Absent End-diastolic Flow Research Articles

Infants of women with severe early pre-eclampsia: the effect of absent end-diastolic umbilical artery doppler flow velocities on neurodevelopmental outcome.

Umbilical artery Doppler flow velocity waveform studies were performed over a period of 4 y on 242 women with severe pre-eclampsia before 34 wk gestation. Sixty-eight (28%) had absent end-diastolic umbilical artery Doppler flow velocities. One hundred and ninety-three infants survived to hospital discharge and were followed at 6-monthly intervals until 48 mo of age. The mean corrected developmental quotient was 94 +/- 8 at 24 mo of age and 87 +/- 9 at 48 mo. Ninety-two percent of the infants had a developmental quotient of >80 at 24 mo and 72% at 48 mo of age. This decline is thought to be due to the impact of social circumstances. There were no differences between the developmental quotients of the infants with normal and those with absent end-diastolic umbilical artery Doppler flow velocities at either 24 or 48 mo of age. At 24 mo of age, infants with absent end-diastolic umbilical artery Doppler flow velocities scored lower in the Performance subscale test (p = 0.03). The developmental quotients of infants from poorer socioeconomic backgrounds were significantly lower than those living in more privileged circumstances. At 48 mo, 153 (97%) of the children presented with normal gross motor development. Four infants had cerebral palsy. No differences were noted in the motor outcomes between the infants of women with normal umbilical artery waveforms and those with absent end-diastolic umbilical artery Doppler flow velocities.

Effect of Antenatal Betamethasone Administration on Placental Vascular Resistance

Placental vascular resistance is increased, as evidenced by absent end-diastolic flow (AEDF) in the umbilical artery, in fewer than 0.5 percent of all pregnancies but in as many as 5 percent of high-risk pregnancies. Oxygen and substrate availability are limited as a result, and fetal growth restriction may ensue. Perinatal mortality is increased. Although no effective treatment is known, diagnostic Doppler ultrasonography in high-risk pregnancies at least would allow intensive fetal surveillance and could substantially lower perinatal mortality. The goal of this study was to learn whether betamethasone might, through augmenting the secretion of corticotropin-releasing hormone, a potent dilator of fetoplacental vessels, lower vascular resistance. Flow velocity waveforms of the umbilical artery were monitored in 28 women with umbilical arterial AEDF in conjunction with betamethasone therapy (two 11.4-mg intramuscular doses given at a 24-hour interval). Women were diagnosed at a median of 27 weeks’ gestation and delivered at 29 weeks. The 21 women who were hypertensive received medication before delivery. The median birth weight for 25 singleton pregnancies was 946 gm. None of the newborn infants had weights above the 50th percentile. Diastolic flow returned within 24 hours of betamethasone therapy in 68 percent of pregnancies, and the effect lasted a median of 3 days. This effect, however, did not correlate with the length of gestation at delivery or with birth weight. Three of four women again had a return of diastolic flow when given a second course of steroid. Although betamethasone reduces placental vascular resistance when umbilical arterial AEDF is present, it is not clear whether this is beneficial or harmful to the fetus. Lancet 1999;353:1404–1407

Umbilical Doppler Waveforms and Placental Villous Angiogenesis in Pregnancies Complicated by Fetal Growth Restriction

In Brief Objective To test the hypothesis that the characteristics of umbilical artery Doppler flow velocity waveforms in growth-restricted fetuses indicate angiogenesis within placental stem and gas-exchanging villi. Methods We examined 18 placentas from singleton fetuses that were normal structurally and chromosomally but were growth-restricted, preterm, and complicated by preeclampsia. Ten cases with positive end-diastolic flow and eight with absent or reverse end-diastolic flow were compared with six gestational age-matched controls. Sections of villous placenta were examined to determine structural composition (percentage of fibrinoid, intervillous space, and villous tissue), relative proportion of villous types (stem, immature intermediate, and gas-exchanging villi), and the frequency distribution of stem arterial vessel calibers and their branching pattern. Results Placentas with positive end-diastolic flow had a significantly (P < .05) higher percentage of gas-exchanging villi (median 69.6%, range 62.5–80.8%) than those with absent or reverse end-diastolic flow (58.3%, 29.9–71.9%) or controls (60.8%, 43.1–65.6%). The gas-exchanging villi from placentas with absent or reverse end-diastolic flow were slender, elongated, poorly branched, and poorly capillarized. There was a progressive trend toward reduced branching of the stem arteries from the controls (median 22%, range 2–38%), through the positive end-diastolic group (17%, 11–20%), to the absent or reverse end-diastolic group (13%, 4–23%). Conclusion Compared with absent or reverse end-diastolic flow, the placentas from growth-restricted fetuses with positive end-diastolic flow showed a normal pattern of stem artery development, accompanied by increased capillary angiogenesis and terminal villous development. These features suggest an adaptive pathway for the placenta in the face of uteroplacental ischemia. Different patterns of umbilical artery Doppler flow velocity waveforms identify characteristic placental lesions that can explain different outcomes in growth-restricted fetuses.

Effect of antenatal betamethasone administration on placental vascular resistance

High placental vascular resistance is an important cause of fetal growth restriction and subsequent perinatal mortality. Identification of affected pregnancies allows appropriate fetal surveillance and delivery, but there are no known therapeutic strategies to decrease resistance and improve blood flow. However, placental corticotropin-releasing hormone (CRH) is thought to be a potent fetoplacental vasodilator, and exogenous corticosteroids can increase placental CRH secretion. Therefore, we examined whether corticosteroids could improve fetoplacental blood flow in pregnancies with increased vascular resistance. A retrospective review of umbilical-artery flow-velocity waveforms (FVWs) before and after betamethasone administration was undertaken in pregnancies with increased placental vascular resistance, as shown by umbilical-artery absent end-diastolic flow (AEDF). FVWs were obtained by pulsed-wave doppler ultrasonography. We studied all 28 pregnancies monitored at the maternal-fetal medicine unit of a university teaching hospital since 1995. The median duration of gestation at presentation with AEDF was 27 weeks (range 23-33). In 19 (68% [95% CI 49-86]) pregnancies, umbilical-artery diastolic flow returned within 24 h after betamethasone administration, consistent with decreased resistance. The median duration of this effect was 3 days (range 2-7). There were no differences in duration of gestation at diagnosis or delivery, or in birthweight between fetuses showing a return of flow after betamethasone and those not showing a return of flow. In pregnancies with umbilical-artery AEDF, betamethasone treatment is associated with decreased placental vascular resistance, possibly induced via increased placental CRH secretion. This study does not provide insights into whether this effect would be beneficial or harmful to the fetus.

Umbilical doppler waveforms and placental villous angiogenesis in pregnancies complicated by fetal growth restriction

Objective: To test the hypothesis that the characteristics of umbilical artery Doppler flow velocity waveforms in growth-restricted fetuses indicate angiogenesis within placental stem and gas-exchanging villi. Methods: We examined 18 placentas from singleton fetuses that were normal structurally and chromosomally but were growth-restricted, preterm, and complicated by preeclampsia. Ten cases with positive end-diastolic flow and eight with absent or reverse end-diastolic flow were compared with six gestational age-matched controls. Sections of villous placenta were examined to determine structural composition (percentage of fibrinoid, intervillous space, and villous tissue), relative proportion of villous types (stem, immature intermediate, and gas-exchanging villi), and the frequency distribution of stem arterial vessel calibers and their branching pattern. Results: Placentas with positive end-diastolic flow had a significantly ( P < .05) higher percentage of gas-exchanging villi (median 69.6%, range 62.5–80.8%) than those with absent or reverse end-diastolic flow (58.3%, 29.9–71.9%) or controls (60.8%, 43.1–65.6%). The gas-exchanging villi from placentas with absent or reverse end-diastolic flow were slender, elongated, poorly branched, and poorly capillarized. There was a progressive trend toward reduced branching of the stem arteries from the controls (median 22%, range 2–38%), through the positive end-diastolic group (17%, 11–20%), to the absent or reverse end-diastolic group (13%, 4–23%). Conclusion: Compared with absent or reverse end-diastolic flow, the placentas from growth-restricted fetuses with positive end-diastolic flow showed a normal pattern of stem artery development, accompanied by increased capillary angiogenesis and terminal villous development. These features suggest an adaptive pathway for the placenta in the face of uteroplacental ischemia.

Necrotizing enterocolitis in infants born to women with severe early preeclampsia and absent end-diastolic umbilical artery doppler flow velocity waveforms.

The aim of this study was to determine the prevalence of necrotizing enterocolitis (NEC) in infants born to a homogeneous group of women with severe preeclampsia before 34 weeks' gestation and who had absent end-diastolic umbilical artery Doppler flow (AEDF) or normal umbilical Doppler flow velocities (NUFV). A total of 242 infants were entered into the study. The mean birth weight was 1260.5 g (SD = 339) and the mean gestational age 30.5 weeks (SD = 2.0). Sixty-eight (28%) infants had AEDF, 43 (18%) had umbilical artery Doppler flow velocities between the 95th and 99th percentile, and 131 (54%) had NUFV. Forty-one (18%) infants developed NEC, of whom 20 (8%) developed definite and advanced NEC (grade 2 and 3). Of these, 16(80%) had grade 2 and 4(20%) had grade 3. Twenty-one (8%) infants developed suspected NEC (grade 1). The mean onset of grade 1 NEC (7.2 days) occurred significantly earlier than in those with grades 2 and 3 NEC (18.7 and 23.3 days, respectively). Of the 21 infants with grade 1 NEC, 10 (48%) had AEDF and 9 (43%) had NUFV. None of the infants with grades 2 or 3 NEC had AEDF. We conclude that although chronically hypoxemic fetuses born to women with severe early onset preeclampsia and AEDF respond by redistributing blood flow to vital organs and away from the gut; the intestinal compromise is of insufficient magnitude to induce intestinal necrosis or NEC. Enteral feeding, however, should be introduced cautiously in infants with AEDF, as so-called suspected NEC developed significantly more often in these infants.

Placental pathology of absent and reversed end-diastolic flow in growth-restricted fetuses

Objective To identify placental histopathology associated with absent and reversed end-diastolic flow demonstrated by umbilical artery (UA) Doppler velocimetry in fetal growth restriction (FGR). Methods Between January 1989 and June 1995, 64 consecutive, nonanomalous singletons at less than the tenth percentile for birth weight were admitted to the neonatal intensive care unit, with UA Doppler velocimetry obtained within 3 days of delivery; 54 of the 64 (84%) had placental histopathology. Umbilical artery Doppler wave forms were classified as having end-diastolic flow ( n = 26), and either absent ( n = 20) or reversed end-diastolic flow ( n = 8). Blinded review of placental histology scored lesions in categories of intraplacental vaso-occlusion, uteroplacental vascular pathology, chronic inflammation, and coagulation. Results Using cases of FGR with end-diastolic flow present as the control population, we found that absent end-diastolic flow cases had significantly more fetal stem vessels with medial hyperplasia and luminal obliteration, and cases of reversed end-diastolic flow had significantly more poorly vascularized terminal villi, villous stromal hemorrhage, “hemorrhagic endovasculitis,” and abnormally thin-walled fetal stem vessels (each P Conclusion In FGR, UA Doppler velocity wave forms do not demonstrate a continuum of placental lesions in which reversed end-diastolic flow reflects more severe placental histopathology than absent end-diastolic flow and enddiastolic flow present. As expected, absent end-diastolic flow cases had more occlusive lesions of the intraplacental vasculature. In reversed end-diastolic flow, lesions suggesting vascular remodeling and/or damage by pathologic conditions of intraplacental flow predominated.

Outcome of 88 pregnancies with absent or reversed end-diastolic blood flow (ARED flow) in the umbilical arteries

Objectives: to investigate both perinatal and postneonatal morbidity and mortality in fetuses with absent or reversed end-diastolic flow (ARED flow) in the umbilical artery. Study design: A 5 year prospective follow-up of 88 fetuses with ARED flow. Results: Sixteen stillbirths, 16 neonatal deaths, six postneonatal deaths and one death at 2 years of age were noted. Out of the 42 fetuses born alive, 36 showed a normal neurological development whereas six were mentally handicapped. Adverse prognosis was more frequently found in the group with absent end-diastolic flow at first examination and then reversed flow until delivery, compared to the groups of always absent or always reversed end-diastolic flows. Conclusions: Prompt delivery is recommended in these high-risk pregnancies in order to prevent long-term sequelae, obviously depending on the local limits of viability. Further studies appropriately designed for assessing long-term neurodevelopment of fetuses with ARED flow, although demanding, are mandatory.

Does increased resistance on umbilical artery Doppler preclude a trial of labour?

Objective: To determine whether patients with increased resistance on umbilical artery Doppler velocimetry could be safely allowed a trial of labour. Design: The Coombe Womens' Hospital is a university teaching hospital which takes tertiary referrals. All singleton pregnancies found to have increased resistance (>2 SD above the mean for gestational age) on umbilical artery Doppler ultrasound between 1993 and 1995 inclusively were identified from the ultrasound database and reviewed, retrospectively. Cases where the umbilical artery waveform reverted to normal or deteriorated to absent end diastolic flow on a subsequent scan were excluded. The 118 cases identified were divided into two groups, those that were delivered by elective caesarean section and those that laboured. Results: Forty-five patients were delivered by elective caesarean section and 73 were allowed to labour. In the group that laboured over 90% delivered vaginally and 9.8% were delivered by emergency caesarean section. Three babies had a cord pH less than 7.20 in the group that laboured. Two babies had an Apgar score of less than 7 at 5 min in the group that were delivered electively. There were no neonatal seizures or perinatal deaths in either of the two groups. Conclusion: This study shows that patients with increased resistance on umbilical artery Doppler can be allowed a trial of labour without compromising the fetal outcome. We would suggest that consideration be given to induction of labour in selected patients as an alternative to elective section.

Serial Amniocenteses in the Management of Twin-Twin Transfusion Syndrome

Serial decompressive amniocenteses were performed at 18-23 weeks of gestation in 23 pregnancies referred due to echographic signs typical of twin-twin transfusion syndrome. The procedures were repeated until delivery or permanent normalization of the amniotic fluid volume both in the donor and the recipient twin sac. The overall survival rate was 57%, but in only 39% of the pregnancies did both twins survive without handicaps. The absence of end diastolic flow in the umbilical artery of the donor twin was associated with poor chances of survival for both fetuses; in contrast, the presence of hydrops or ascites in the recipient twin did not worsen the prognosis. A policy of aggressive amniotic fluid decompression may achieve permanent resolution of the fluid in over 50% of the pregnancies complicated by twin-twin transfusion syndrome.

Fetal arterial Doppler-IUGR and hypoxia

Vascular resistances of various fetal arreas are assessed by Doppler ultrasound. The PI, RI and S/D indices are measured on the cerebral, renal, aortic and umbilical Doppler spectrum. Ratios of these indices based on the comparison of the cerebral (Rc) and the umbilical (Rp) resistances, or carotid (Rcc) and umbilical resistances, or cerebral (Rc) and aortic (Rao) resistances (Rc.Rp or Rp/Rcc, or Rc/Rao), measure the flow redistribution between the placenta and brain. The umbilical resistance indices, when greater than the upper limit of the normal range (>2sd) are frequently associated with IUGR. (Sensitivity about 65 to 70%). Absent end diastolic flow is most of the time associated with severe IUGR and hypoxia and poor fetal outcome. A fairly good correlation was found between the existence of significantly decrerased (<.2sd) cerebral resistance and the development of post asphyxial encephalopathy in the neonate (Specificity 75% Sensitivity 87%). The earliest detectors of IUGR and hypoxia are the cerebral-umbilical cerebral-carotid, or cerebral-aortic ratios (Sensitivity 85% specificity 90%). When used as predictor of poor perinatal outcome in growth retarded fetuses, the cerebral umbilical ratio shows a sensitivity of 90% compared with 78% of the middle cerebral artery, and 83% for the umbilical artery indices. Changes of this ratio are well correlated with the fetal pO 2 changes. The renal flow response to hypoxia depends on the degree of hypoxia. Opposite responses were found in case of moderate, and severe IUGR or hypoxia. Thus, it is too early to conclude if the renal indices are reliable parameters for the evaluation of fetal hypoxia. The sensitivity in predicting IUGR was for the aortic PI: 41% and for the aortic BFC (Blood flow classes): 57%. In predicting delivery for fetal distress, the corresponding values were 76 and 87%, respectively. Because the resistance indices are heart rate-dependent, it is dangerous to draw any conclusion from one single value of any of these parameters. Only several successive measurement of the Doppler indices or of their ratio, may lead to a reliable evaluation of fetal hemodynamics. In the case of significant IUGR with abnormal Doppler indices it is recommended to repeat the Doppler measurements daily both at the cerebral and umbilical or aortic level in order to follow up the fetal flow redistribution which is highly correlated with the fetal pO 2 changes.

Oxygen and placental villous development: Origins of fetal hypoxia

The increasing practice of preterm delivery in the fetal interest for conditions such as pre-eclampsia or intrauterine growth restriction (IUGR) has provided an opportunity to study placental structure in pregnancies with prenatal evidence of fetal compromise. These data suggest that the origin of fetal hypoxia in IUGR with absent end-diastolic flow in the umbilical arteries is due to a failure of oxygen transport from intervillous space to umbilical vein. Failure of the fetoplacental circulation to extract oxygen from the intervillous space under such circumstances means intervillous Po o is closer to maternal arterial values than under physiological conditions. Correspondingly the placental villi are chronically exposed to a higher oxygen tension than under normal circumstances — the term ‘hyperoxia’, relative to normal intraplacental oxygenation, is proposed to describe this situation. Both the trophoblast and villous core react to increased oxygen despite fetal hypoxia. These results challenge the generally accepted concept of ‘placental hypoxia’ in all circumstances where fetal hypoxia might arise. Therefore three categories are proposed for the origins of fetal hypoxia: (1) preplacental hypoxia; (2) uteroplacental hypoxia; and (3) postplacental hypoxia. Examples for these three disease states are listed in this review and the structural reaction patterns of placental villi to these differences in oxygenation are discussed.

Placental pathology of absent and reversed end-diastolic flow in growth-restricted fetuses

To identify placental histopathology associated with absent and reversed end-diastolic flow demonstrated by umbilical artery (UA) Doppler velocimetry in fetal growth restriction (FGR). Between January 1989 and June 1995, 64 consecutive, nonanomalous singletons at less than the tenth percentile for birth weight were admitted to the neonatal intensive care unit, with UA Doppler velocimetry obtained within 3 days of delivery; 54 of the 64 (84%) had placental histopathology. Umbilical artery Doppler wave forms were classified as having end-diastolic flow (n = 26), and either absent (n = 20) or reversed end-diastolic flow (n = 8). Blinded review of placental histology scored lesions in categories of intraplacental vaso-occlusion, uteroplacental vascular pathology, chronic inflammation, and coagulation. Using cases of FGR with end-diastolic flow present as the control population, we found that absent end-diastolic flow cases had significantly more fetal stem vessels with medial hyperplasia and luminal obliteration, and cases of reversed end-diastolic flow had significantly more poorly vascularized terminal villi, villous stromal hemorrhage, "hemorrhagic endovasculitis," and abnormally thin-walled fetal stem vessels (each P < .005). In FGR, UA Doppler velocity wave forms do not demonstrate a continuum of placental lesions in which reversed end-diastolic flow reflects more severe placental histopathology than absent end-diastolic flow and end-diastolic flow present. As expected, absent end-diastolic flow cases had more occlusive lesions of the intraplacental vasculature. In reversed end-diastolic flow, lesions suggesting vascular remodeling and/or damage by pathologic conditions of intraplacental flow predominated.

OGO 6353 Dopplervelocimetry of umbilical artery with absence of end diastolic flow and perinatal results

OGO 6353 Dopplervelocimetry of umbilical artery with absence of end diastolic flow and perinatal results

Effect of absent end diastolic flow velocity in the fetal umbilical artery on subsequent outcome

Sixty babies, delivered over a six and a half year period, who had absent end diastolic frequency (AEDF) in the umbilical artery, were studied. Individually matched control pregnancies for gestational...

Pathological basis for abnormal umbilical artery doppler waveforms in pregnancies complicated by intrauterine growth restriction: A review

Summary The abnormal umbilical artery Doppler waveform represented by absent enddiastolic flow velocity (AEDFC) identifies a group of preterm fetuses with intrauterine growth restriction (IUGR) at high risk of perinatal death due chronic hypoxia from compromised umbilical artery blood flow. Initial studies of AEDFV placentae suggested a loss of small stem arterioles, though by immunohistochemical localization with an antibody to α-smooth muscle actin, we were unable to demonstrate any selective loss of even the smallest vessels in the 10–25 μM post-fixation diameter range. Further studies of villous ultrastructure and immunohistochemical localization of matrix molecules (laminin and collagens I, III and IV) demonstrated evidence of villous fibrosis and trophoblast aging. Parallel scanning electron microscopy studies demonstrated reduced numbers of malformed peripheral villi, whose capillaries were elongated and only poorly branched. Several of the structural differences in the terminal villi of this IUGR group, such as reduced cytotrophoblast proliferation and stromal fibrosis, are incompatible with the prevailing view of placental hypoxia in preterm IUGR with AEDFV. Reduced numbers of malformed terminal vili would be predicted to both increase capillary vascular impedance, and compromise placental gas exchange. Despite the known reduction in uteroplacental arterial blood flow in IUGR with AEDFV in the umbilical arteries, there is a greater fall in extraction of oxygen from the intervillous space: as such that maternal blood leaving the placenta has a higher content than under normal circumstances. Our data challenge the presumption of “placental hypoxia” in this subset of preterm IUGR pregnancies complicated by AEDFV in the umbilical arteries, which has both scientific and clinical implications.

Intrauterine growth restriction with absent end-diastolic flow velocity in the umbilical artery is associated with maldevelopment of the placental terminal villous tree

OBJECTIVE: Our purpose was to evaluate the structure of placental terminal villi and their capillaries in pregnancies complicated by intrauterine growth restriction with absent end-diastolic flow velocity in the umbilical artery. STUDY DESIGN: Glutaraldehyde-perfusion-fixed villous tissue and a plastic cast of the vessels in at least two cotyledons were prepared from 10 cases with intrauterine growth restriction and 9 gestational age-matched control placentas. The structure and dimensions of 20 terminal capillary loops per cast were determined by scanning electron microscopic examination, and their appearances were correlated with the peripheral villi of the perfusion-fixed villous tissue. RESULTS: Capillary loops in the growth-restricted cases were sparse in number and significantly longer than in the control cases (218 μm [72] vs 137 μm [30], mean and SD, p < 0.05). They exhibited fewer branches (4.0 [1.9] per loop vs 6.1 [2.2], p < 0.05) and a majority of loops were uncoiled (79% vs 18%, p < 0.05). The villous tissues from the growth-restricted cases demonstrated elongated villi, consistent with the cast findings. The trophoblast surface was wrinkled and in some areas covered by fibrin plaques. CONCLUSIONS: The terminal villous compartment of the placenta appears to be maldeveloped in preterm intrauterine growth restriction pregnancies where absent end-diastolic flow velocity is demonstrated in the umbilical artery before delivery. These findings are consistent with an increase in fetoplacental vascular impedance at the capillary level and may account for the impaired gas and nutrient transfer in this disorder. (Am J Obstet Gynecol 1996;175:1534-42.)

Ultrasound predictors of neonatal outcome in intrauterine growth restriction.

Our purpose was to assess the value of commonly performed ultrasound parameters in predicting neonatal outcome of fetuses with intrauterine growth restriction (IUGR). One hundred twenty-seven patients were identified on ultrasound examination to have IUGR. Estimated weight percentile, amniotic fluid volume, umbilical artery Doppler velocimetry, and head circumference/abdominal circumference ratio were compared with neonatal outcome. Thirty infants had severely adverse courses. The degree of growth restriction was strongly associated with adverse outcome and neonatal death. Umbilical artery Doppler waveforms with absent or reverse end-diastolic flow were predicted of neonatal death, bronchopulmonary dysplasia (BPD), necrotizing enterocolitis (NEC), and adverse outcome in general. Oligohydramnios was predictive of adverse outcome and neonatal death. Logistic regression also showed that absent or reverse end-diastolic flow and oligohydramnios were independent predictors of adverse outcome. Ultrasound findings of low estimated weight percentile, absent or reverse end-diastolic umbilical blood flow, and oligohydramnios are independent predictors of adverse neonatal outcome of growth restricted fetuses.

Venous Doppler in the fetus with absent end-diastolic flow in the umbilical artery.

High perinatal mortality has been reported in association with the finding of absent end-diastolic flow velocities in the umbilical artery. The fetus is known to centralize its circulation during hypoxemia and abnormal venous blood flow velocities have been reported in cases of heart failure and imminent asphyxia. The aim of this study was to evaluate blood flow velocities recorded with Doppler ultrasound in the umbilical vein, inferior vena cava and middle cerebral artery as predictors of survival in 17 fetuses with absent or reversed end-diastolic flow in the umbilical artery. There were five perinatal deaths, all having abnormal umbilical cord venous pulsations. An increased proportion of diastolic blood flow velocity in the middle cerebral artery as a sign of hypoxia was found in 12 fetuses without a relationship to perinatal mortality. An increased proportion of retrograde blood flow in the inferior vena cava was recorded in only one fetus, which died on the same day of congestive heart failure, suggesting fetal heart sparing in the remaining complicated pregnancies. The results suggest that abnormal end-diastolic umbilical venous pulsation in the cord is a late and ominous sign of a severely compromised fetus, while abnormal blood flow velocimetry in the middle cerebral artery might be an earlier sign of fetal hypoxia, with a better prognosis.

Outcomes of severely abnormal umbilical artery Doppler velocimetry in structurally normal singleton fetuses

To construct a management guide for preterm pregnancies complicated by severely abnormal umbilical artery Doppler velocimetry. A retrospective chart review was conducted on all cases of absent or reversed end-diastolic flow umbilical artery Doppler velocimetry identified through an ultrasound data base. Maternal and perinatal outcome variables were retrospectively reviewed and analyzed using both parametric and nonparametric statistical techniques. Seventy-one cases were identified over a 5-year period. After excluding multiple gestations, anomalous fetuses, and two cases that were terminated before 24 weeks' gestation, 56 singleton gestations remained for analysis. Among the 56 subjects, there were 45 survivors and 11 deaths (five fetal and six neonatal deaths). Nonsurvivors had a significantly lower gestational age at diagnosis and delivery. Nonsurviving live-born neonates had lower Apgar scores and were significantly smaller; however, there were no differences in proportion or severity of fetal growth restriction in survivors and nonsurvivors. There were no differences in last biophysical profile before delivery or interval from diagnosis of reversed end-diastolic flow to delivery. Predictors of nonsurvival were the presence of reversed end-diastolic flow and oligohydramnios. Perinatal mortality for reversed end-diastolic flow was 333/1000 and 94/1000 for absent end-diastolic flow. Risk for perinatal death was highly gestational age dependent. For delivery at less than 26 weeks, survival was one of four; at 26-27.9 weeks, survival was seven of 12; and at 28 weeks or greater, survival was 37 of 40. Whereas severely abnormal umbilical artery blood flow poses significant risk for pregnancy, perinatal mortality is dominated by gestational age at diagnosis and delivery. This may reflect the severity of the disease or the low survival of very immature gestations. Interventions on behalf of the fetus at very early gestational ages should be undertaken with caution.