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Hyaline Membrane Disease
  1. K. Boughton,
  2. Gillian Gandy,
  3. Douglas Gairdner

    II: Lung Lecithin


    The lecithin content of lung, together with its surface tension properties, were determined in 34 stillbirths, and 61 neonatal deaths. Lecithin content ranged widely from 1·5 to 18·6% of dry lung tissue.

    In 24 cases the `palmitic-lecithin' was also measured; it formed 44-79% of the total lecithins. Since the two were related linearly, changes in palmitic-lecithin could be adequately studied by measuring total lecithins.

    Lecithin content was negatively correlated with minimum surface tension of lung extract in both fresh stillbirths and neonatal deaths. Cases with hyaline membranes had lung lecithin in the lower range (< 8% dry tissue). Lung lecithin content may be a measure of surfactant reserve.

    After 29 weeks' gestation, fresh stillbirths and neonatal deaths, other than those with hyaline membranes, had normal lung surfactant. The exception was a small group of infants having immature lungs lacking surfactant, and who survived less than 2½ hours; some of these, it is surmised, would have developed hyaline membranes had they survived longer. This was consistent with the fact that well-formed hyaline membranes were only found in infants that had survived for at least 3 hours.

    Surfactant deficiency probably develops only after birth (except in very immature infants), and as a consequence of an initial rapid consumption of surfactant to form a lining layer covering the alveolar surface, when a gas-liquid interface is created by aeration of lung. Surfactant deficiency, by promoting interstitial pulmonary oedema, is thought to be the immediate cause of hyaline membrane disease.

    A scheme for the pathogenesis of hyaline membrane disease is set out. It provides a possible mechanism for the different ways in which surfactant deficiency may arise in immature and mature infants.

    Cases where hyaline membranes occur with normal surfactant fall into three groups: (1) Cases with hyaline membrane disease that have survived several days, the lungs being in the stage of repair. (2) Cases with massive lung haemorrhage, with severe anaemia from haemolytic disease, or with heart failure; extravasation of oedema fluid or blood may be the common factor in this group. (3) Infants of diabetic mothers.

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    II: Lung Lecithin