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OBJECTIVE: To determine whether 40 mg/kg phenobarbital given to term infants with severe asphyxia would result in a lower incidence of seizures in the newborn period and an improved neurologic outcome. METHODS: We conducted a randomized, controlled, prospective study. Entry criteria included (1) an initial arterial pH less than or equal to 7.0 with a base deficit 15 mEq/L or more, (2) Apgar score less than or equal to 3 at 5 minutes of age, or (3) failure to initiate spontaneous respiration by 10 minutes of age. Sample size was calculated to detect a 50% reduction in the incidence of neonatal seizures. RESULTS: No differences were present between treatment and control groups with respect to severity of asphyxia assessed by initial arterial pH, base excess, cerebrospinal fluid lactate dehydrogenase concentration or detection of CSF creatine kinase of its BB isoenzyme. Seizures occurred in 9 of 15 infants in the treatment group and 14 of 16 infants in the control group (p = 0.11). No adverse effects were observed from phenobarbital on heart rate, respiratory rate, blood pressure, or arterial blood gas values. Three-year follow-up revealed normal outcome in 11 of 15 infants in the treatment group and 3 of 16 in the control group (p = 0.003). CONCLUSION: Phenobarbital, when administered in a dose of 40 mg/kg intravenously over 1 hour in term, severely asphyxiated newborn infants appeared to be safe and was associated with a 27% reduction in the incidence of seizures and a significant improvement in neurologic outcome at 3 years of age.

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Group B streptococcus (GBS) is a common cause of early-onset sepsis in neonates. The most recent reviews describing incidence, diagnosis, treatment, and outcome evaluated data on patients from the early 1980s. To obtain current information about this disease, we retrospectively evaluated data on neonates with GBS early-onset sepsis from nine hospitals in the United States between Jan. 1, 1987, and Dec. 31, 1989. There were 245 infants with GBS bacteremia identified among 61,809 live births, resulting in an incidence of 0.32%. Ninety-six infants (39%) were preterm (less than 38 weeks of gestational age). Maternal risk factors for infected preterm and term infants were similar. Antibiotics were administered during parturition in 10% of infants with bacteremia. Mothers of preterm infants received antibiotics up to 48 hours before delivery; mothers of term infants received antibiotics less than 4 hours before delivery. All preterm infants with bacteremia had symptoms; 22% of term infants with bacteremia had no symptoms. Group B streptococcal meningitis was confirmed in 6.3% of infants. Although 86% survived, GBS sepsis increased the birth weight-specific mortality rate up to eightfold in preterm infants and more than 40-fold in term infants. Although the incidence of GBS early-onset sepsis is not changing, we speculate that the improved birth weight-specific survival rate and the changing clinical presentation are due to improved intrapartum and neonatal management.

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In a randomized, controlled study, human surfactant derived from amniotic fluid was administered within 12 hours of birth to infants with severe respiratory distress syndrome who were born at 24 to 32 weeks of gestation weighing less than or equal to 1500 gm. A second dose of surfactant was given to patients in the treatment group if they met ventilator requirements indicating relapse or lack of response to the initial dose. No significant improvement was observed in mortality rate (9/28 vs 15/31) or incidence of bronchopulmonary dysplasia (5/28 vs 3/31) when surfactant-treated infants were compared with control subjects, although there was a significant reduction in initial respirator and inspired oxygen requirements and the arterial/alveolar oxygen ratio improved. In addition, there was a significant reduction in pulmonary air leak in treated infants (10/28 vs 20/31; p less than 0.05). Retreatment was associated with an attenuated ventilatory response and with a higher mortality rate (7/14) than that of infants who did not require a second dose (2/14; p = 0.05), indicating a more severe form of disease. Multiple discriminant analysis, including eight independent variables, revealed that increasing birth weight, earlier age at surfactant treatment, and female gender were significantly associated with survival. These data suggest that early surfactant treatment may reduce mortality rates in very low birth weight infants with severe respiratory distress syndrome, as well as reduce ventilator requirements and the incidence of pulmonary air leaks.

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Serial extracellular volume (ECV) changes were measured in 18 infants of less than 32 weeks gestation. Results were compared with changes in body weight, fluid and sodium intake, urine output, and serum sodium concentration. Mean +/- SD ECV decreased from 550 +/- 116 mL/kg on day 1 to 359 +/- 66 mL/kg on day 14. Thereafter, mean ECV/kg remained between 336 +/- 42 and 349 +/- 54 mL/kg. Clinical hydration and serum sodium concentration usually remained normal during this reduction of stabilization of ECV/kg. Six episodes of hyponatremia occurred at 11 to 31 days of age. Mean ECV/kg was significantly lower in infants with hyponatremia compared with infants of similar age with normal serum sodium concentration (303 +/- 36 mL/kg vs 368 +/- 56 mL/kg, P less than 0.01). Sodium intake in the two groups was similar. We conclude that ECV in the VLBW infant decreases postnatally and is regulated within a range similar to that in older infants, and that postnatal natriuresis in the first 2 weeks of life represents physiologic reduction of the expanded ECV of the fetus. Late hyponatremia may indicate excessive sodium loss and ECV depletion.

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Body water compartment changes were assessed during postnatal weight loss in 14 infants with respiratory distress syndrome. Total body water and extracellular volume were measured by dilution methods on the first day of life and again between the third and sixth days of life. Extracellular volume changes were calculated between the first and second determinations by measurement of chloride balance. Fluid therapy was prescribed to allow negative net water balance and a 1% to 3% reduction in body weight per day. All infants had concurrent reductions in body weight, total body water, and extracellular volume. Progressive daily extracellular volume reduction concurrent with weight loss was also apparent from chloride balance data. The correlation of changes in body weight with extracellular volume in individual subjects was poor (r = 0.05). We speculate that variations between sodium and free water balance in the sick preterm infant may be responsible for variability in the distribution of postnatal body water losses. Assessment of hydration in the newborn infant should include consideration of sodium balance and alterations of serum osmolality, and changes in body weight.

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We assessed pulmonary function and compression deformities in 76 preterm infants less than or equal to 34 weeks gestation who had premature rupture of membranes (PROM) for longer than 5 days (mean +/- SD 18.8 +/- 15.4 days, range 6 to 90 days). Twenty-one of the 76 infants had oligohydramnios and positional deformities at birth; however, only two infants met all the criteria for the oligohydramnios tetrad. All 21 required assisted ventilation from the moment of birth. Twenty infants had clinical evidence of pulmonary hypoplasia; 18 of these died. Pulmonary hypoplasia was confirmed by significantly low wet lung weights, low lung DNA content, or low radial alveolar counts in the 13 infants with postmortem examinations. Fifty-five infants with PROM for longer than 5 days did not have positional deformities. Twenty-one required assisted ventilation, of whom 10 had severe oligohydramnios. Eleven of the 21 died; autopsies were performed. All had normal wet lung weights, but seven had significantly decreased radial alveolar counts, implying a less severe but still fatal form of pulmonary hypoplasia. None of the remaining 34 infants had lung disease, and only three had oligohydramnios. We conclude that pulmonary hypoplasia can result from PROM associated with severe oligohydramnios of as short as 6 days duration. Furthermore, fatal pulmonary hypoplasia can occur with little or no external deformation.

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The incidence of rickets was found to be 32% (39/125) in a retrospective review of consecutive survivors of very low birth weight in whom serial radiographic and biochemical data were obtained. A higher proportion of these infants were black, had a greater initial weight loss, and had a longer hospitalization; there was a prevalence of births in the spring. Soy formula, supplemented with calcium and vitamin D but not phosphorus, was used predominantly in both groups; cumulative calcium, phosphorus, vitamin D, and caloric intakes were the same. We believe that the etiology of rickets in VLBW infants is multifactorial; however, nutritional deficiency is of central importance. Soy isolate formula, as well as human milk and many other commercially available formulas, do not provide sufficient calcium and phosphorus to keep pace with rates of intrauterine accretion. Supplementation with calcium, phosphorus, and vitamin D, beginning as soon as possible after birth, is indicated.

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