Aetiological factors in the respiratory distress syndrome of the newborn

Previous investigations into the respiratory distress syndrome have established that the infants lack pulmonary surface active factor, and thus alveolar stability. Inactivation or greatly reduced production of this substance is more likely than congenital absence. The extensive atelectasis which ensues leads to decreased lung compliance, ventilatory insufficiency, vascular shunts and respiratory and metabolic acidosis. It has been shown to be largely a condition of premature gestation, and significant associations found with antepartum haemorrhage, maternal diabetes, birth asphyxia and the male sex. Largely as the result of animal studies on the pulmonary circulation, and the experimental production of respiratory distress, prenatal asphyxia has been postulated as a likely cause. An analysis has been made of maternal and infant factors relating to premature births over a six-year period. Infants developing the respiratory distress syndrome as defined by strict criteria, and their mothers, have been compared with those who avoided this complication. Since immaturity is known to be the one constant factor in aetiology, it was realized that an en bloc comparison of these two groups might lead to mothers and their infants of dissimilar gestation being compared, so that in addition, infants in the two groups above and below a birth weight of 1500 g have been contrasted with each other as well, and chi-squared tests of significance used. Since there were many factors being analysed, there was much to be gained by regression and correlation analyses as well, to discriminate the most important variables between the groups and their association one with another. The results confirm the already published associations. They are also considered to show that Caesarean section predisposes of itself to the development of RDS, a question previously controversial. They establish that pre-natal asphyxia as judged by relatively crude manifestations of foetal distress is indeed likely to be significantly associated in certain Infants; and that infants who are small for their gestation period are less likely to develop the syndrome. When Infants IS00 g or below were analysed separately there were found to be no helpful factors discriminating RDS infants from others. It is suggested, since many of these significantly associated conditions are shown to be interrelated, that the syndrome may develop in response to any one of a number of factors or to a combination of them. Inspiratory gasping in utero and increased pulmonary capillary permeability, due to pre-natal asphyxia, may be the cause of the increased fluid content which has been shown present in these infants' lungs. Such an increase, in the larger infants, may then parallel the amount of fluid normally found in the lungs of very small infants, an amount which decreases with birth weight. This fluid and delay in its removal may compromise the pulmonary circulation further, leading to alveolar cell damage and hence decreased production of pulmonary surface active factor, already diluted or inactivated by the extra fluid. In the most immature, the sheer mechanical disadvantage of breathing may be equally important