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Biomedical subjects

K J Moise

Publications and source records attributed to K J Moise.

At least 109 records · Page 6Linked to original sources

The effect of indomethacin on the pulsatility index of the umbilical artery in human fetuses.

Pulsed and continuous-wave Doppler ultrasonography was used to assess blood velocities in the ductus arteriosus and the pulsatility index of the umbilical artery in 20 fetuses (1 pair of twins and 18 singletons) at 23 to 33 weeks' gestation during maternal indomethacin therapy for preterm labor or polyhydramnios. There was no statistically significant difference in the pulsatility index of the umbilical artery during maternal indomethacin treatment (mean +/- SD, 1.11 +/- 0.20) when compared with baseline values (1.12 +/- 0.19) in all 20 fetuses studied. An increase in the peak systolic and diastolic blood velocities in the ductus arteriosus consistent with ductal constriction was noted in 9 fetuses. Analysis of the umbilical artery pulsatility index values before and during indomethacin in this subgroup of fetuses failed to reveal a statistically significant change (1.12 +/- 0.19 vs. 1.11 +/- 0.20). Indomethacin therapy does not influence the pulsatility index of the umbilical artery at the gestational ages studied.

Blood Flow Velocity↗

Acute fetal hemodynamic alterations after intrauterine transfusion for treatment of severe red blood cell alloimmunization.

One of the compensatory hemodynamic mechanisms seen in the anemic human fetus is an increased cardiac output. With Doppler techniques, cardiac output was measured in 21 fetuses before and immediately after 38 intrauterine transfusions for severe red cell alloimmunization. Umbilical venous pressures were measured before and after transfusion; amniotic fluid pressure was also quantitated. After subtraction of amniotic pressure, umbilical venous pressure increased by 1.7 +/- 2.8 mm Hg (p less than 0.01). Left and right ventricular output declined by 19% and 22%, respectively (p less than 0.001). Four factors are known to affect cardiac output: heart rate, cardiac contractility, preload, and afterload. Fetal heart rate and mean acceleration, a measure of myocardial contractility, were unchanged after transfusion. A calculated mean increase in the fetoplacental volume of 18% in conjunction with an increase in umbilical venous pressure would indicate that cardiac preload was increased. We propose that intravascular intrauterine transfusion leads to an increased cardiac afterload, possibly by increasing blood viscosity. The fetal heart responds to the increased afterload by a decrease in stroke volume, leading to a fall in cardiac output.

Blood Transfusion, Intrauterine↗

Flow velocity waveforms of the vascular system in the anemic fetus before and after intravascular transfusion for severe red blood cell alloimmunization.

Sixteen intravascular transfusions were performed in 16 anemic human fetuses. To investigate the status of the vascular system with Doppler ultrasonography before and after correction of anemia, pulsatility index values were obtained for the flow velocity waveforms of the middle cerebral artery, internal carotid artery, anterior cerebral artery, thoracic aorta, abdominal aorta, renal artery, femoral artery, and umbilical artery before and the day after the correction of anemia. The fetuses were divided into two groups: (1) fetuses with a hematocrit level between 2 and 4 SDs below the normal mean value for gestational age and (2) fetuses with a hematocrit value less than 4 SDs below the normal mean value for gestational age. No significant differences were observed in the pulsatility index values of the vessels studied before and after correction of anemia in both groups of fetuses. These data suggest that the pulsatility index cannot be used as an indicator of fetal anemia at the hematocrit values studied.

Anemia, Hemolytic, Autoimmune↗

In utero resolution of hydrops fetalis following the death of one twin in twin-twin transfusion.

A case of massive hydramnios involving a twin-twin transfusion syndrome is presented with death of the larger twin and the development of hydrops fetalis in the surviving smaller twin. The amniotic fluid volume of the surviving twin became normal and the hydrops fetalis resolved spontaneously in utero. Concomitant with the resolution of the hydrops fetalis, the umbilical cord systolic to diastolic ratio improved. At the time of delivery, the hydrops had resolved. The liveborn infant died 11 days later secondary to pulmonary hypertension and cardiorespiratory failure. Although the fetal status improved in utero, the pulmonary hypertension postdelivery resulted in neonatal death.

Adult↗

Increased severity of fetal hemolytic disease with known rhesus alloimmunization after first-trimester transcervical chorionic villus biopsy.

Fetomaternal hemorrhage secondary to chorionic villus biopsy has the potential to accelerate fetal hemolytic disease in the pregnant patient previously sensitized to red cell antigens. A case of poor fetal outcome after first-trimester transcervical chorionic villus sampling in an alloimmunized patient is reported. An increase in antibody titers was associated with the demise of a hydropic fetus early in the second trimester. Maternal red cell alloimmunization is suggested as an absolute contraindication for chorionic villus sampling performed for genetic indications.

Adult↗

Fetoplacental blood volume estimation in pregnancies with Rh alloimmunization.

Direct intravascular fetal transfusion under ultrasound guidance has become an important method of treating fetal anemia secondary to maternal red cell alloimmunization. An estimate of normal circulating volume would be useful in selecting the volume of donor blood to be transfused to achieve a desired final hematocrit. Thirty-five fetuses between 21 and 35 weeks of gestation underwent 67 direct intravascular transfusions. The fetoplacental volume relative to fetal weight estimated by ultrasound was found to be relatively constant throughout gestation at approximately 100 cm3/kg. The severity of fetal hemolytic disease and its treatment with intrauterine transfusions did not appear to alter the fetoplacental volume. A nomogram for fetoplacental blood volume versus gestational age is described.

Blood Transfusion, Intrauterine↗

Flow velocity waveforms of the umbilical and cerebral arteries before and after intravascular transfusion.

Thirteen intravascular transfusions were performed in 13 human fetuses who were anemic because of severe red-cell alloimmunization. To investigate the status of the umbilical and cerebral circulations by pulsed Doppler ultrasound, we studied the fetal middle cerebral artery (N = 13), internal carotid artery (N = 11), anterior cerebral artery (N = 11), and umbilical artery (N = 13) before, within the first 2 hours after, and the day after intravascular transfusion. The gestational age at the time of transfusion was 21-31 weeks (mean +/- SD 25 +/- 3.1). The fetal hematocrits before transfusion ranged from 12-32% (23.4 +/- 6.1), whereas the hematocrit after transfusion was between 25-42% (35 +/- 5). The net blood volume transfused (volume infused--volume removed) ranged between 7.5-31.0 mL (16.0 +/- 7.4). The hematocrit of the transfused blood varied between 68-81% (74 +/- 4). Repeated-measures analysis of variance indicated significant differences in the pulsatility index values of the four vessels studied. The same analysis indicated significant differences in the pulsatility index values at the three time points. Multiple comparison tests showed that the pulsatility index was reduced significantly immediately after transfusion for each vessel studied, but returned to pretransfusion levels by the next day. These data suggest a change in vascular impedance soon after transfusion as a consequence of direct intravascular transfusion.

Anemia↗

Effect of indomethacin on the fetal ductus arteriosus during treatment of symptomatic polyhydramnios.

Ten pregnancies with 13 fetuses complicated by symptomatic polyhydramnios were treated with indomethacin. A baseline fetal echocardiogram was obtained before therapy, repeated 24 hours after the initiation of indomethacin and then performed weekly provided that the ductus arteriosus remained patent. The mean duration of indomethacin therapy was 28.3 +/- 18.9 days. The starting dose in all patients was 25 mg orally every six hours. The ductus arteriosus was noted to constrict in four patients, with the development of tricuspid regurgitation in one. One of the constrictions occurred after 23 days of therapy. In one patient with constriction a reduction of the indomethacin dosage was not associated with constriction, while in the other three, constriction was still evident at a reduced dosage. All constrictions and the tricuspid regurgitation resolved in utero within 24 hours after discontinuation of the indomethacin. We recommend careful monitoring of the fetal ductus arteriosus when treating symptomatic polyhydramnios with indomethacin.

Ductus Arteriosus↗

Uterine blood flow velocity waveforms in pregnant women during indomethacin therapy.

Continuous-wave Doppler ultrasound was used to assess blood flow velocities and determine the pulsatility index of the uterine arteries in ten pregnant women at 23-33 weeks' gestation during indomethacin therapy for preterm labor or polyhydramnios. There was no statistically significant difference in the pulsatility index of the uterine arteries during maternal indomethacin treatment (mean +/- SD 0.85 +/- 0.29) compared with pre-treatment values (0.85 +/- 0.23). Although studies in animals have reported that indomethacin increases uterine impedance to flow, it appears that it does not affect the uterine impedance in humans.

Blood Flow Velocity↗

Serial maternal blood donations for intrauterine transfusion.

Because of concern regarding viral disease transmission, 21 pregnant women who had been alloimmunized to various red-cell antigens donated 77 units of blood (range two to six donations) for intrauterine transfusion to their anemic fetuses. Patients received supplemental iron and vitamin therapy throughout the blood donation period. Before the first donation, the mean (+/- SD) maternal hematocrit was 34.4 +/- 2.8%, whereas at delivery it was 33.4 +/- 3.5%. Maternal hematocrit was noted to decline slightly between the first and second donations but returned to pre-donation values with subsequent donations. No adverse maternal or fetal effects occurred secondary to repeated donations. Use of maternal designated-donor red cells for intrauterine transfusion offers potential advantages over the use of random allogeneic red blood cell units.

Adult↗

Doppler assessment of the renal blood flow velocity waveform during indomethacin therapy for preterm labor and polyhydramnios.

To investigate the effects of indomethacin on the human fetal renal blood flow velocity waveform, 17 fetuses whose mothers were treated for preterm labor (N = 8) or polyhydramnios (N = 9) were studied. There were five growth-retarded fetuses (all in the group with polyhydramnios), 11 normal fetuses, and one fetus with red-cell alloimmunization. The indomethacin dose in all patients was 25 mg orally every 6 hours. The gestational age of the fetuses studied varied between 24-35 weeks (mean +/- SD 29.6 +/- 2.8). The fetal renal artery was studied at its origin from the aorta before and during the first 24 hours of indomethacin therapy. Seven fetuses manifested ductal constriction. Three fetuses also manifested tricuspid regurgitation. All ductal constrictions and the tricuspid regurgitations resolved in utero after discontinuation of indomethacin. There were no significant differences in the pulsatility index values of the renal artery before and during indomethacin therapy. These results suggest that there is no change in fetal renovascular parameters detectable with pulsatility index measurements during the first 24 hours of maternal indomethacin therapy.

Ductus Arteriosus↗

Indomethacin therapy in the treatment of symptomatic polyhydramnios.

Eight gravidas with symptomatic polyhydramnios were managed with maternal indomethacin therapy. The mean gestational age at presentation was 28.6 +/- 3.5 weeks. Only patients requiring serial amniotic fluid decompressions for rapid amniotic fluid reaccumulation were enrolled in the study. An initial amniotic fluid decompression was performed and, when a second decompression was required, indomethacin was initiated. Amniotic fluid volume was measured with a para-amino hippuric acid dilution technique before and during indomethacin therapy. Fetal urine output, studied by serial bladder dimension ultrasonography, declined significantly during indomethacin therapy (P less than .05). Only one patient required further amniotic fluid decompression while on indomethacin. The mean (+/- SD) amniotic fluid volume was 1529 +/- 1070 mL after the initial amniocentesis, and was 2355 +/- 820 mL at the second amniocentesis just before indomethacin therapy. The mean amniotic fluid volume during indomethacin therapy was 1608 +/- 914 mL. We recommend initial amniotic fluid decompression followed by indomethacin therapy for the management of symptomatic polyhydramnios as an alternative to serial amniotic fluid decompressions.

Adult↗

Outcome of twin-twin transfusion diagnosed before 28 weeks of gestation.

To develop prognostic indicators for those patients diagnosed with twin-twin transfusion before 28 weeks' gestation, we conducted a retrospective analysis of all cases diagnosed at Baylor College of Medicine from January 1985 through April 1989. Twenty-seven cases of twin-twin transfusion were diagnosed by ultrasound; the criteria for diagnosis were polyhydramnios in one amniotic cavity and oligohydramnios in the other cavity. The mean (+/- SD) age at diagnosis was 21.9 +/- 2.9 weeks and the mean age at delivery was 26.8 +/- 4.9 weeks. Gestational age at diagnosis was similar in survivors and non-survivors (21.7 +/- 3.7 versus 22.2 +/- 2.8 weeks; P = .35); however, surviving infants were delivered later in gestation (31.9 +/- 3.5 versus 25.9 +/- 3.4 weeks; P = .000008). The overall survival rate was 21%. Fetal hydrops correlated with poor survival. Amniocentesis for decompression and tocolysis failed to decrease perinatal mortality.

Adult↗

Relationship between human development and disappearance of unusually large von Willebrand factor multimers from plasma.

von Willebrand factor (vWF) multimers were examined in fetal, umbilical cord, and neonatal platelet-poor plasma (PPP) specimens. Sixty-five of 65 (100%) fetal PPP samples aged less than 35 weeks and seven of ten (70%) fetal samples aged greater than 35 weeks had unusually large vWF (ULvWF) multimers. Thirty of 46 (65%) cord PPP samples from neonates ranging in gestational age from 34 to 41 weeks had ULvWF. There was no significant relationship between either gestational age at time of delivery or birth weight and likelihood of finding ULvWF multimers in cord PPP samples. No maternal PPP sample contained ULvWF multimers. Serial heelstick samples from 16 preterm and term neonates were analyzed for 8 weeks. ULvWF multimers disappeared from the PPP of ten of the neonates during this time. The PPP of four neonates had vWF patterns similar to those in normal adult PPP throughout the sampling period. The ULvWF multimeric forms of fetal and neonatal PPP samples were similar to those constitutively released from endothelial cells. They were not as slowly migrating in a very porous 0.5% agarose gel system as the ULvWF multimers released from Weibel-Palade bodies in response to the calcium ionophore A23187. A vWF protomer was present in 97% of fetal samples, 83% of cord blood specimens, and 11% of neonatal heelstick samples, but was not found in any maternal sample. These results indicate that control mechanisms operative in older children and adults to prevent circulation of ULvWF multimers and vWF protomeric forms are normally acquired late in uterine life or during the neonatal period. ULvWF multimers, which are normal components of fetal, most cord, and some neonatal plasma samples, may contribute to in utero and postnatal hemostasis.

Autoradiography↗

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor.

To investigate the effects of nifedipine on the human fetal circulation, 11 fetuses whose mothers were treated with nifedipine for treatment of preterm labor were studied. Maximum velocity waveforms were obtained in the middle cerebral artery (n = 8), renal artery (n = 6), ductus arteriosus (n = 8), and umbilical artery (n = 10). Transvalvular maximal velocity waveforms were obtained across the aortic (n = 11) and pulmonary (n = 7) valves. Maternal uterine arteries also were studied (n = 7). Doppler data were collected before and 5 hours after nifedipine therapy. Patients received an oral loading dose of 30 mg of nifedipine followed by a second oral dose of 20 mg 4 hours later. No significant difference in the flow velocity waveforms was found in the vessels studied 5 hours after the initial dose. These results suggest that short-term nifedipine therapy does not influence either fetal or uteroplacental circulation as evaluated with the Doppler technique.

Adolescent↗