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Lecithin Sphingomyelin Ratio

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). Neonatal RDS is characterized by increased work of breathing, fetal acidosis, the need for supplemental oxygen, and surfactant replacement therapy. 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. The fetal risk of RDS can be estimated by performing a fetal lung maturity profile.

Surfactant is a complex mixture of lipids, proteins, and carbohydrates. Most of the lipids are phospholipids including lecithin (L), sphingomyelin (S), disaturated lecithin, phosphatidyl 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. Lecithin must be stabilized by PI and/or PG to have maximal surface tension reducing activity. The relative concentrations of these phospholipids determine the state of fetal lung maturity. The L/S ratio and percentages of PI, PG, and disaturated lecithin are determined by two dimensional thin layer chromatography and reflectance densitometry.

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. Around 32 to 33 weeks gestation, lecithin and sphingomyelin concentrations are about equal. Subsequently, lecithin begins to increase, with an abrupt rise at 35 weeks. Lecithin continues to steadily increase until term. Sphingomyelin concentrations level off at 32 weeks and begin to decrease. PI increases in parallel with lecithin until 35 weeks and subsequently declines. PG becomes detectable at 36 weeks.In the mature lung, lecithin comprises 50 to 80% of the total surfactant lipid. Fetal lung maturity occurs during the 2 to 3 weeks period when the L/S ratio increases to 2.0 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%).

Results are interpreted as follows:

Immature

Premature

Inter-

mediate

Caution

Mature

Mature

Post

Term

Post Maturity

L/S

<1.0

1.0 - 1.5

1.5 - 1.9

2.0 - 2.2

2.5 - 3.8

5.2

8.0

% Disat L

10 - 40

<40 - 40

40 - 50

>50

>50

>50

>50

% PI

Trace - 5

5 - 12

12 - 20

20 - 25

20 - 15

15 - 10

10 - 5

%PG

0

0

0

0-2

2 - 10

10 - 12

12 - 15

Weeks

26 - 30

30 - 34

34 - 35

35 - 36

37 - 40

41 - 42

>42

An L/S ratio greater than 2.2 is considered mature. The combination of an L/S ratio >2.2, >50% disaturated lecithin, a high percentage of PI, and the presence of PG usually indicates maturity.

Diabetes delays development of the fetal lung. Fetuses of mothers with 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.

Generally, fetal lung maturity testing is not necessary when the gestational age is >37 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.

Bloody samples give inaccurate L/S ratios, because whole blood has an L/S ratio of 1.5 and plasma has a ratio of 1.6. A high L/S in a bloody sample usually indicates maturity, but a ratio close to 2 is unreliable and uninterpretable. Meconium has an L/S ratio of 1.2 and causes falsely low L/S ratios. Samples contaminated by urine, indicated by a creatinine value >5 mg/dL, are not acceptable. Specimens left for long periods of time at room temperature may have falsely decreased lecithin because of phosphodiesterases in the amniotic fluid. Vaginal pool specimens yield inaccurate results if they are often contaminated with mucus, cellular debris, or bacteria.

Specimen requirement is 15 mL (5 mL minimum) of amniotic fluid. Specimen should be placed in ice immediately after collection.

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