Abnormal antenatal lung growth
Abnormal antenatal lung growth, which may result in pulmonary hypoplasia (incomplete lung development), is common: it has been reported to be present in 15– 20% of early neonatal deaths. The mortality rate is high, particularly if the abnormal growth has occurred either as a consequence of oligohydramnios with rupture of the membranes between 14 and 19 weeks of gestation, or in association with a congenital diaphragmatic hernia (CDH). It may be primary, but more usually occurs as a consequence of a variety of problems, which can largely be divided into those conditions that reduce intra-thoracic space, fetal breathing movements or amniotic fluid volume. It is also found in association with trisomy 18 and 21. Pulmonary hypoplasia may have a genetic basis, as the condition occasionally occurs in twins and families. Both pre- and post-natal malnutrition can adversely affect lung growth. Vitamin A is essential for normal alveolar development and vitamin A deficiency decreases alveolar septal development.
Determining whether a fetus has an important chromosomal abnormality is key to providing appropriate counselling to parents regarding antenatal intervention with the aim of promoting lung growth. In the first trimester, however, both amniocentesis and chorion villus sampling have been associated with an excess of infant respiratory symptoms and abnormal lung function at follow-up.
Antenatal interventions that aim to prevent abnormal antenatal lung growth include: amnio-infusion, which can facilitate ultrasound examination but has not been shown to improve lung growth; and thoraco-amniotic shunting, which results in effective drainage of pleural effusions, facilitating resuscitation, but is usually performed too late in pregnancy to influence lung growth. In utero surgical repair of CDH has been attempted, but a more promising technique is obstruction of the normal egress of fetal lung fluid by placing a balloon in the trachea.
Pre-natal antioxidant supplementation might be expected to influence fetal lung growth and development, and to reduce the oxidative stress implicated in the development of BPD. However, follow-up of infants entered into a randomised trial did not demonstrate improved infant respiratory outcome following maternal high-dose vitamin C and E supplementation.