Fetal Cerebral Circulation Research Articles

OC253: Three‐dimensional power Doppler analysis of cerebral circulation in normal and growth‐restricted fetuses

To evaluate the fetal cerebral circulation by using three-dimensional (3D) power Doppler ultrasound in normal and growth-restricted fetuses. In total, 125 singleton pregnancies were studied. One hundred of them were in normal healthy pregnant women with normally grown fetuses between 17 and 40 weeks of gestation. Their data were used to construct normal ranges throughout pregnancy. They were compared with the other 25 pregnant women who had fetal growth restriction (FGR) with Doppler-defined placental insufficiency. 3D power Doppler ultrasound and quantitative 3D histogram analyses were used to assess fetal cerebral 3D vascular indices: vascularization index (VI), flow index (FI) and vascularization–flow index (VFI). Both FI and VFI correlated positively with gestational age while VI remained stable throughout pregnancy. All the 3D vascular indices were higher in fetuses with FGR than in the control group. The proportion of fetuses detected as having hemodynamic redistribution was much higher when using 3D power Doppler indices than by means of the MCA-PI (52% vs. 20%; P = 0.002). There were nine cases (36%) of oligohydramnios. While all of them had hemodynamic redistribution according to the 3D power Doppler indices, only five cases were diagnosed with this according to MCA-PI measurements (P = 0.04). Cerebral blood flow increases with gestation. All the fetal cerebral 3D vascular indices are increased in fetuses with FGR and they are more sensitive than MCA measurements in detecting fetal hemodynamic redistribution.

Hypoxic regulation of the fetal cerebral circulation

Fetal cerebrovascular responses to acute hypoxia are fundamentally different from those observed in the adult cerebral circulation. The magnitude of hypoxic vasodilatation in the fetal brain increases with postnatal age although fetal cerebrovascular responses to acute hypoxia can be complicated by age-dependent depressions of blood pressure and ventilation. Acute hypoxia promotes adenosine release, which depresses fetal cerebral oxygen consumption through action of adenosine on neuronal A1 receptors and vasodilatation through activation of A2 receptors on cerebral arteries. The vascular effect of adenosine can account for approximately half the vasodilatation observed in response to hypoxia. Hypoxia-induced release of nitric oxide and opioids can account for much of the adenosine-independent cerebral vasodilatation observed in response to hypoxia in the fetus. Direct effects of hypoxia on cerebral arteries account for the remaining fraction, although the vascular endothelium contributes relatively little to hypoxic vasodilatation in the immature cerebral circulation. In contrast to acute hypoxia, fetal cerebral blood flow tends to normalize during acclimatization to chronic hypoxia even though cardiac output is depressed. However, uncompensated chronic hypoxia in the fetus can produce significant changes in brain structure and function, alteration of respiratory drive and fluid balance, and increased incidence of intracranial hemorrhage and periventricular leukomalacia. At the level of the fetal cerebral arteries, chronic hypoxia increases protein content and depresses norepinephrine release, contractility, and receptor densities associated with contraction but also attenuates endothelial vasodilator capacity and decreases the ability of ATP-sensitive and calcium-sensitive potassium channels to promote vasorelaxation. Overall, fetal cerebrovascular adaptations to chronic hypoxia appear prioritized to conserve energy while preserving basic contractility. Many gaps remain in our understanding of how the effects of acute and chronic hypoxia are mediated in fetal cerebral arteries, but studies of adult cerebral arteries have produced many powerful pharmacological and molecular tools that are simply awaiting application in studies of fetal cerebral artery responses to hypoxia.

Acute changes of cerebral venous blood flow in growth-restricted human fetuses in response to uterine contractions.

The fetal cerebral venous circulation during acute hypoxic stress provoked by uterine contractions has not been studied previously. The aim of this study was to explore the cerebral venous circulation during an oxytocin challenge test (OCT) in intrauterine growth-restricted (IUGR) fetuses. Doppler recordings of blood flow in the vein of Galen (GV), straight sinus (SS) and transverse sinus (TS) before and during uterine contractions and relaxation were obtained at the same time as electronic fetal heart rate (FHR) monitoring in 44 term IUGR fetuses. The OCT was classified as negative (normal FHR) or positive (late FHR decelerations). Non-parametric statistics were used to test differences between OCT groups. In OCT-negative cases (n = 39), de novo pulsations occurred in the GV, and SS flow velocities increased during contractions compared with basal measurements. There were no significant differences in TS flow. Flow recordings were less often obtained from OCT-positive cases (n = 5), making comparisons with OCT-negative cases uncertain. In uncompromised IUGR fetuses an acute cerebral venous hyperperfusion develops in response to uterine contractions. Pulsations in the GV are detected but are unlikely to be an ominous sign in this situation. The more centrally located TS was less discriminating for acute cerebral venous blood flow changes.

P242: Assessment of fetal cerebral arterial and venous blood flow before and after birth according to type of delivery

Objective: To determine whether antenatal steroids administration alter the Doppler flow indices of the umbilical, middle cerebral and uterine arteries and to determine the exact time that antenatal steroid administration affects the biophysical profile in fetuses. Methods: A prospective study was conducted in 20 fetuses between 26 and 34 weeks’ menstrual age at risk of preterm delivery. Two intramuscular injections of 12 mg of betamethasone were given to the mother 24 hours apart. The Doppler examination included the assessment of the pulsatility index of the umbilical artery (UA PI), the middle cerebral artery (MCA PI) and the pulsatility index of uterine arteries (Ut PI) before treatment, and 24, 48 and 72 hours after the first dose of betamethasone. All fetuses underwent biophysical profile testing prior to and on 24, 48 and 72 hours after steroid administration. We compared the percentage of fetuses with biophysical profile parameters present for each of the five components of the BP using statistical methods where appropriate. Neonatal outcome, including Apgar score, menstrual age at delivery, admission to and length of stay in the neonatal intensive care unit and mortality were analysed in all subjects. Results: The mean delivery time was 32.4 (27–36 weeks). There was a statistically significant difference in the frequency of the following findings in the precompared to post-steroid measurements: absence of body movements, non-reassuring fetal heart rate tracings, and absence of breathing movements. Initially none of the biophysical profile score was < or =8 whereas at 24, 48, and 72 hrs 10, 40 and 50% of them were respectively < or =8. No significant variation was noted in both the fetal and maternal Doppler velocimetry indices. Conclusion: Biophysical profile scores were decreased in more than 40% of fetuses within 48 hours of antenatal steroid administration, but neonatal outcome was not affected. On the contrary, Doppler velocimetry of the umbilical and fetal cerebral circulation appears to be reliable for the assessment of fetuses previously exposed to antenatal steroids. It seems that Doppler studies have the potential to differentiate the steroid induced changes in fetal biophysical profile from those due to fetal compromise.

OC130: Computer analysis of three-dimensional power angiography images of fetal cerebral, lung and placental circulation in normal and high-risk pregnancy

OC130: Computer analysis of three-dimensional power angiography images of fetal cerebral, lung and placental circulation in normal and high-risk pregnancy

Changes in fetal blood flow in hypoxemia during labor

Objective: The aim of this study was evaluation of intrapartum Doppler velocimetry changes in fetuses with signs of fetal hypoxemia in fetal pulse oximetry (arterial hemoglobin saturation &lt;30%).Study design: Examinations were performed on 44 women in labor with singleton pregnancies. The subject of analysis was Doppler blood flow velocimetry in umbilical cord, fetal brain and lung. In all cases the following examinations were performed: blood flow velocimetry in middle cerebral artery (MCA), umbilical artery (UA), and pulmonary vein (PV). Among fetuses with normal Doppler velocimetry at the time of admission, we selected those with cephalic presentation and non‐reassuring fetal heart rate pattern during labor. The fetuses were included to the group of fetal pulse oximetry monitoring. All cases with signs of fetal distress in ctg and intrapartum fetal arterial oxygen saturation &lt;30% for at least 5 min were included to the study group. Fetuses with abnormal ctg and fetal oxygen saturation &gt;30% constituted the control group.Results: Doppler indices (PI, RI) in MCA were significantly lower in the presence of reduced oxygen saturation. Pulsatility and resistance index in UA in the study group were higher, comparing to the control group. But, there was no statistically significant difference between both groups in analyzing parameters. There were no statistically significant changes in parameters describing blood flow in pulmonary veins in both studied groups.Comments: The combined intrapartum fetal monitoring, including pulse oximetry and Doppler blood flow velocimetry, proved that the reduction of fetal arterial oxygen saturation (&lt;30%) is associated with changes in hemodynamics of fetal cerebral circulation. It has been not observed any changes in blood flow in umbilical artery and pulmonary vein in the presence of decreased fetal saturation.

WS12‐05Umbilical and fetal cerebral circulation and fetal growth

BackgroundFetal growth is determined by its genetic potential and growth support. The aim of our prospective study was to find out does the growth support (placental factor and blood flow) or genetic potential play a primary role in fetal growth.MethodFrom 27 to 41 gestational weeks an umbilical artery (RI1), a middle cerebral artery resistance index (RI2) and umbilical‐cerebral (U/C) ratio were measured. Several US measurements in 3–4 week intervals of the same pregnancy were done. After delivery, fetuses were divided into the three groups (AGA, LGA, SGA) according to their birth‐weights. Pregnancies with gestational diabetes were excluded from the study.ResultsThere were not statistically significant differences between the average values of RI1 (age related) in the groups of AGA and LGA fetuses. However, the mean values of RI1 (according to gestational age) in the mentioned two groups of fetuses were significantly lower than in the group of SGA fetuses, as well as their mean values of U/C ratios.ConclusionPlacental factor is equally and efficiently functioning in the both groups of AGA and LGA fetuses. The genetic regulating factor of fetal growth can be adequately expressed in conditions of appropriate uteroplacental and umbilical blood supply. In other words, in identical or at least similar conditions of umbilical blood supply, fetal growth is exclusively influenced by its genetic potential.

The influence of variations in blood flow on pulsed Doppler ultrasonic heating of the cerebral cortex of the neonatal pig

Pulsed Doppler ultrasound examination of the fetal cerebral circulation may cause potentially harmful temperature elevations in brain tissue immediately beneath the insonated segment of the skull. This study measured the effect of variations in cerebral blood flow on ultrasonic heating of the cerebral cortex of anaesthetised, neonatal pigs. Wide and narrow ultrasound beams were used. Pulsed ultrasound exposures were delivered in 90 s bursts at 5.8 μs pulse length, pulse repetition frequency 8 kHz and centre frequency 3.5 MHz. Studies were performed with the target at the focus of a fixed, stationary beam of 0.3 cm −6 dB beam width (narrow beam) and I spta 1.4 W/cm 2 ( n = 11), or with the target in the near field of a fixed, stationary beam of 1.6 cm −6 dB beam width (wide beam) and I spta 3.6 W/cm 2( n = 5). The 90 s ultrasound exposures were performed under three different conditions of ambient cerebral blood flow: baseline (during normocarbic, normoxic conditions), increased (during hypercarbic, hypoxic conditions) and absent (postmortem). Cerebral blood flow was measured using the radiolabelled microsphere technique. In the narrow beam studies, cerebral blood flow during baseline was 34 ± 4 ml/min/100 g, rising to 109 ± 32 ml/min/100 g during the increased phase ( p < 0.001); in the wide beam studies baseline flows were 29 ± 9 ml/min/100 g, whereas flows in the increased phase were 128 ± 32 ml/min/100 g ( p < 0.001). There was no difference in the heating curves for normal, increased and absent cerebral blood flow for exposure to the narrow beam, when mean temperature increases of 1.5°C at 90 s were recorded in each case ( p > 0.21, power > 0.8). However, the heating curves for the wide beam were significantly different for the three rates of blood flow with mean temperature increases of 1.9°C (normal flow), 1.7°C (increased flow) and 2.4°C (no flow) recorded at 90 s ( p < 0.05).

Dynamic changes in the middle cerebral artery perfusion in normal full-term human fetuses in relation to the timing of behavioral state.

Our aim is to evaluate serial changes in normal full-term fetal cerebral circulation according to the behavioral states. Flow velocity waveforms in the middle cerebral artery and fetal heart rate (FHR) were well recorded in ten of 19 cases by pulsed Doppler ultrasonography and actocardiography over 45 min, respectively. Behavioral states were classified as resting or active phase by FHR patterns. Resistance indices (RIs) were calculated every 5 s as an average of two consecutive waveforms, and median RI was chosen in each 2-min segment. In order to evaluate changes in median RI from active-to-resting transition to resting-to-active one statistically, differences in RI between two 2-min segments were examined using Mann-Whitney U-test. As a result, median RI was decreased to the minimum one in the active-to-resting transition for 12 min in all cases: significant decrease to the 2-min segment with the minimum one (P<0.01). Various types of increase to the maximum median RI during resting phase followed the minimum one: significant increase from the 2-min segment with the minimum one to that with the maximum one in all cases (P<0.001 in eight cases, P<0.01 in two cases). Thereafter, median RI was decreased from the end of resting phase in the resting-to-active transition for 12 min in all cases: significant decrease from the last 2-min segment of resting phase in all cases (P<0.01). We reveal that fetal cerebral circulation changes dynamically in relation to the timing in each behavioral state.

Perinatal brain injury.

Perinatal brain damage in the mature fetus is usually brought about by severe intrauterine asphyxia following an acute reduction of the uterine or umbilical circulation. The areas most heavily affected are the parasagittal region of the cerebral cortex and the basal ganglia. The fetus reacts to a severe lack of oxygen with activation of the sympathetic-adrenergic nervous system and a redistribution of cardiac output in favor of the central organs (brain, heart and adrenals). If the asphyxic insult persists, the fetus is unable to maintain circulatory centralization, and the cardiac output and extent of cerebral perfusion fall. Owing to the acute reduction in oxygen supply, oxidative phosphorylation in the brain comes to a standstill. The Na+/K+ pump at the cell membrane has no more energy to maintain the ionic gradients. In the absence of a membrane potential, large amounts of calcium ions flow through the voltage-dependent ion channels, down an extreme extra-/intracellular concentration gradient, into the cell. Current research suggests that the excessive increase in levels of intracellular calcium, so-called calcium overload, leads to cell damage through the activation of proteases, lipases and endonucleases. During ischemia, besides the influx of calcium ions into the cells via voltage-dependent calcium channels, more calcium enters the cells through glutamate-regulated ion channels. Glutamate, an excitatory neurotransmitter, is released from presynaptic vesicles during ischemia following anoxic cell depolarization. The acute lack of cellular energy arising during ischemia induces almost complete inhibition of cerebral protein biosynthesis. Once the ischemic period is over, protein biosynthesis returns to preischemic levels in non-vulnerable regions of the brain, while in more vulnerable areas it remains inhibited. The inhibition of protein synthesis, therefore, appears to be an early indicator of subsequent neuronal cell death. A second wave of neuronal cell damage occurs during the reperfusion phase. This cell damage is thought to be caused by the postischemic release of oxygen radicals, synthesis of nitric oxide (NO), inflammatory reactions and an imbalance between the excitatory and inhibitory neurotransmitter systems. Part of the secondary neuronal cell damage may be caused by induction of a kind of cellular suicide programme known as apoptosis. Interestingly, there is increasing evidence from recent clinical studies that perinatal brain damage is closely associated with ascending intrauterine infection before or during birth. However, a major part of this damage is likely to be of hypoxic-ischemic nature due to LPS-induced effects on fetal cerebral circulation. Knowledge of these pathophysiological mechanisms has enabled scientists to develop new therapeutic strategies with successful results in animal experiments. The potential of such therapies is discussed here, particularly the promising effects of intravenous administration of magnesium or postischemic induction of cerebral hypothermia.

Cerebral Doppler blood flow velocimetry and central hemodynamics in the ovine fetus during hypoxemia-acidemia.

The purpose of this study was to assess the effects of hypocapnic hypoxia, acidemia and the combination of hypoxia/acidemia on blood flow velocity variables in the fetal cerebral circulation. Chronically instrumented fetal sheep were used and the ewes were induced to breathe a hypoxic gas mixture for about 90 min. This caused an initial period of hypoxemia followed by a period of mixed hypoxemia/acidemia. When the ewe was reoxygenated, the fetus experienced a period of normoxic acidemia. The fetal cerebral circulation was assessed by recording Doppler blood flow velocity waveform variables in a cerebral vessel and the umbilical artery, using standard ultrasound equipment. External carotid artery blood flow was maintained during hypoxic and hypoxic/acidotic periods despite a fall in cardiac output. In the cerebral vessel, mean maximum velocity (time-averaged maximum velocity), minimum diastolic velocity and maximum systolic velocity manifested increases during hypoxic and hypoxic-acidotic periods, but pulsatility index did not change due to the effect of reduced heart rate on pulsatility index. Umbilical artery pulsatility index increased in the hypoxic and hypoxic-acidotic periods, despite unchanged mean maximum velocity, minimum diastolic velocity and maximum systolic velocity. With acute hemodynamic changes, the measurement of pulsatility index can yield misleading results. For clinical and experimental research on the fetal cerebral circulation, more attention should be paid to the individual Doppler variables, especially to the mean maximum velocity, than to the pulsatility index alone. Changes in mean maximum velocity recorded from the cerebral artery seem to reflect changes in the cerebral arterial flow.

Maternal anxiety in late pregnancy and fetal hemodynamics

The aim of this study was to investigate if fetal circulation is affected by maternal anxiety, 37 nulliparous women were studied prospectively in the third trimester of pregnancy, with self-rate tests of anxiety (STAI). Doppler ultrasound examination of the umbilical artery and fetal middle cerebral artery was performed at 37–40 gestational weeks. The pulsatility index (PI) was calculated and corrected for heart rate. The women were divided into groups of increasing levels of anxiety. The fetuses of women with high trait anxiety scores had significantly higher PI values in the umbilical artery ( p = 0.0056), significantly lower PI values in the fetal middle cerebral artery ( p = 0.0029) and significantly lower cerebro-umbilical PI ratios ( p = 0.0002), suggesting a change in blood distribution in favor of brain circulation in the fetuses. Maternal weight, weight-increase, height, age, marital status, smoking habits, drinking habits and socioeconomic factors known to affect fetal well-being did not interfere with these findings. No significant differences in birth-weight, length and head circumference were found between infants born to mothers with higher trait anxiety levels compared to mothers with lower trait anxiety levels. Our results suggest that maternal stress, in terms of trait anxiety, influences fetal cerebral circulation.

Prediction of cerebral blood flow in fetal lambs by carotid artery ultrasonic flow transducer.

To determine whether common carotid artery blood flow measured with an ultrasonic flow transducer would predict brain blood flow in fetal sheep, we measured unilateral common carotid artery blood flow and compared this to simultaneous measurements of total brain blood flows made by radioisotope-labelled microsphere techniques. We studied anaesthetized, exteriorized fetal sheep with intact umbilical circulation after ligation of extracranial, extracerebral arteries and placement of a common carotid artery flow transducer; five fetuses at 120 d gestation had 19 total comparison measurements. As measured by microsphere technique, mean basal blood flow during undisturbed conditions to regional brain areas were similar to normal values reported for the exteriorized ovine fetus; these flows were highly correlated to fetal PaCO2 and successfully varied over a wide range (total brain 9.1-200.4 ml/min/100g and total cortex 6.1-153.1 ml/min/100g) in subsequent experimental conditions of hypercapnia or occluded blood flow. Blood flow as measured by flow transducer significantly correlated (P < or = 0.01) with microsphere measurements of blood flow to total brain (r = 0.56) and total cortex (r = 0.62); regional flow to cerebellum (r = 0.70) and thalamus (r = 0.60) also correlated to transducer measurements. Stronger correlations were observed at low-flow conditions to total brain (r = 0.83) and to total cortex (r = 0.90). As measured by microsphere technique, right and left cortical blood flows were highly correlated (P = 0.0001, r = 0.97), indicating that the flow transducer or surgical manipulation did not disturb the distribution of cerebral blood flow. The mean values for zero flow reference of the transducer were < 1.5% of mean basal flow values. It is concluded that the common carotid artery flow transducer technique developed in this study provides an accurate prediction of blood flow to total brain and total cortex over a wide range of values in fetal sheep. This technique provides a methodologic advantage to sequential experimental interventions and may prove advantageous to studies of fetal sheep cerebral circulation.

Doppler velocimetry of the fetal middle cerebral artery in patients with preterm labor and intact membranes.

A prospective cohort study was conducted to determine whether preterm labor is associated with changes in the impedance to blood flow of the fetal middle cerebral artery. Doppler velocimetry studies were performed in 194 consecutive patients with preterm labor and intact membranes. Pulsatility indices of the middle cerebral artery and umbilical artery were determined on admission. Results were expressed as ratio of the observed pulsatility index to mean value for gestational age expressed as delta MCA PI and delta UA PI, respectively. The prevalence of preterm delivery (< 37 weeks) and delivery within 24 hours of admission was 55.2% (107/194) and 15.5% (30/194), respectively. Patients with an examination-to-delivery interval within 24 hours had significantly lower mean delta MCA PI than that of patients delivered at > or = 37 weeks and > or = 4 weeks after the examination (P < 0.01). Fetuses with a delta MCA PI at or below 0.88 had a relative risk of 2 (95% confidence interval, 1.32 to 2.9) who were delivered within 24 hours compared to controls (sensitivity 76.7%, specificity 62.8%, positive predictive value 26.7%, negative predictive value 93.5%). Stepwise logistic regression analysis indicated that the relationship between delta MCA PI and examination-to-delivery interval remained statistically significant after correcting for cervical dilatation (P < 0.001). Our data indicate that preterm parturition is associated with a decrease in the impedance to flow in the fetal cerebral circulation.

Fetal cerebral blood flow velocity during labor and the early neonatal period.

This study was performed to elucidate circulatory changes in the fetal cerebral circulation during uncomplicated labor and in early neonatal life. Eighteen healthy term singleton fetuses were followed longitudinally during labor. Using the transabdominal approach, and the color Doppler technique, the middle cerebral artery was identified and Doppler flow velocity waveforms recorded between and during uterine contractions. Neonatal recordings were made by insonating the middle cerebral artery from the temporal region before and immediately after the cutting of the umbilical cord, and at 1 hour and 1 day after birth. The recorded Doppler signals were evaluated for pulsatility index, heart rate, peak systolic flow velocity, end-diastolic flow velocity and time-averaged maximum velocity. There was no change in the pulsatility index between and during contractions (1.39 +/- 0.36 and 1.40 +/- 0.39, respectively, mean +/- SD). A significant decrease in the pulsatility index compared to fetal values was seen 4 min after birth (1.06 +/- 0.30, p < 0.01). One hour after birth, the pulsatility index values increased significantly (1.52 +/- 0.25, p < 0.001), to fall again between I hour and 1 day after birth (0.95 +/- 0.26, p < 0.001). Mechanical compression of the skull, blood gas changes and a decrease in ductal shunting may all have contributed to these changes. The present study has shown physiological neonatal circulatory adaptation and onset of breathing to cause manifest changes in cerebral blood flow velocity.

The effect of cordocentesis on umbilical and middle cerebral artery blood flow velocity waveforms.

To investigate the effect of cordocentesis on the umbilical and fetal cerebral circulation. Cross sectional study. Department of Obstetrics and Gynaecology, Regional Referral Centre for Fetal Medicine, Klagenfurt Hospital, Austria. Thirty pregnant women undergoing diagnostic cordocentesis at 18 to 38 weeks' gestation. The pulsatility index (PI) in the umbilical artery and fetal middle cerebral artery was measured by pulsed Doppler ultrasound before and immediately after cordocentesis. Change in umbilical artery PI and middle cerebral artery PI. Cordocentesis was associated with a significant decrease in both umbilical artery PI (median -0.18, range -2.21 to 1.5, P < 0.004) and middle cerebral artery PI (mean -0.15, SD 0.32, P < 0.03) and the decrease in umbilical artery PI was most marked when cordocentesis was performed transplacentally. In four cases, there were absent or reversed frequencies at the end of diastole (EDF) in the umbilical artery before cordocentesis, and in all cases there were positive EDF after the procedure. In contrast, one of the 26 cases with positive EDF developed reversed EDF following the procedure. Acute alterations in the waveforms from both the umbilical and fetal cerebral circulation can be induced by cordocentesis. The decrease in resistance in the fetoplacental circulation could be attributed to the release of vasodilators, and the increase in resistance observed in some cases could be secondary to arterial vasospasm. Better understanding of the underlying mechanisms might help in making cordocentesis a safer procedure.

The “brain-sparing” effect: Antenatal cerebral Doppler findings in relation to neurologic outcome in very preterm infants

Our purpose was to study the relationship between fetal cerebral circulation and neurologic outcome. In 117 high-risk fetuses (gestational age 25 to 33 weeks) flow velocity waveforms were recorded from the umbilical and medial cerebral arteries. The ratio between umbilical and cerebral pulsatility indexes was calculated. A ratio above a predefined tolerance limit was used as an index for the "brain-sparing" effect. Neonatal neurosonography and neurologic examination were used as outcome parameters. Antenatally raised ratios are associated with poor obstetric outcome (fetal death and fetal growth retardation). The incidence of intracranial hemorrhages and ischemic lesions was not different for infants with a normal or raised prenatal ratio. The incidence of neurologic abnormalities was the same for both ratio groups. The "brain-sparing" effect is a mechanism to prevent fetal brain hypoxia rather than a sign of impending brain damage.

Effects of maternal administration of 3% carbon dioxide on umbilical artery and fetal renal and middle cerebral artery Doppler waveforms

OBJECTIVE: The null hypothesis is that umbilical, middle cerebral, and renal artery pulsed Doppler velocity waveforms in the normal term fetus may be affected during short-term maternal inhalation of 3% carbon dioxide gas mixture.STUDY DESIGN: Seventy-two observations were made on 14 term fetuses before and during maternal 3% carbon dioxide gas mixture inhalation. The umbilical, middle cerebral, and renal arteries of these fetuses were sampled with pulsed Doppler velocity. waveforms and recorded on a strip chart at a preset speed of 50 mm/sec. Doppler waveforms' were analyzed for differences in the systolic peak to end-diastolic velocity ratio for these three vascular beds. Peak flow velocity and time velocity integral were also analyzed for the cerebral and renal vascular beds. The data were analyzed with the paired t test.RESULTS: A significant decrease in the systolic-to-diastolic-velocity ratio of the middle cerebral artery occurred with 3% carbon dioxide inhalation (p \\lt 0.02). The other vascular beds had no demonstrable change.CONCLUSION: Transient maternal breathing of 3% carbon dioxide gas mixture selectively causes a decrease in resistance in the fetal cerebral circulation. (AM J OBSTET GYNECOL 1992;167:1668-71.)

Fetal and neonatal cerebral circulation: a pulsed Doppler study.

We studied the relation between the fetal cerebral circulation and changes in the cerebral circulation directly after birth. With a combined real time ultrasound/pulsed Doppler technique flow velocity waveforms from the fetal umbilical- and carotid-circulation were monitored. Pulsatility Index (PI) was computed and the ratio between Umbilical PI and Carotid PI was calculated. Flow velocity waveforms of the cerebral circulation before birth were related to anterior cerebral artery flow velocity waveforms recorded immediately after birth. The study shows that changes in flow velocity waveforms associated with the intra uterine brain-sparing effect are related to poor obstetrical outcome. Furthermore is shown that the brain-sparing effect in the fetal period is associated with higher PI values in the cerebrovascular circulation in the neonatal period. It is suggested that changes in these PI values, representing changes in cerebrovascular resistance, might be indicative of cerebral ischemia in the neonate.

Fetal cerebral circulation assessment by Doppler ultrasound in normal and pathological pregnancies

During normal pregnancies (n = 40) the cerebral index ( Rc = S − D S ) (with S = systolic and D-telediastolic amplitudes) is always higher than the placental index (Rp), and the cerebro/placental ratio ( Rc Rp ) greater than 1. Of 29 pregnant women with hypertension (including two twins), 17 delivered normally (Rc, Rp and CPR normal), 14 delivered an hypotrophic fetus, in 12 out of these 14 pregnancies one of the two indices (Rc or Rp) was abnormal and the cerebro/placental ratio, CPR, was always less or equal to 1. CPR sensitivity was 86% the specificity 100%. In 11 pregnancies with idiopatic fetal-growth retardation, the CPR was less or equal to 1 in eight cases (73% of the cases), and greater than 1 in three cases (three false-negative results).