Umbilical pressure measurement in the evaluation of nonimmune hydrops fetalis.

OBJECTIVE

Nonimmune hydrops fetalis continues to have a perinatal mortality rate > 50%. Although many abnormalities are associated with nonimmune hydrops fetalis, the direct mechanism by which the hydrops occurs is often obscure, even after delivery. There are at least three possible mechanisms for hydrops: heart failure (whether primary or a secondary effect of obstructed venous return), lymphatic malformation, and liver or peritoneal disease. The development of safe access to the fetal circulation by cordocentesis allows for the measurement of the umbilical venous pressure, which is closely related to the fetal central venous pressure. The premise that nonimmune hydrops fetalis of cardiac origin could be distinguished from that of noncardiac origin was examined by measuring the umbilical venous pressure.

STUDY DESIGN

Umbilical venous pressure was measured during indicated diagnostic cordocentesis in three groups of fetuses: 20 with nonimmune hydrops fetalis, four with a cardiac malformation but without nonimmune hydrops fetalis, and eight with immune hydrops (fetal hemolytic disease). In 16 of 20 fetuses with nonimmune hydrops fetalis the serum total protein and albumin concentrations were also measured.

RESULTS

Presumed inadequate cardiac output, as indicated by an elevated umbilical venous pressure, was the mechanism of nonimmune hydrops fetalis in 13 of 20 (65%). The pathologic condition included arrhythmia, cardiothoracic abnormalities, severe polycythemia and hyperviscosity, viral infection, and severe anemia. Successful antenatal treatment normalized the umbilical venous pressure. Nonimmune hydrops fetalis secondary to noncardiac mechanisms did not progress in severity and was not amenable to antenatal therapy. Hypoproteinemia and hypoalbuminemia were found in only six of 16 cases and were similarly distributed between cardiac and noncardiac mechanisms.

CONCLUSIONS

This is the first report where the measurement of umbilical venous pressure was applied to the evaluation of nonimmune hydrops fetalis. Cardiac dysfunction was the most common mechanism causing hydrops. The finding of a normal umbilical venous pressure greatly reduces the likelihood that the heart is the cause of the hydrops, even when there is a coexistent heart malformation. This immediate information allows the practitioner either to focus on therapeutic interventions that might lower the umbilical venous pressure or to look for noncardiac causes for the hydrops.