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The ability of the fetus to survive outside of the uterus is greatly dependent on proper pulmonary function. Pulmonary surfactant is needed to reduce the surface tension of the air-liquid interface of the alveolar lining, so that alveoli don’t collapse upon expiration. Infants born with a deficiency of pulmonary surfactant are at increased risk of developing respiratory distress syndrome (RDS). The incidence of RDS is dependent on gestational age, with more RDS occurring in younger fetuses. For instance, the risk of RDS is 0% at 40 weeks, 2% at 36 weeks, and 8 to 23% at 34 weeks, depending on birth weight. RDS can occur at term, especially with Rh isoimmunization and maternal diabetes.

Surfactant is a complex mixture of lipids, proteins, and carbohydrates. Most of the lipids are phospholipids including lecithin (L), sphingomyelin (S), disaturated lecithin, phophatidyl inositol (PI), and phosphatidyl glycerol (PG). All of these phospholipids are manufactured by the fetal lung, possess surface tension activity, and are secreted into the amniotic fluid. Lecithin is present in the lung in the highest concentration, but must be stabilized by PI and/or PG to have maximal surface tension reducing activity. The relative concentrations of these phospholipids determine the degree of fetal lung maturity. The fetal risk of RDS can be estimated by measuring amniotic fluid phospholipid concentrations.

In early pregnancy, the concentration of lecithin is very small, while that of sphingomyelin is much greater. Lecithin begins to be secreted into amniotic fluid by the developing fetal lung between 24 and 26 weeks of gestation. At 30 to 32 weeks, lecithin concentration remains relatively low, less than or equal to sphingomyelin. PI concentration is also low at this time and PG is nonexistent. Subsequently, sphingomyelin concentration levels off and lecithin begins to increase, with an abrupt rise at 35 weeks. PI increases in parallel with lecithin until 35 weeks and subsequently declines. PG becomes detectable at 36 weeks. Fetal lung maturity is established during the 2 to 3 week interval when the L/S ratio increases to 2.2 or more, PI decreases, and PG becomes detectable. Because PG appears later in gestation, it is a good indicator of maturity (positive predictive value >95%). 

Generally, fetal lung maturity testing is not necessary when the gestational age is >39 weeks because fetal lungs are usually mature. Unfortunately, complications such as diabetes and Rh isoimmunization retard fetal lung development. Women with these complications may require testing. Testing is also not usually necessary when the gestational age is <30 weeks, because most fetuses are expected to have immature lungs. However, a number of disorders accelerate pulmonary maturity including maternal hypertension, preeclampsia, HELLP syndrome, premature rupture of the membranes, intrauterine growth restriction, maternal smoking and drug use, and maternal hemoglobinopathies. Women with one of these complications and preterm labor or premature rupture of the membranes may require testing. 

The Abbott TDX Fetal Lung Maturity II (FLM II) test was introduced in January 2001. This is a rapid automated fluorescence polarization assay based on the partitioning of a fluorescent dye between the surfactant particles and albumin present in amniotic fluid. Because the dye is a synthetic derivative of lecithin, it has solubility and binding characteristics comparable to surfactant phospholipids. The surfactant particles have a relatively small size and rotate freely during the interval between absorption of polarized light and emission of fluorescent light, resulting in a high degree of fluorescence depolarization. Conversely, the much larger albumin molecules do not rotate as rapidly and, therefore, absorb and emit polarized light in the same plane. The degree of net polarization is proportional to the surfactant to albumin (S/A) ratio. For example, a specimen with low amounts of surfactant relative to albumin exhibits high net polarization because rotation of albumin molecules is slower than rotation of surfactant molecules. In contrast, a specimen with high amounts of surfactant relative to albumin has low net polarization.

Albumin concentration remains relatively stable during the third trimester, providing an internal standard that compensates for changes in amniotic fluid volume. The final result is expressed as mg of surfactant per g of protein. Lungs are considered immature if the S/A is <35 mg/g and mature if S/A is >55 mg/g. Indeterminate lung maturity status is indicated if S/A is between 35 and 55 mg/g. The results of our study indicated that an FLM-II value of 55 mg/g or greater correlated perfectly with an L/S ratio of 2.2 or greater. 

Insulin dependent diabetes delays fetal lung development. Fetuses of mothers with insulin dependent diabetes mellitus need to have PG levels >2% to ensure lung maturity, because RDS may develop in spite of a mature L/S ratio, a high percentage of disaturated lecithin, and high PI.   

Fifteen mL of specimen is necessary to perform both FLM-II and the fetal lung profile. If insufficient volume is received, only the FLM-II will be performed. Frozen specimens can be tested by FLM-II if they have not been centrifuged and are less than 72 hours old. 

The reference ranges for nondiabetic and diabetic patients are listed in the following table.

Unfortunately, Abbott Diagnostics has discontinued the this test. Today, most hospital laboratories have replaced it with Lamellar Body Counts.