Stress and Fetal Lung Maturity

Dobbie, Henry Gordon (1987) Stress and Fetal Lung Maturity. MD thesis, University of Glasgow.

Abstract

It has been the clinical impression for many years that certain 'stressful' pregnancy complications appear to be associated with a generally improved neonatal outcome. The reason for this is unclear but is has been proposed that a hostile intrauterine environment may, perhaps as a result of relative hypoxia, promote the release of hormones such as cortisol and catecholamines. These hormones may facilitate the maturational processes, particularly in the lung, and so help to prepare the fetus for extrauterine life. Certainly, and despite advances in neonatal care, respiratory problems remain the most common cause of death in normally-formed live-born babies (Chamberlain et al 1975), being responsible for about 1500 deaths in England and Wales alone in 1980 (HMSO 1980). Even if the baby survives, however, the need for prolonged ventilatory support may lead to the development of bronchopulmonary dysplasia and other causes of chronic respiratory insufficiency (Levine and Dubowitz 1982, Tarrow-Mordi and Wilkinson 1986). Other problems such as intraventricular haemorrhage, patent ductus arteriosus and pneumothorax are also related to respiratory immaturity (Greenhough and Roberton 1985, Whittle et al 1986). The improvements in neonatal care have resulted in survival rates of over 88% for babies weighing greater than 1000 g in some units (Greenhough and Roberton 1985). In view of the excellent survival rates for the small baby, the obstetrician when faced with a difficult management problem not unnaturally has a low threshold for preterm delivery often, as is increasingly the trend, without prior assessment of fetal lung maturity. With more and more small babies receiving assisted ventilation, knowledge of the natural development of the respiratory system in the human fetus is essential. The aims of this thesis were: 1. To evaluate certain obstetric factors, considered to influence fetal lung maturity. 2. To investigate what controls respiratory maturity in the human fetus. 3. To evaluate human fetal adrenal cortisol and medullary activity from mid-trimester until term. The basis of the study centres on the concept of fetal stress in utero being the interlinking factor between the various obstetric problems and fetal lung maturity. However, many of the current ideas regarding human fetal lung development have been derived from animal experiments, the results of which may not be applicable to the human. A timetable of events can, however, be defined using a combination of animal and human data and a review of the current literature is contained in Chapters 2 and 3. Chapter 2 outlines what is currently known of the normal development of the human fetal lung. The anatomical, physiological and biochemical development are discussed and the evidence presented suggesting an important role for the fetal stress hormones cortisol and the catecholamines. A number of animal studies have suggested that corticosteroids can cause an induction of the enzymes involved in surfactant synthesis and that the catecholamines, especially adrenaline, facilitate the release of surfactant (the surface-active lung phospholipids) and the clearance of lung fluid at birth, all helping to optimise neonatal lung function. These animal expriments are supported by clinical studies suggesting a reduction in the incidence of respiratory problems following treatment of the pregnant mother with corticosteroids and various Beta sympathomimetic drugs. Various factors, both physiological and pathological, considered to influence fetal lung maturity in the human are discussed in Chapter 3, with regard to both clinical and biochemical lung maturity. In addition, the available evidence linking the obstetric factors with the human fetal adrenocortical and sympathoadrenal responses is presented. A total of 381 babies were investigated in this study, of which 189 were born at or prior to 35 weeks' gestation. Lung maturity was assessed clinically by the occurrence of the respiratory distress syndrome and the requirement for neonatal ventilation and biochemically by measurement of amniotic fluid phospholipids. The fetal stress responses were assessed by measuring, in blood sampled from the umbilical artery at birth, the cortisol, noradrenaline and adrenaline levels and pH. These measurements were also made in maternal venous blood at time of delivery. (Abstract shortened by ProQuest.).

• Item Type: Thesis (MD)
• Qualification Level: Doctoral
• Keywords: Medicine, Obstetrics
• Date of Award: 1987
• Depositing User: Enlighten Team
• Unique ID: glathesis:1987-77563
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 14 Jan 2020 09:05
• Last Modified: 14 Jan 2020 09:05
• URI: https://theses.gla.ac.uk/id/eprint/77563