Ventricular volume overload in the human fetus: observations from fetal echocardiography.

We examined two groups of fetuses in which echocardiography had been performed and in which ventricular volume overload eventually led to fetal hydrops. The first group (18 fetuses) had atrioventricular valve regurgitation and almost all of the fetuses had structural heart disease. No fetus in this group survived the neonatal period; only two of the pregnancies in this first group were terminated. A second group of three fetuses had ventricular volume overload from sacrococcygeal teratomas at 21 to 24 weeks' gestation. These fetuses also had nonimmune hydrops (or it developed), but they did not have structural heart disease or atrioventricular valve regurgitation. Combined ventricular output in this group was calculated by Doppler ultrasound to be greater than twice the normal output for fetuses of the expected gestational weight. The proportion of the combined output to the lower body and the placenta was increased with the increase to the teratoma, exceeding the increase to the placenta. In one fetus, serial study demonstrated increasing output and the development of hydrops. Intrauterine surgery was undertaken to control the high output failure. The abnormal variables tended to revert to normal after replacement of blood loss, and the hydrops disappeared. The pregnancy continued until the spontaneous rupture of membranes at 26 weeks' gestation forced delivery by cesarean section. The infant died from severe hyaline membrane disease. These findings suggest that, in some circumstances, fetal hydrops is a late sign of cardiac failure and heralds incipient death.(ABSTRACT TRUNCATED AT 250 WORDS)