Doppler umbilical artery studies in the twin-twin transfusion syndrome.

Eleven patients with twin pregnancies were identified as having twin-twin transfusion syndrome on the basis of like-sex twins with monochorionic placentation and umbilical venous blood hemoglobin differences exceeding 50 g/L at delivery. Umbilical artery velocity-time waveform studies had been performed in these pregnancies as part of a large series of 456 twin pregnancies. In all 11 cases, the systolic-diastolic (S-D) ratio differences between the twins were less than 1 unit (mean 0.4 +/- 0.2), indicating that in twin-twin transfusion, umbilical artery S-D ratios are concordant even in the presence of discordancy in fetal size.

Umbilical artery waveforms in triplet pregnancy.

Twenty patients with triplet pregnancies underwent continuous-wave Doppler ultrasound umbilical artery waveform studies as part of a multiple-pregnancy surveillance program. One or more infants was small for gestational age in nine of these triplet pregnancies. In all of these cases, at least one abnormal umbilical artery velocity waveform was present. Two infants were stillborn, and both had a grossly abnormal umbilical artery waveform (absent diastolic flow) recorded consistently for several weeks before fetal death. The use of umbilical artery Doppler studies may delineate those triplet pregnancies in which more intensive fetal surveillance is appropriate.

Reduced fetal platelet counts in pregnancies with abnormal Doppler umbilical flow waveforms.

Fetal and maternal platelet counts were correlated with antenatal assessment of the umbilical-placental waveform. Forty singleton pregnancies were studied using Doppler ultrasound, and placental resistance was categorized as normal or high according to the systolic/diastolic ratio. We performed platelet counts on maternal and cord blood taken at the time of cesarean section. The high-resistance group had a mean fetal platelet count (218 +/- 53 x 10(3)/microliters) significantly lower than that of the normal-resistance group (314 +/- 76 x 10(3)/microliters) (P less than .001). This difference was evident in both the hypertensive and nonhypertensive subgroups of the high-resistance group. There was no difference in mean maternal platelet counts between the high- and normal-resistance groups.

The effects of prostacyclin and thromboxane analogue (U46619) on the fetal circulation and umbilical flow velocity waveforms.

In placental insufficiency and pre-eclampsia the relative production rates of prostacyclin and thromboxane by the placenta and umbilical vessels are altered and the Doppler umbilical flow velocity waveform shows a high resistance pattern. To investigate the control of umbilical placental blood flow by those eicosanoids either prostacyclin (10 micrograms/min), or the thromboxane analogue U46619 (10 ng/min) was infused into the distal aorta of 12 chronically catheterized fetal lambs at day 125. Thromboxane produced a rise in mean arterial pressure and a rise in the systolic diastolic ratio of the umbilical artery flow waveform (2.6 to 3.1; P less than 0.05). Umbilical blood flow did not change and there was no evidence of altered flow to other organs. Prostacyclin caused a fall in fetal mean arterial pressure and a decrease in the umbilical artery systolic diastolic ratio (2.9 to 2.4; P less than 0.05). Prostacyclin produced a three-fold increase in lung perfusion (and the onset of fetal breathing movements) and this was associated with a 90% reduction in muscle blood flow (hindlimb muscle flow reduced from 12.5 to 1.1 ml.min-1 100g-1; P less than 0.01). We conclude that the local release of thromboxane in the fetal placental vascular bed could account for the rise in systolic diastolic ratio seen in umbilical placental insufficiency.