Physiology of fetal lung fluid clearance and the effect of labor.
Respiratory morbidity in near term (> or =34 and <37 weeks) infants delivered spontaneously or by elective cesarean section (ECS) has been well documented in the literature, and accounts for a significant number of admissions to intensive care units among these neonates. Given the high rates of near-term deliveries in the USA and worldwide, the public health and economic impact of morbidity in this subgroup is considerable. Causes of respiratory distress include transient tachypnea of the newborn (TTNB), surfactant deficiency, pneumonia, and pulmonary hypertension. There is considerable evidence that physiologic events in the last few weeks of pregnancy coupled with the onset of spontaneous labor are accompanied by changes in the hormonal milieu of the fetus and its mother, resulting in rapid maturation and preparation of the fetus for delivery and neonatal transition. A surge in endogenous steroids and catecholamines accompanies term gestation and spontaneous vaginal delivery, and is responsible for some of the maturational effects. Rapid clearance of fetal lung fluid clearance plays a key role in the transition to air breathing. The bulk of this fluid clearance is mediated by transepithelial sodium reabsorption through amiloride-sensitive sodium channels in the alveolar epithelial cells with only a limited contribution from mechanical factors and Starling forces. Disruption of this process can lead to retention of fluid in air spaces, setting the stage for alveolar hypoventilation. When infants are delivered near-term, especially by cesarean section (repeat or primary) before the onset of spontaneous labor, the fetus is often deprived of these hormonal changes, making the neonatal transition more difficult. This chapter discusses the physiologic mechanisms underlying fetal lung fluid absorption and explores potential strategies for facilitating neonatal transition.
Jain
Lucky
L
Emory University School of Medicine, Atlanta, GA 30322, USA.
Eaton
Douglas C
DC
D000818:Animals; D001826:Body Fluids / Q000502:physiology*; D002585:Cesarean Section; D005260:Female; D005325:Fetal Organ Maturity / Q000502:physiology*; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000502:physiology*; D007743:Labor, Obstetric; D008168:Lung / Q000502:physiology*; D011247:Pregnancy; D011650:Pulmonary Alveoli / Q000502:physiology; D011653:Pulmonary Diffusing Capacity / Q000502:physiology; D011654:Pulmonary Edema / Q000503:physiopathology; D012127:Respiratory Distress Syndrome, Newborn / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D012964:Sodium / Q000378:metabolism
D005938:Glucocorticoids; D012964:Sodium