Pulmonary follow-up of moderately low birth weight infants with and without respiratory distress syndrome.

Pulmonary function was measured in 18 children aged 6 to 9 years who had been born prematurely (mean birth weight 1760 +/- 555 g) and who had each received greater than 100 hours (mean 177 +/- 74 hours) of mechanical ventilation for respiratory distress syndrome (RDS). We used as controls 26 children aged 6 to 7 years who had been born prematurely (mean birth weight 1636 +/- 554 g) but who had required no treatment for pulmonary disease. Results for total lung capacity, FEV1, ratios of functional residual capacity and residual volume to total lung capacity, specific airway conductance, and alveolar plateau slope did not differ in the RDS and control groups. Eight of the 18 children in the RDS group had had radiologic evidence of bronchopulmonary dysplasia at 30 days and oxygen dependence at 30 days, but did not differ from the control group for any of the indices of pulmonary function. However, FEV1 and specific airway conductance were significantly reduced in the premature control group compared with children born at term. Therefore, factors associated with prematurity rather than combined effects of RDS and its treatment determined pulmonary function at age 6 to 9 years.

Continuous monitoring of PO2 during apnea of prematurity.

We studied the changes in PO2 during 72 isolated episodes of apnea of prematurity in 20 low-birth-weight infants. A stable PO2 prior to the onset of apnea was observed in 65% of the episodes. A falling PO2 was noted in only 18% of the cases. The mean initial PO2 was 75 mm Hg and no infant was hypoxic (PO2less than 40 mm Hg) immediately prior to apnea. The mean PO2 fell to 60 mm Hg at the end of apnea and continued to fall to a mean low PO2 of 46 mm Hg. The mean PO2 at recovery was 79 mm Hg. We concluded that in this group of premature infants, hypoxia is not the initiating even in the apnea of prematurity. Furthermore, we noted that arterial oxygen tension continues to fall despite the reestablishment of respiratory efforts, that the rate of recovery from apnea is slower than the rate of fall, and that bradycardia associated with apnea is not initiated by hypoxemia.

Amniotic fluid fluorescence polarization value as a predictor of respiratory distress syndrome.

Fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene in amniotic fluid lipid aggregates was measured to determine the ability of this technique to prospectively predict respiratory distress syndrome. Prior retrospective studies have shown that an FP value of less than or equal to 0.336 correlated best with a lecithin to sphingomyelin ratio of greater than 2.0. Fluorescence polarization values of amniotic fluid samples obtained within 48 hours of birth from 161 pregnancies were correlated with neonatal outcome. Samples from 149 pregnancies had FP values of less than or equal to 0.336 and samples from 12 pregnancies had FP values of greater than or equal to 0.336. No infants delivered from the former group developed RDS and eight of 12 infants from the latter group developed RDS (P less than 0.001). In the entire population the test had a sensitivity of 100% and a specificity of 97%. When 37 infants with birth weights less than 2,500 gm were studied, the FP value remained a highly reliable predictor of the infant at risk for developing RDS (P less than 0.001). In this subset the test had a sensitivity of 100% and a specificity of 90%. L-S ratios were performed on 96 samples and the results correlated well with FP values (P less than 0.001). We conclude that the amniotic fluid FP value is a reliable index of fetal lung maturity and the risk for developing RDS. The FP value also has specific technical and diagnostic advantages over the L-S ratio.

The hemodynamic effects of intrauterine hypoxia: an experimental model in newborn lambs.

An experimental animal model of intrauterine hypoxia and respiratory distress in newborn lambs was produced by inducing maternal hypotension. Serial hemodynamic data indicated that the oxygenation defect in the lambs was due to right-to-left shunting of blood through fetal channels rather than within the lungs. Shunting was mainly across the foramen ovale, but, in severely distressed animals, significant right-to-left shunt also occurred through the ductus arteriosus. Left-to-right shunts across the ductus arteriosus were found in lambs with milder respiratory distress. The implications of perinatal hypoxia as it affects the pulmonary vascular bed in human neonates with the respiratory distress syndrome (hyaline membrane disease) and persistence of the fetal circulation are discussed. It is speculated that the early pulmonary vascular esponses in the two diseases may be identical.

Renal response of the lamb fetus to partial occlusion of the umbilical cord.

The role of the fetal kidney during impairment of placental exchange was studied in eight fetal lambs, intact in utero; a standard asphyxial insult for a period of 1 hour was produced by occluding the umbilical cord sufficiently to lower the fetal heart rate by 35 +/- 5 beats/min and the pH by 0.15 units. This asphyxial stress caused a fall in urine output from a control of 0.17 to 0.03 ml/kg/min and of glomerular filtration rate from 1.2 to 0.3 ml/min; release of the occlusion was followed by mild diuresis. The fall in urine output was accompanied by a rise in total primary solutes including concentrations of electrolytes; this rise continued for 1 to 2 hours following the release of the occlusion. Because of the low urinary output during the period of occlusion, there was a fall in excretion of electrolyte; an increase in net acid excretion occurred only after the release of the cord. These experiments show that, although the fetal kidney is capable of contributing to elimination of acid following compression of the cord, there may be an associated net loss of water and electrolytes.