Low amniotic pressure in oligohydramnios-Is this the cause of pulmonary hypoplasia? Umberto Nicolini, MD, Nicholas M. Fisk, MD,* Charles H. Rodeck, MD, David G. Talbert, PhD, and Jonathon S. Wigglesworth, MD London, England The mechanism by which oligohydramnios produces lung hypoplasia is not understood. The current theory that extrinsic compression of the fetal thorax causes hypoplasia, either by inhibiting breathing movements or by squeezing out lung liquid, is not supported by observational or experimental data, or by our finding of decreased amniotic pressure around the fetus in oligohydramnios. We hypothesize that lung hypoplasia results from excess loss of lung liquid because of a reduction in amniotic pressure, and hence an increase in the alveolar-amniotic pressure gradient. The magnitude of this increased pressure gradient is calculated to exceed the small standing tracheal pressure; thus low amniotic pressure overcomes the normal laryngeal retentive mechanisms and allows a larger quantity of lung liquid to escape. In the prevention of pulmonary hypoplasia, a role is suggested for the instillation of artificial amniotic fluid to restore normal amniotic pressure. (AM J OSSTET GVNECOL 1989;161:1098-101.) Key words: Pulmonary hypoplasia, oligohydramnios, amniotic fluid, lung liquid Lung hypoplasia is a m<u or cause of neonatal mor- tality and morbidit y. Although its pathophysiology is poorly understood , known predisposing factors include oligohydramnios, diaphragmati c hernia , hydrothorax , skeletal dysplasias, and neuromu scular disorders. No sing le theory adequately explains lung hypoplasia in such a wide range of conditions. Oligohydramnios, the most common association, is thought to cause lung hy- popla si a by extrinsic compression of the fetal thorax. Alternatively, extrinsic compre ssion of the abdomen mi ght produce upward pressure on the diaphragm, and hence lung compression and hypoplasia. This con- cept of fetal compression by the uterine wall is sup- po rted by other sequelae of oligohydramnios such as talipes, Potter's facies, and a rthrogryposis. However, it fa il s to explain the selective effect of compression on the lung. Other fetal viscera are presumably similarly compressed, yet their growth is unimpaired. There- fore there appears to be a specific effect on lung de- velopment. Current theories on the cause of pulmonary hypoplasia Fetal breathing movements. Inhibition of fetal bre athing movements has been suggested to predict pulmonary hypoplasia in the presence of oligohydram- nios.l Fetal breathing movements may promote lung From the Royal Postgraduate MedIcal Schoo l, Institute of Obstetncs and Gynaecology, Queen Charlotte's and Chels ea HospItals. R eprints not available. *Dr. Fisk was supported by a Glad ys Dodds FellowshIP from the College of Obstetn aanJ and Gynaecologzsts. 611113061 1098 growth by cyclic expansion and retraction of pulmo- nary parenchyma . Certainly, lung hypoplasia occurs with lack of fetal breathing movements in experimental animals" and fetal neuromuscular disease. 3 Conversely, a mechanism by which oligohydramnios might inhibit fetal breathing movements remains obscure. Extrinsic compression is not a probable explanation because the thor acic component of fetal breathing movements is minor compared with the diaphragmatic excursion. Furthermore, experimentally both oligohydramnios and inhibition of fetal breathing movements have been shown to be additive, not alternative, insults to lung development.' Pulmonary hypoplasia after oligohy- dramnios has a histologic appearance that is distinct from other conditions in which inhibition of fetal breathing movements appears to be the mechanism.' Fina lly, more recent reports suggest that lung hypo- plasia associated with oligohydramnios may be unre- lated to the presence or absence of fetal breathing movements." Lung fluid. Lung liquid acts as an internal stent around which the lung develops, a nd its reduction im- pairs lung growth.'· 7. 8 In fetal sheep , chronic tracheal dr ainage causes lung hypoplasia,'· 8 whereas tracheal ligation prevents it by blocking egress of fluid. 7 Laryn- geal atresia causes an increase in alveolar number and lung volume and, as seen in Fraser's syndrome, the resulting lung liquid retention allows normal pulmo- nary development despite the coexisting oligohydram- nios caused by renal agenesis ." Reduction in lung liquid volume may result from failure of retention, increased outflow, or both. Fluid normally escapes into the am- niotic cavity at a rate that is three to eight times higher