A study of inflation of the lungs of the newborn; a preliminary report.
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Conference Article| December 01 1985 Respiratory distress syndrome and its treatment with surfactant C. J. MORLEY C. J. MORLEY 1Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QQ, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1985) 13 (6): 1091–1092. https://doi.org/10.1042/bst0131091 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation C. J. MORLEY; Respiratory distress syndrome and its treatment with surfactant. Biochem Soc Trans 1 December 1985; 13 (6): 1091–1092. doi: https://doi.org/10.1042/bst0131091 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search Keywords: RDS, respiratory distress syndrome This content is only available as a PDF. © 1985 Biochemical Society1985 Article PDF first page preview Close Modal You do not currently have access to this content.
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The lungs of newborn infants, particularly those who are premature or born to diabetic mothers, frequently contain membranes of eosinophilic material, which line the distal respiratory passages and are almost always associated with extensive atelectasis. They are found in an estimated 20%-40% of liveborn infants who die in the first few days of life. They may be found, furthermore, in as much as 70% of those early neonatal deaths in which no other major abnormality is encountered. These membranes and the atelectasis that accompanies them are the most commonly found abnormality in early neonatal death. The last decade has been one of intensive investigation and study of pulmonary hyaline membranes and their associated phenomena in the newborn. They are no longer merely a pathologic entity to be recognized on postmortem examination. Their clinical and radiologic features have been clarified, and the resultant syndrome is now the concern of the cardiac
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In a recent publication 1 on the subject of obstructive pulmonary atelectasis, two etiologic factors were described as being essential to its production, viz., bronchial obstruction and labored respiration or expiration against resistance. The latter of these two factors was contrary to the observations of Lee, 2 Coryllos and Birnbaum 3 and others, 4 who had produced the condition experimentally with regularity, and who believed a quiet, shallow respiratory cycle to be one of the important factors in its etiology. This idea has been carried down from the time of Pasteur 5 who, observing several cases of massive atelectasis associated with postdiphtheritic paralysis of the diaphragm, believed it due to a reduction in the depth of respiration. When an attempt was made to reproduce the results of other investigators, the factor of straining respiration was accidently encountered and massive atelectasis produced with routine regularity in its presence. That straining respiration
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When considering diseases of the lungs during pregnancy, one must remember that there are certain normal physical changes and signs in the chest due to pregnancy. As the growth of the uterus continues there is slight congestion of the lungs with an increased lateral expansion, the excursion of the diaphragm is decreased and the breathing becomes more costal. These changes are, as a rule, more pronounced in the primipara than in the multipara, because there is less relaxation of the abdominal muscles in the former. It becomes immediately apparent, therefore, that such conditions bring about an ideal nidus for the harboring of infection and explains somewhat the reason why quiescent infections in the lungs may be activated. This is particularly true of women with arrested pulmonary tuberculosis who become pregnant. It is an astounding fact that approximately 50,000 women in the child-bearing period die each year from tuberculosis and that
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Newborn infants with severe atelectasis seldom survive long enough to develop secondary cardiac changes other than dilatation, but in rare instances survival is sufficiently prolonged to permit hypertrophy of the myocardium of the right ventricle, giving the heart the characteristic anatomic configuration of cor pulmonale as seen in older age groups. The clinical findings associated with these secondary changes in the heart may be more striking than those of the primary disease of the lungs, and because the clinical behavior of the atelectasis-cor-pulmonale lesion-complex can so closely simulate that of a congenital malformation of the heart, the correct etiologic diagnosis is often made only after death and examination of the lungs and heart at necropsy. Apparently these facts are not generally appreciated, for in the modern English language literature there are only two reports * which consider in detail the pulmonary heart disease secondary to atelectasis of the newborn. It would
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For a number of years we have been struck by the absence of truly pathologic lesions as a cause of death among many of the immature infants born in the Pennsylvania Hospital. Many of these infants appeared to have died of respiratory failure, as evidenced by cyanosis and gasping respirations in the presence of seemingly normal cardiac function. In fact, it was usual for the heart to continue beating even after respirations had ceased. Numerous embryologic studies on the development of the fetal lung and the lining of the alveoli have been made; yet in the literature there has been little discussion of the clinical significance of the results of such studies. Although death in the premature infant is undoubtedly caused by a complex mechanism which includes anatomic and metabolic dysfunction of numerous organs, it seemed desirable to make an anatomic study of the fetal lung to determine what bearing
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Summary An analysis of 30 cases of newborn infants with hyaline membranes in the lungs has led to the conclusion that these membranes are of no significant functional importance in the vast majority of castas. In more than half of the cases death was considered due to pneumonia. In cases where there was no pneumonia or demonstrable extrapulmonary cause of death the significant factor in the prevention of the gaseous exchange in the lungs was primary and/or secondary atelectasis. The atelectasis was not only located in parts of the lungs corresponding to the membranes. The clinical diagnosis of “membrane asphyxia” in the sense of “asphyxia caused by membrane formation” must be limited to cases with very abundant and widespread membranes causing secondary atelectasis.
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PNEUMONIC changes can be found the lungs of a substantial proportion of the fetuses which die utero the late stages of gestation. Similar alterations found the lungs of percentage of liveborn infants who for only a few hours or day. In the first instance it is certain, the second it is generally assumed that the process had its origin within the uterus. In additional number of both stillborn and liveborn infants, it may be demonstrated by microscopic examination that there is excessive quantity of sac contents within the lungs. The pathogenetic factors responsible for both intrauterine pneumonia and for excessive aspiration of contents have never been definitely established. still exit profound differences of opinion on every aspect of the process of intrauterine respiration. The following represent expert opinions on the question as to whether the fetus breathes or not. Snyder and Rosenfeld state that in the full-term fetus sponataneous rhythmic respiratory movements occur which may continue many hours. Davis and Potter maintain that amniotic fluid is normally aspirated into lungs as part of intrauterine respiratoy activity and concluded that an adquatic existence for the fetus is normal during intrauterine Windle has arrived at the opposite conclusion. In 1939 he wrote,One is tempted to entertain the false assumption that respiration at birth is a continuation of respiratory-like phenomena indulged normally throughout fetal life. This is contrary to fact. Sir Joseph Barcroft came to the same conclusion. There is during the second half of fetal life inhibition of the nervous mechanism responsible for respiratory movements. If there were not the fetus would be drowned before it was born.
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The literature of recent years is replete with articles dealing with the early pneumonic complications following anesthesia and operation. The frequency and gravity of these conditions have everywhere been recognized. But as their etiology was obscure, the suggested means for prophylaxis were many, but unavailing. A great impetus, however, was given to research in this field with the postulation of the theory that these complications are caused primarily by an altered physiology, depressed respiration. This decreased pulmonary ventilation prevents the tracheobronchial secretions from being removed by nature's processes, and, remaining in situ, these secretions block the air passages, thus often imprisoning pathogenic bacteria. The air in the areas of the lungs supplied by the bronchioles or in the bronchi closed by these plugs of mucus is soon absorbed. Thus atelectasis is caused, its extent depending on the size and number of the air passages so occluded. The imprisoned bacteria, being
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Abstract
There seems to be no reasonable doubt that the lungs in a newborn expand progressively during the first few days of life. Some degree of atelectasis seems to be perfectly normal. This is indicated by a number of roentgenographic studies (including those here reported); by the reported findings of pathologists; by the fact that in experimental animals the lungs inflated very unevenly; and by the fact that aeration of only a portion of the lung is needed for complete oxygenation of the blood. The relation of atelectasis to neonatal death is not entirely clear and is probably not always the same. The infant may die from other causes before the lungs are fully expanded. Atelectasis may develop secondarily to other debilitating conditions. The frequent coincidence of prematurity and extensive atelectasis is impressive. It may be that the lungs are so incompletely formed that they cannot expand. On the other hand, atelectasis and massive collapse in the adult is a serious condition and there seems to be no good reason to suppose that this cannot also occur in infants and be serious per se.
The air pressures found necessary to expand the lungs in rabbit fetuses were found to be about ten times what adult humans use in quiet respiration and were of about the same magnitude as the pressures found necessary to expand the lungs of stillborn humans. An attempt to produce atelectasis in newborn rabbits by chilling was most inconclusive. Atelectasis did develop in three of 15 animals used in the experiment, but the relation to chilling was not at all clear.
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