In congenital diaphragmatic hernia (CDH) pulmonary hypoplasia is variable depending on the size of the diaphragmatic defect and the amount and timing of visceral herniation. In CDH pulmonary hypoplasia may arise from loss of lung fluid, decreased fetal breathing secondary to diaphragmatic dysfunction, and decreased intrathoracic volume. The lungs in CDH appear to be arrested in the saccular phase of development with poorly developed airspaces and thickened interalveolar septums. Pulmonary hypoplasia and decreased lung compliance contribute to the increased susceptibility to ventilation-induced lung injury seen in CDH. Persistent pulmonary hypertension of the newborn is the failure of the normal circulatory transition after birth. Four major components of surfactant proteins have been identified: surfactant protein A and D are hydrophilic and protein B and C are hydrophobic. A surfactant deficiency is clearly seen in the experimental lamb model of CDH.

This chapter first discusses the measurement of amniotic fluid and the technique of measuring the depth of amniotic pool. It then describes the causes, diagnosis, and treatment of both polyhydramnios and oligohydramnios. Amniotic fluid can be semi-quantified reliably using two-dimensional ultrasound measurement of the depth of amniotic pocket and presented with amniotic fluid index (AFI) or maximum vertical pool or pocket (MVP). Combination of clinical and ultrasound assessment often allows accurate diagnosis of the underlying causes of oligohydramnios and polyhydramnios, which are heterogeneous and are usually not treatable or reversible prenatally. The aim of management is to prevent the adverse consequences resulting from extreme deviations of amniotic fluid volume. In polyhydramnios, serial amnioreduction may help to relieve the maternal pressure symptoms. In oligohydramnios caused by ruptured membranes, serial amnioinfusion may be considered to prevent pulmonary hypoplasia. Both interventions are only supported by small and uncontrolled observational studies.