Clement A. Smith

Idiopathic respiratory distress syndrome of the newborn

AN I N F O R M A L discussion of hyaline membrane disease or the respiratory distress syndrome was held on July 2I, I959, at the IX International Congress of Pediatrics in Montreal. The following were the participants: Dr. E. K. Ahvenainen, Jyvaskyla, Finland Dr . Dr. Dr. Dr. Dr. Dr Dr Dr. Dr. Dr Dr. Dr Dr Virginia Apgar, New York Peter Auld, Boston and Montreal Mary Ellen Avery, Baltimore Heinrich Baar, Pownal, Maine Kurt Benirschke, Boston Eric Burnard, New York Albert Claireaux, London Stewart Clifford, Boston Myron Cohen, Baltimore Charles Cook, Boston Beryl Corner, Bristol John Craig, Pittsburgh V. Mary Crosse, Birmingham

Studies of respiratory physiology in the newborn infant. II. Observations during and after respiratory distress.

An invitation to participate in this publication honoring Professor Wallgren confers no small distinction on any American pediatrician. It also imposes a high standard of scientific scholarship upon those so invited. The Harvard group working with newborn infants are more hopeful of meeting that standard because of the recent presence of one of Dr. Wallgrens own staff in our laboratory, a happy circumstance which has considerably increased the information we can contribute to this publication. Although we are submitting only a preliminary report of studies now in progress, the opportunity of presenting the data here was too tempting to be resisted by this international team of admirers of Professor Wallgren, C. A. S.

Arterial blood gas tensions and acid-base balance in the management of the respiratory distress syndrome†

Serial measurements of arterial oxygen tension (during 100 per cent oxygen breathing)and acid-base balance were used to follow the course of 51 newborn infants with respiratory distress. Serial Pa O2 provided the most useful guide to progression and severity of the disease. A retrospective analysis of the data obtained at first sampling (within 10 hours of birth) made possible a prognostic classification based on initial Pa O2 and pH.

Ether in the blood of the newborn infant

0 BSTETRIC anesthesia may disturb the onset of respiration at birth by producing either (a) anoxia, or (b) anesthesia, or (c) both of these states. Thus, on the one hand (a), the oxygen supply of the mother’s blood may be affected so as to diminish the amount of oxygen available to the fetus during the last critical moments when it is still dependent upon the placental circulation. Under such circumstances the infant may be born with the nervous control of respiration temporarily or permanently damaged by anoxia. Evidence has been put forward by various authors1-3 to show that the onset of neonatal respiration may be disturbed in this way by the use of too much nitrous oxide gas, and perhaps during the administration of other anesthetic agents. On the other hand, (b) as might be expected, some anesthetic substances may themselves pass through the placenta and accumulate in the fetal blood in concentrations sufficient to render respiration shallow or delayed at birth from actual narcosis, despite adequate fetal blood oxygen levels. There are probably situations, (c) in which both the former and the latter disturbances affect the baby, but we have felt that delayed respiration or apnea, due entirely to the directly narcotizing effect of the anesthetic, was primarily the mechanism involved when babies were slow to breathe after delivery under ether. Although Eastman’ found that in eight infants so delivered, the blood -oxygenation was slightly below that expected in deliveries without anesthesia, a similar comparison in a somewhat larger series4 showed the oxygen levels of babies delivered during ether anesthesia to be somewhat higher than the levels in the unanesthetized controls. Moreover the infants of this series who displayed some degree of apnea were not worse off for oxygen than were the others who breathed promptly. In earlier papers the average amounts of nitrous oxide and of cyclopropane4 in the maternal and the fetal blood at birth have been stated, but no figures have been found in the literature to indicate how much ether may enter the blood durin, 0 the average delivery and how this is distributed between the maternal and fetal circulations. Because of this gap in our knowledge, and because we have reason to believe that any neonatal respiratory difficulty nssign.&l& to tlhe anesthetic in deliveries under ether is usually a narcotic and not an anoxic phenomenon, it

Maternal acid-base status and neonatal respiratory distress in normal and complicated pregnancies

Abstract In order to investigate the possible etiological importance of maternal blood-gas and acid-base status in the respiratory distress syndrome, studies were made on the arterial blood of mothers at delivery and on cord and on 1 hour arterial samples of their infants. A total of 79 maternal samples, 76 cord bloods, and 30 1 hour infant samples were studied. The maternal blood data indicated that neither maternal hypoxia nor acidosis at delivery was etiologycally important in the 14 infants who developed respiratory distress. Moreover, clinical and cord blood biochemical studies also suggested that the presence of intrauterine asphyxia as deduced from such information was not an important etiological factor in this syndrome. Infant arterial samples suggested that maternal metabolic acidosis, when present, was associated with acidosis in the infant which persisted at least 1 hour.

Water and Electrolyte Economy in Newborn Infants of Diabetic Mothers

The excessive size and weight and the increased mortality of infants born to diabetic mothers continue as puzzles for obstetricians and pediatricians ( 2 4 ) . In an attempt to reveal some abnormality of body components a t birth, water, electrolyte and nitrogen balances were measured in such infants during the period of postnatal adjustment. This report presents the results of studies carried out during the first three days of life on 19 diabetic mothers’ infants and compares them with previously reported similar observations on normal control infants ( 5 ) .

Postnatal growth and development of infants born after diethylstilbestrol administration during pregnancy.

Abstract The prophylactic administration of diethylstilbestrol in pregnancy to prevent those accidents associated with progesterone deficiency was introduced in 1946 by Smith, Smith, and Hurwitz. 1 The success of this treatment in preventing abortion, 2 reducing the incidence and severity of late pregnancy complications, and increasing fetal salvage 3, 4 has led to its continued and extensive use in this hospital. Previously reported clinical studies indicated that the newborn infants of stilbestrol-treated mothers exhibited no deleterious effects from the Smith and Smith regime. In fact, weights and lengths of infants born prematurely to stilbestrol-treated mothers exceeded those expected at their gestational age, 3, 4 a finding presumably related to the reduced fetal loss observed. Because all of these data covered only the prenatal and immediately postnatal periods, the present study of postnatal development was undertaken.

Acceptance of the Howland Award: (From the American Pediatric Society, April 28, 1976, St. Louis, Missouri)

Acceptance of the Howland Award: (From the American Pediatric Society, April 28, 1976, St. Louis, Missouri)

90 Vascular Responses to Oxygen Breathing in the Newborn Infant

During the course of measurements of pulmonary function in newborn infants breathing 60–100 % oxygen, we have previously noted frequent, rapid and significant decreases in hematocrit and hemoglobin levels. The present investigation has been designed to confirm and elucidate this finding. 14 newborn infants varying in gestational age from 36–37 weeks, in birth weight from 2.7–4.6 kg and in postnatal age from 1–18 h breathed 60 % O2 by demand valve for periods of 60–70 min. Hematocrit (Hct), hemoglobin (Hb), total protein (TP) and blood gases were followed throughout and blood volume (CO method) was measured in 3 infants. Within 10 min of onset of O2 breathing prompt decreases of Hb, Hct, TP were seen reaching levels of 20 % below control values by 60 min. These changes promptly reversed upon resumption of air breathing. TP changes were seen to be more consistent and marked than changes in Hct or Hb. The response was seen with arterial O2 tensions of as low as 116 mm Hg. Total blood volume increases of 40–60 ml/kg were noted during O2 breathing in 3 infants. These data suggest auto-infusion of tissue fluid from some vascular bed in response to O2 breathing; this may imply an increase in precapillary resistance with consequent decrease in capillary pressure and derangement of the Starling equilibrium. Preliminary investigations indicate that bradycardia and increased peripheral vascular resistance are involved in this phenomenon. (APS)

Further studies on ventilation/perfusion relations in the newborn's lung

Radioisotope scanning of the lungs following the intravenous administration of macroaggregated albumin (MAA) labeled with I TM provides an assessment of the distribution of pulmonary blood flow between the r ight and left lung and between different areas of the same lung. The safety and validity of this technique have been tested in animals and man. In adults, the distribution of radioactivity between the r ight and left lung closely correlated with the oxygen consumption of each lung measured by bronchospirometry (r ~ 0.98, p ~ 0.001). Eight lung scintiscans were done in 6 patients with severe hyaline membrane disease (HMD) following the intravenous administration of 0.1 to 0.2 ml. of 1 per cent MAA labeled with 10 to 15 /~c of I TM. All patients required oxygen by face mask to relieve cyanosis. Four of the infants died, and all had H M D on histologic examination. An arterialized capillary pH greater than 7.30 was associated with a normal scan. Patients with a pH of 7.29 or less had either a relative decrease in the perfusion of one lung or nearly complete shunt ing of radioactivity to the liver and spleen via extrapulmonary right-to-left shunts. The diminution of pulmonary blood flow to one lung seen on the scans correlated with the increased severity of the disease on that side seen on the chest films. These findings are consistent with previous observations that effective pulmonary blood flow may be reduced in se~zere HMD. The lung scintiscan also demonstrates tha t the distribution of pulmonary circulation in H M D may be nonuniform.