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Fetal lung maturity testing: the end of an era

Respiratory distress syndrome is a major cause of neonatal morbidity and mortality that is most commonly caused by a deficiency in lung surfactant in premature infants. Therefore, laboratory tests were developed to measure the presence and/or concentration of lung surfactant in amniotic fluid in order to estimate maturity of the fetal lung. Although these tests were once widely employed, their utilization by physicians has decreased in recent years. Several studies have shown that demonstration of a mature fetal lung index by antenatal testing does not improve neonatal outcomes. Instead, decreased respiratory and nonrespiratory morbidities are most highly correlated with gestational age of the fetus. Therefore, fetal lung maturity testing may have passed the point of being clinically useful. Keywords:  amniotic fluid • fetal lung maturity testing • lamellar body count • respiratory distress syndrome • surfactant

Fetal lung development The development of the human lung is a highly regulated process that begins at just 3 weeks of gestation and continues through 8 years of age [1] . The final stages of development prepare the lung for its role as a gas exchange organ. Between weeks 24 and 38 of gestation, alveolarization begins to occur at the terminal branches of the developing lung and type II pneumocytes start producing pulmonary surfactant, a lipoprotein mixture that regulates surface tension at the air–liquid interface [2] . Lung surfactant production & function Pulmonary surfactant consists of lipids and proteins that are assembled in the endoplasmic reticulum and Golgi apparatus of type II pneumocytes and are packaged into secretory granules called lamellar bodies. After exocytosis into the alveolar space, lamellar bodies unfold into a structure known as tubular myelin, which supplies the lipids necessary for regulation of surface tension in the lungs. This surface tension is essential to maintain

10.2217/BMM.14.7 © 2014 Future Medicine Ltd

Melanie L Yarbrough1, David G Grenache2 & Ann M Gronowski*,1 Department of Pathology & Immunology, Washington University School of Medicine, St Louis, MO 63110, USA 2 Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112, USA *Author for correspondence: Tel.: +1 314 362 0194 Fax: +1 314 362 1461 gronowski@ wustl.edu 1

airway patency and support the elastic recoil of the airways during respiration. Phospholipids constitute approximately 90% of the composition of surfactant. The principal phospholipids present in surfactant arelecithin (also known as phosphatidylcholine) and phosphatidylglycerol (PG), while phosphatidylinositol and sphingomyelin are present in much lower abundance [3] . The synthesis of lecithin gradually increases from 28 weeks of gestation until birth, with the highest production occurring at week 36. Similarly, phosphatidylinositol first appears at 28 weeks of gestation, but reaches peak production between 32 and 35 weeks. PG is the last phospholipid to be produced, making its first appearance in surfactant at 36 weeks and continuing to rise until birth [4] . A primary function of lung surfactant is to decrease surface tension at the air–liquid interface in the lungs. Highly polar water molecules at the interface experience large forces of attraction that increase surface tension. The amphipathic properties of surfactant phospholipids permit the formation of a film at the air–liquid interface that lowers the

Biomarkers Med. (2014) 8(4), 509–515

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ISSN 1752-0363

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Review  Yarbrough, Grenache & Gronowski surface tension of water, allowing the alveoli to expand and contract during gas exchange without collapsing [5] . Respiratory distress syndrome Pulmonary surfactant deficiency due to prematurity is the most common cause of respiratory distress syndrome (RDS) in newborns. The lack of surfactant results in higher surface tension, causing collapse of small alveoli and overinflation of large alveoli. This leads to atelactasis that results in perfused but unventilated alveoli that contribute to hypoxia, hypercapnia and acidemia. The resulting ischemia in the lungs leads to a secondary surfactant deficiency that further exacerbates the condition [6] . The incidence of RDS decreases with increasing gestational age. Therefore, the risk of RDS is highest in premature infants, with the likelihood >60% at 29 weeks, 20% at 34 weeks and

Fetal lung maturity testing: the end of an era.

Respiratory distress syndrome is a major cause of neonatal morbidity and mortality that is most commonly caused by a deficiency in lung surfactant in ...
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