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The cardiovascular effects of dopamine were evaluated in 14 severely asphyxiated neonates. After a period of stabilization, either dopamine 2.5 micrograms/kg/minute or placebo was infused in a randomized double-blind protocol. In seven dopamine-treated infants, echocardiographically determined shortening fraction and mean velocity of circumferential fiber shortening increased when compared to preinfusion values (P less than 0.05). There was no significant change in these echo indices of cardiac function in the placebo-treated group. Systolic blood pressure rose in the dopamine group when compared to predopamine infusion values and to the postinfusion values of the placebo group (P less than 0.001 and 0.025, respectively). Diastolic blood pressure increased to a small degree in the dopamine group. There was no significant change in heart rate or echocardiographically measured systolic time intervals. Low doses of dopamine increase cardiac performance and raise systolic blood pressure in the severely asphyxiated neonate.

Hypoxanthine, the end product of purine metabolism, is usually very elevated in body fluids during severe hypoxia. We measured hypoxanthine in the cerebrospinal fluid of hydrocephalic preterm infants (12 with posthemorrhagic, one with congenital hydrocephalus) to determine whether hydrocephalus is associated with anaerobic metabolism of brain tissue. Cerebrospinal fluid hypoxanthine was undetectable in normal infants. In hydrocephalic infants, the concentration of hypoxanthine ranged from 7.5 mumol/L to 28 mumol (means = 14.3 mumol/L). The hypoxanthine concentrations fell from a mean of 12.8 mumol/L to a mean of 2.0 mumol/L (P less than 0.05) with successful treatment of the ventriculomegaly by lumbar puncture or by ventriculoperitoneal shunt. Patients with acute posthemorrhagic hydrocephalus had similar concentrations of hypoxanthine (means = 14.5 mumol/L) as patients with late or with congenital hydrocephalus (means = 13.8 mumol/L), indicating that brain hypoxia is probably a consequence of the ventriculomegaly and not of the hemorrhagic insult.

We have compared the actual contribution of surfactant deficiency in respiratory distress syndrome to left-to-right shunting across a patent ductus arteriosus in premature infants with severe RDS by performing serial phospholipid analysis of tracheal aspirates and echocardiograms, and we have correlated these findings with the infants' clinical courses and management of ventilation. This analysis was combined with surgical or pharmacologic closure of PDA if a significant shunt existed. Qualitative surfactant abnormalities at birth and the subsequent maturation of phospholipids after birth were similar in all three groups of infants (Group 1, RDS alone; Group 2, RDS+PDA in infants weighing >1.2 kg; Group 3, RDS+PDA in infants ≤ 1.2 kg). The largest infants had isolated RDS (Group 1) and, after a brief period of stabilization after birth, had declining ventilatory and oxygen requirements. Infants in Group 2 had a gradual decrease in ventilatory and oxygen requirements which was accelerated markedly by cessation of PDA shunting. Infants in Group 3 had increasing ventilatory and oxygen requirements despite a maturing tracheal aspirate phospholipid pattern; their course, especially if they were asphyxiated, was characterized by early development of a significant left-to-right shunt and worsening clinical condition which improved following ablation of the shunt. The data suggest that severe RDS presents as a developmental spectrum and provides the justification for a controlled trial of very early closure of the PDA in the very low-birth-weight infant with severe RDS.

This report summarizes a consecutive experience with 59 preterm infants with clinical, radiographic, and echocardiographic findings of a large patent ductus arteriosus. Thirty-five infants who met defined criteria received indomethacin, and 24 infants underwent PDA ligation. Analysis of the clinical course of these infants revealed no selective indomethacin morbidity and suggests that infants undergoing ligation require more prolonged ventilator therapy with increased exposure to FiO2 greater than or equal to 0.3. Mortality rates between ligated and pharmacologically treated groups were similar. This study documents that inhibition of prostaglandin synthesis to constrict and close the PDA in the premature infant is an effective alternative to operative closure.

The course and complications of fifty-two infants with patent ductus arteriosus requiring closure were assessed prospectively. Twenty-six infants with a PDA received indomethacin for pharmacologic closure of the PDA, and 26 underwent ligation. The current study analyzes and compares the longitudinal follow-up with respect to somatic growth, neurologic function, psychomotor and mental development, and renal, ophthalmologic, and audiologic function in 21 infants in each group who entered the follow-up. No selective morbidity was attributable to PDA closure with indomethacin when compared to surgically treated infants.

Examination of the brains of 69 infants revealed spongiform changes restricted to myelinated tracts of the brainstem in seven of them. This type of myelinopathy consistently develops in experimental animals after hexachlorophene intoxication. Common factors in affected infants were multiple exposures to hexachlorophene, prematurity with low birth weight, and the presence of dermal rashes or wounds.

The surfactant phospholipids in the tracheal effluent of eight pairs of preterm twins were followed, serially. In four pairs only one of the twins had RDS; in the other four pairs both twins had RDS. Twins with and without RDS had markedly different surfactant phospholipids. Phosphatidylglycerol was absent in all twins with RDS. L/S ratios in tracheal effluent increased after birth in infants with and without RDS. With recovery from RDS, phosphatidylinositol increased. The study helps confirm previous studies of the necessity of the acidic phospholipids, PI and PG, in stabilizing lecithin, as well as that surfactant composition can be independent of gestational age.

MYOCARDIAL INFARCTION in the neona te usually occurs in association with congeni ta l hear t disease?..2 There have been isolated case reports of myocardial infarct ion occurring dur ing the per inata l period in the absence of recognized predisposing factors. A case is reported here which suggests that embol i sm of systemic vessels via fetal circulatory pathways may occur in complicated deliveries, which predispose the neona te to hypoxia and hemostasis, with resul tant t h rombus formation.

We performed a randomized, prospective clinical trial comparing intratracheal administration of human surfactant with conventional treatment with intermittent mandatory mechanical ventilation alone for treatment of severe respiratory distress syndrome in preterm infants of less than 30 weeks gestation. Twenty-two infants (mean gestational age 27.0 weeks, mean birth weight 987 gm) were given surfactant, and 23 infants (mean gestational age 27.2 week, mean birth weight 1055 gm) received intermittent mandatory ventilation. Infants given surfactant required less FiO2 during the first week, had lower mean airway pressure during the first 48 hours, and had improved ventilatory index and a/A PO2 ratio. Death or the occurrence of bronchopulmonary dysplasia was significantly less among infants given surfactant (P = 0.019). Pneumothorax, pulmonary interstitial emphysema, and need for FiO2 greater than or equal to 0.3 for greater than 30 days was significantly less in the surfactant group. This trial confirms the efficacy of treatment with human surfactant in preterm infants with severe respiratory distress syndrome.