he importance of amnionic fluid volume estimation is indicated by its inclusion into virtually all schemes in which fetal health is assessed (Ff0en, 2008). This is based on the rationale that diminished utero placental perfusion may lead to lower fetal renal blood low, decreased urine production, and ultimately, oligohydramnios (Chap. 11, p. 231). The American College of Obstetricians and Gynecologists (2016) concludes that data available from randomized trials indicate that the use of the deepest vertical pocket measurement, as opposed to the AFI, to diagnose oligohydramnios is associated with a reduction in unnecessary interventions without an increase in adverse perinatal outcomes (Nabhan, 2008; Reddy, 2014).
restricted fetuses, several fetal vascular circuits including the umbilical artery, middle cerebral artery, and ductus venosus have been evaluated as diagnostic tools for fetal well-being (Chap. 44, p. 854). Maternal uterine artery Doppler velocimetry has also been assessed as a modality to predict placental dysfunction, with the goal to balance stillbirth against the risks of preterm delivery (Ghidini, 2007). Even the efects of sildenail in pregnant sheep have been evaluated using Doppler velocimetry (Alanne, 2017). he rationale is that sildenafil would improve placental blood low in the presence of placental insuiciency. This proved untrue, as sildenail was associated with detrimental efects on fetal cardiovascular dynamics.
Waveforms were irst studied in the umbilical arteries late in pregnancy, and abnormal waveforms correlated with placental villous hypovascularity. Of the small placental arterial channels, 60 to 70 percent need to be obliterated before the umbilical artery Doppler waveform becomes abnormal. Such extensive placental vascular pathology has a major efect on fetal circulation. According to Trudinger (2007), because more than 40 percent of the combined fetal ventricular output is directed to the placenta, obliteration of placental vascular channel increases aterload and leads to fetal hypoxemia. This in turn leads to ventricular dilation and redistribution of middle cerebral artery blood low. Ultimately, pressure rises in the ductus venosus due to afterload in the right side of the fetal heart (Baschat, 2004). Clinically, abnormal Doppler waveforms in the ductus venosus are a late inding in the progression of fetal deterioration due to chronic hypoxemia.
he umbilical artery systolic-diastolic (SID) ratio is considered abnormal if it is >95th percentile for gestational age or if diastolic low is either absent or reversed (Chap. 10, p. 213). Absent or reversed end-diastolic low signiies greater impedance to umbilical artery blood low (Fig. 44-8, p. 854). It is reported to result from poorly vascularized placental villi and is seen in extreme cases of fetal-growth restriction (T odros, 1999). According to Zelop and colleagues (1996), the perinatal mortali ty rate for absent end-diastolic flow was about 10 percent, and for reversed end-diastolic low, it approximated 33 percent.
Spinillo and associates (2005) studied neurodevelopmental outcome at 2 years of age in 266 growth-restricted fetuses delivered between 24 and 35 weeks' gestation. Of infants who had shown absent or reversed umbilical artery low, 8 percent had evidence of cerebral palsy compared with 1 percent of those in whom Doppler low had been normal.