Pulmonary function in premature infants. Rupture of the amniotic membranes.

Abstract

Recent studies in animals have suggested that antenatally administered steroids may accelerate fetal lung maturation and prevent the development of respiratory distress following premature delivery [7, 13, 16, 18, 21, 23]. Further studies in human pregnancies complicated by premature rupture of the amniotic membranes [l, 3, 4,19, 24], in trauterine growth retardation [6], or maternal heroin addiction [22] have all been consistent with the hypothesis that an intrauterine stress may promote secretion of cortisone by either the mother or fetus and hasten the development of pulmonary surfactant, thereby reducing the incidence of hyaline membrane disease. Such Stresses are not without risks to the fetus. In particular, the fetus exposed to the risk of prolonged rupture of the amniotic membranes is an increasing risk of infection as the time between rupture of the amniotic membranes and delivery lengthens [11, 20]. In such cases the perinatologist must weigh and balance the risks of prematurity, hyaline membrane disease, and infection against the possible benefits of increased maturity at birth, particularly in terms of pulmonary function. The purpose of the present investigation was to apply Standard techniques of pulmonary function testing to a group of premature infants to determine whether or not prolonged rupture of the membranes had any significant effect on pulmonary function. Curriculum vitae