Does an expanding fetal abdominal mass produce pulmonary hypoplasia?

Fetal pulmonary hypoplasia has been related to multiple factors. In an effort to define which fetuses may benefit from prenatal intervention to prevent or reverse pulmonary hypoplasia, we studied the relative contribution of an enlarging abdominal mass in the fetus. We produced abdominal masses in fetal rabbits at 24 days gestation by two methods. In one group, a small cylindrical chip of Takasen, (a synthetic polymer that expands to 50 times its size in 1 week; Grobeast, Pop Art Co, Cleveland, OH) was inserted into the peritoneal cavity of the fetal rabbit; in another group, the bladder neck was obstructed with a surgical clip. Amniotic fluid volume was restored at the surgical procedure. Sham-operated littermates served as controls. At cesarean delivery on day 30, fetal lung, liver, and body weights were measured, and the abdominal masses were quantitated by volume displacement of the removed mass or bladder. In both groups large abdominal masses of comparable size were produced. Newborns with the synthetic abdominal mass did not have significant pulmonary hypoplasia, but often had a prune belly deformity of the abdominal wall, whereas newborns with bladder obstruction had significant pulmonary hypoplasia. Liver weight was not significantly affected. We conclude that a fetal abdominal mass does not independently produce pulmonary hypoplasia, possibly because the "mass effect" is relieved by distension of the abdominal wall rather than elevation of the diaphragm; the pulmonary hypoplasia that occurs in bladder outlet obstruction is probably due to the associated oligohydramnios rather than the mass effect of the dilated urinary tract; and prenatal decompression of an abdominal mass or dilated urinary tract is not justified to prevent pulmonary hypoplasia in the absence of oligohydramnios.