Is fetal thoracic compression really the underlying mechanism of lung hypoplasia in oligohydramnios? An experimental...

Compression of the fetal thorax by the uterine wall is one of the theories proposed to explain the mechanism of lung hypoplasia in association with oligohydramnios. However, the reduction in the intrathoracic space and the evidence of compression on the fetal thorax have not been demonstrated in detail. Therefore an experimental study was planned to determine the effects of oligohydramnios on available intrathoracic space and lung volume in the rabbit fetus. Amniotic fluid was shunted into the peritoneal cavity between 23 and 31 days of gestation. Intrathoracic space and lung volumes (TV and LV), and lung and body weight (LW and BW) values were measured in our study and control fetuses at term. Lung weight/body weight, lung volume/thorax volume, thorax volume/body weight ratios were calculated and the values of the fetuses with shunting and controls were compared. The difference between TV/BW ratios was not significant. LW/BW and LV/TV ratios were significantly reduced in experimental fetuses compared to the controls. Chronic drainage of amniotic fluid into the peritoneal cavity resulted in reduced LW/BW and LV/TV ratio, but did not effect TV/BW ratio. The low LV/TV ratio in the fetuses with shunting despite similar TV/BW ratio suggested that the diaphragm had been elevated. This is also an explanation for the observation of reduced chest circumference and chest circumference/abdominal circumference ratio in prolonged premature rupture of the membranes in vivo. The developing fetal lungs would undergo not only transthoracic but also trans-abdomino-diaphragmatic compression. However, it is unlikely in the tubular shaped rabbit uterus. In oligohydramnios amniotic fluid dynamics or physical characteristics with its contents should be disturbed. A previous experimental study with herniation of the amniotic sac causing lung hypoplasia through reduced intraamniotic pressure without oligohydramnios also questioned the role of fetal compression. Although fetal lung development was significantly impaired, the thoracic cage was not affected by amniono-peritoneal shunting. Therefore, we suggest that lung hypoplasia resulted from another mechanism rather than thoracic compression.