Clearance of Fluid From Airspaces of Newborns and Infants

Abstract

After completing this article, readers should be able to: 1. Describe fetal lung fluid secretion, its application on lung development, and its reabsorption immediately after birth. 2. List the primary cellular mechanism responsible for lung fluid absorption. 3. Describe clinical conditions in newborns and infants associated with impaired sodium transport. 4. Describe how sodium transport can be influenced by fetal lung maturity. When the airspaces of the lungs are filled with fluid, normal gas exchange cannot take place, and there is marked respiratory distress and the need for intensive care. This occurs in only two situations: failure to clear fetal lung liquid at birth and leakage of fluid from the vasculature filling the alveoli (alveolar pulmonary edema). Fluid that is secreted into the fetal airspaces to enable normal lung development must be absorbed at the time of birth for a normal transition from fetal to postnatal life. Failure to do so can lead to two well-known clinical syndromes: transient tachypnea of the newborn (TTN) and when there is coexistent relative surfactant deficiency, neonatal respiratory distress syndrome (nRDS). Pulmonary edema can be caused postnatally by many disorders; those that occur frequently during the neonatal period are patent ductus arteriosus or structural congenital heart disease with marked left-to-right shunting. It is not only biologically reasonable to assume that clearance of such airspace fluid would be beneficial to the patient, but studies in adults suffering from pulmonary edema have shown that the lung’s ability to clear such fluid correlates with survival. In this article, we review how the epithelium of the lung uses the active transport of sodium (Na+), followed by chloride (Cl−) and water, from the apical to basolateral side of the alveolar lining cells to clear fluid and how the underlying mechanisms for active Na+ transport are influenced by the degree of …