedure was performed, and the degree of fetal smallness. CONCLUSION: Cordocentesis induces the rapid release of vasoactive substances and the effect differs between normally grown and growth-restricted fetuses. This may explain the different hemodynamic response and the higher rate of complications occurring in the latter group after cordocentesis.
This study was performed to investigate whether fetal blood sampling and/or transplacental puncture are associated with changes of blood flow velocity waveforms in umbilical artery and fetal circulation. The pulsatility index (PI) was measured from umbilical artery, thoracic descending aorta, renal artery, and middle cerebral artery immediately before and after fetal blood sampling (n = 28) or third trimester amniocentesis (n = 32). No significant changes in PI values were evidenced after amniocentesis performed either transamniotically (n = 21) or transplacentally (n = 11). Fetal blood sampling induced a significant decrease of PI values in all the vessels investigated. However, in presence of a transplacental procedure (n = 15) the amplitude of the decrease of PI in umbilical artery was significantly higher than after a transamniotic procedure (n = 13), while no differences were evidenced in the other vessels tested. These findings indicate that umbilical cord puncture at the time of fetal blood sampling is associated with a decrease in PI in umbilical artery and several peripheral arterial vessels. The isolated placental puncture does not induce Doppler-detectable hemodynamic effects, while in conjunction with cord needling, it increases the amplitude of the effects in umbilical artery.
The objective of this study was to evaluate the effect of fetal blood sampling on atrioventricular blood flow velocity waveforms. Flow velocity waveforms were measured from mitral and tricuspid valve immediately before and after fetal blood sampling in 25 normally grown and 10 growth-retarded fetuses. This latter group was characterized by abnormal Doppler indices in umbilical artery and middle cerebral artery suggestive of uteroplacental insufficiency as the causative factor of the impaired growth. The flow velocity parameters studied were peak velocity during early and active ventricular filling, time velocity integral, and fetal heart rate. Different indices were then calculated as expressions of ventricular diastolic function and cardiac output. In normally grown fetuses, both peak velocity during early diastole and time velocity integral values significantly increased after fetal blood sampling from both atrioventricular valves, whereas no significant changes were evidenced in the other parameters considered. Gestational age at the time of the procedure was positively related to the amplitude of these changes. In growth-retarded fetuses, fetal blood sampling induced a significant decrease in time velocity integral value form tricuspid valve, suggestive of a fall in right ventricle output. The amplitude of the decrease was significantly related to the severity of acidosis in umbilical vein. In conclusion, the cardiac hemodynamic response to fetal blood sampling differs between normally grown and growth-retarded fetuses. This difference may explain the higher rate of complications occurring in the latter group of fetuses after blood sampling.
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The objective of this study was to analyze the effects of cordocentesis on velocity waveforms recorded from the inferior vena cava and to evaluate differences, if any, in the hemodynamic response between normally grown and growth-retarded fetuses. Twenty-five normally grown fetuses and 20 growth-retarded fetuses were considered for this study. This latter group was characterized by abnormal Doppler indices in the umbilical artery and the middle cerebral artery suggestive of uteroplacental insufficiency as the causative factor of the impaired growth. Flow velocity waveforms were measured from the inferior vena cava immediately before and after cordocentesis and the % reverse flow during atrial contraction calculated. In normally grown fetuses the % reverse flow values did not vary significantly after cordocentesis, while in growth-retarded fetuses this index increased significantly after the procedure (p < or = 0.001). Furthermore, the amplitude of this increase was inversely related to pH levels in umbilical vein (p = 0.004). In conclusion, in growth-retarded fetuses cordocentesis induces an increase of % reverse flow in the inferior vena cava, while no modifications occur in normally grown fetuses. This suggests the presence in growth-retarded fetuses of an impaired cardiac adaptive mechanism to cordocentesis that may explain the higher incidence of complications occurring in such fetuses.
Flow velocity waveforms were recorded by Doppler ultrasonography from the uterine arteries, umbilical artery, thoracic descending aorta, renal artery and middle cerebral artery in fetuses of 57 pregnancies complicated by preterm labor with intact membranes. The uterine artery resistance index was significantly increased in patients with preterm labor when compared to reference limits for gestation, but no relationship was found with the time interval between Doppler recordings and delivery. The group of fetuses (n = 15) delivered within 48 h from entry to the study showed significantly reduced pulsatility index values from the middle cerebral artery when compared to fetuses delivered later or to the normal reference limits for gestation. No significant differences were found in the other vessels studied. In conclusion preterm delivery is associated with alterations in fetal cerebral waveforms and knowledge of these changes may prove useful in the evaluation of patients with preterm labor.
Objective of this study was to establish the relationship in growth retarded fetuses between acid-base status in fetal blood obtained by cordocentesis and time interval between blood sampling and occurrence of antepartum heart rate late decelerations. Eighteen growth retarded fetuses scheduled for cordocentesis were considered for this study. All fetuses were free from structural and chromosomal abnormalities, characterized by absent end diastolic velocity waveforms in umbilical artery and later delivered for the development of antepartum heart rate late decelerations. Regression analysis showed that the time interval between cordocentesis and delivery was significantly related to pO2 (r = 0.46; p < or = 0.05) and pH (r = 0.57; p < or = 0.01) delta values but not with pCO2 values. Stepwise multiple regression analysis demonstrated that the severity of fetal acidosis significantly and independently predicted the length of this time interval even after controlling for confounding variables such as pO2 values, gestational age, presence of hypertension, or umbilical vein pulsations. The knowledge of this relationship may be useful in the clinical management of growth retarded fetuses.
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Integration of multi-modal biomedical images of the heart (PET, SPET, MRI, Echocardiography) is a diagnostic procedure of increasing interest. Different registration techniques can be used to spatially correlate two independent tomographic scans of the same patient, each technique presenting relative merits and limitations. Integration of cardiac with respect to neurological images is difficult, because the heart is a non-rigid and moving organ. The experiences of this approach of integrated diagnosis are thus limited to date. However, registration of PET, SPET, MRI, Echocardiographic images has been described with accuracy considered acceptable for clinical applications. Registration techniques for the integration of multi-modal biomedical images of the heart, the clinical applications of cardiac image fusion and the experiences reported in the literature are presented in this paper.
The authors report their experience in three cases of Fournier's disease, observed in recent years. It has made them suspect a disease relapse may always be possible. After having thoroughly gone into this matter, they delved into some aetiologie, clinical and therapeutic notes. They found out the necessity of an early diagnosis increases the possibilities of success upon this dangerous necrotic inflammation, because it has, nowadays, a high death-rate. Finally, they remark on the advantage of the collagen aetherologous to guide and speed up the process of cicatrization of the wound.
Fetal intrauterine behaviour is not a stable situation but a continuous alternation of states characterized by significant changes in fetal motility, heart rate, hemodynamics, metabolism and response to stimulation. Associations between fetal heart rate patterns and movements occur from 26-28 weeks of gestation onwards. As fetuses grow older these variables become gradually more related temporally and clustered in behavioural states similar to those present in newborns. This article describes the technique of recording and analyzing fetal behaviour, its development in normal pregnancy and its influence on different physiological parameters that are assessed in clinical practice. Furthermore the deviations from the norm occurring in compromised fetuses are described.
The objectives of this study were (1) to detect vasoactive intestinal polypeptide in fetal blood obtained by cordocentesis (2) to examine possible changes in growth retarded fetuses and to establish relationships between its levels and fetal blood acid-base status as well as fetal haemodynamics as assessed by Doppler ultrasonography. Vasoactive intestinal polypeptide was measured in umbilical vein blood obtained at cordocentesis in 12 growth retarded fetuses and in 13 control fetuses. Umbilical vein pH and PO2 values were determined in all the cases. Before the procedure, Doppler indices were calculated from umbilical artery, middle cerebral artery, renal artery, cardiac outflow tracts and inferior vena cava. Simple and multiple stepwise regression analysis were performed to examine the relationships between Doppler indices, acid-base status and vasoactive intestinal polypeptide levels. In control fetuses, vasoactive intestinal polypeptide was always detectable in cord blood and its levels did not change with gestational age. In growth retarded fetuses, vasoactive intestinal polypeptide levels were higher and significantly related to umbilical vein PO2 levels, Pulsatility Index in umbilical artery, middle cerebral artery and renal artery, while no relationship was found with umbilical vein pH, cardiac and venous Doppler indices. Stepwise multiple regression demonstrated middle cerebral artery Pulsatility Index to be the best explanatory variable for vasoactive intestinal polypeptide levels. In conclusion, vasoactive intestinal polypeptide blood levels are increased in growth retarded fetuses and this increase is inversely related to the Doppler measured impedance to flow in middle cerebral artery.