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Fetus lung maturation

Lung maturation in the fetus is regulated by the fetal secretion of cortisol. Treatment of the mother with large doses of glucocorticoid reduces the incidence of respiratory distress syndrome in infants delivered prematurely. When delivery is anticipated before 34 weeks of gestation, intramuscular betamethasone, 12 mg, followed by an additional dose of 12 mg 18-24 hours later, is commonly used. Betamethasone is chosen because maternal protein binding and placental metabolism of this corticosteroid is less than that of cortisol, allowing increased transfer across the placenta to the fetus. [Pg.884]

Prenatal glucocorticoid therapy to enhance fetal lung maturation reduces neonatal morbidity and mortality. However, adverse effects of serial courses of betamethasone on mother and fetus can occur. [Pg.41]

Thyroid hormones also accelerate fetal lung maturation. Fetal thyroid hormone levels may be increased by antenatal administration of thyrotropin-releasing hormone (TRH), a tripeptide that crosses the placental barrier, stimulates fetal pituitary production of thyroid stimulating hormone (TSH), and which, in turn, increases fetal thyroid hormone production (Chapter 33). This indirect method of enhancement of fetal thyroid hormone production is utilized because thyroid hormones do not readily cross the placental barrier. Insulin delays surfactant synthesis and so fetal hyperinsulinemia in diabetic mothers may increase the incidence of RDS even in the full-term infant. Androgen synthesized in the fetal testis is the probable cause of a slower onset of surfactant production in male fetuses. Prophylactic, or after onset of RDS, administration of synthetic or natural pulmonary surfactants intratracheally to preterm infants improves oxygenation and decreases pulmonary morbidity. [Pg.408]

Fetal lung maturation can be accelerated with antenatal corticosteroids. The National Institutes of Health (NIH) consensus conference in 1994 concluded that all fetuses between 24 and 34 weeks gestation at risk for preterm delivery should receive corticosteroids regardless of gender, race, maternal infection, and availability of surfactant. A report by the National Institutes of Child Health and Development Neonatal Research Network noted that antenatal steroid use was associated with fewer pulmonary problems and mortality. Many women who are appropriate candidates are... [Pg.559]

This is the scientific rationale for administering corticosteroids. They are administered to a client who is in preterm labor because they accelerate lung maturation, resulting in surfactant development in the fetus. [Pg.191]

Functional Development of the Fetus The fetal organs mature during the third trimester but not at the same rate. This section reviews the lung, liver, kidneys, and blood development of the fetus. [Pg.2159]

During labour, the fetus can tolerate some degree of hypoxia and acidosis. The first respiratory movements inflate the lungs, and if they arc mature and have adequate surfactant, there is a tenfold reduction in pulmonary vascular resistance. Gaseous exchange is quickly established. so that PO, ri.ses and PCO, falls. [Pg.64]


See other pages where Fetus lung maturation is mentioned: [Pg.884]    [Pg.1264]    [Pg.202]    [Pg.916]    [Pg.917]    [Pg.1417]    [Pg.260]    [Pg.519]    [Pg.869]    [Pg.2153]    [Pg.2156]    [Pg.15]    [Pg.681]    [Pg.809]    [Pg.681]    [Pg.836]    [Pg.185]    [Pg.2660]    [Pg.978]    [Pg.477]    [Pg.1135]    [Pg.89]    [Pg.198]    [Pg.531]   
See also in sourсe #XX -- [ Pg.558 , Pg.560 ]




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