The fetal lungs are the last organ system to “mature” so that survival outside the womb is possible. Maturity involves several components. First, there must be sufficient surface area within the lung to allow sufficient exchange of gases (oxygen in and carbon dioxide out) to support metabolic functions. This is accomplished by millions of small sacs called alveoli that give the lungs a sponge-like appearance. Second, the alveoli must develop to the point that the inner lining of cells (epithelial cells) that come in contact with inspired air are very thin – gas exchange can only occur over a short distance between the blood vessels in the alveoli and the air that fills the alveoli. Third, the alveoli must be able to remain open so that the air can get into them and gas exchange can take place. The first two events are generally quite complete by about 32-34 weeks, however, the third is the most essential component from that point on and it is the focus of our fetal lung maturity testing as we shall explain.
Alveoli are like little bubbles. The laws of physics predict that because of the high ratio of surface tension to volume of little bubbles, their tendency is to collapse. To prevent this from happening, certain cells in the lungs – the type II alveolar cells – begin to excrete chemicals that can reduce the surface tension in the alveoli. These chemicals are called ‘surfactants’ and they are a complex combination of phospholipids and apoproteins. When sufficient surfactants are produced that the alveoli can remain open to function, the fetal lungs are considered ‘mature’. Prior to this time, the baby is at risk for developing respiratory distress syndrome (RDS). RDS occurs in about 1% of all pregnancies and it can have serious short- and long-term consequences, involving both the lungs and other organs, that can extend beyond the neonatal period in its most severe forms.
When babies are very premature, RDS is the result of a combination of both alveolar epithelial cell immaturity (the lining cells have not yet thinned out) and a deficiency of surfactants. Later in pregnancy (“near term”), severe RDS can sometimes also occur but at this point it is usually the result of insufficient surfactants alone – but the end result can be just as devastating. Certain medical conditions can delay surfactant production in babies, the most common being maternal diabetes with poor blood sugar control and isoimmunization (such as Rh-disease). Large babies (macrosomic) are also at greater risk for RDS even if maternal diabetes is not contributing to the fetal size. Babies who have developed heart failure (hydrops fetalis) for any number of reasons can also have a relative deficiency of surfactants (as well as pulmonary edema). For reasons that are not entirely clear, babies delivered by cesarean section, particularly, when this is done prior to the onset of labor, are also at increased risk for respiratory difficulties.
The amniotic fluid is mostly fetal urine, but it is mixed with effluent from the fetal lungs as well. The fluid from the fetal lungs contains surfactants and other indicators of type II alveolar cell activity. When we perform an amniocentesis to assess fetal lung maturity, we are looking for direct and/or indirect evidence to support the presumption that there is adequate surfactant present to minimize the risk for RDS. One should realize that all of the tests we will discuss have some degree of “false positivity” – an indicator suggesting lung maturity, but the baby still develops respiratory problems – however, there is enough experience with their use that a “mature” value with a test result generally means the baby has at least a 95% chance of not developing RDS.
Having provided this information as background, the actual tests commonly used to evaluate fetal lung maturity will be discussed in our next post….