Postneonatal infant mortality in infants to a neonatal intensive care unit.

The postneonatal infant mortality (PNIM) of 2,205 infants admitted to a neonatal intensive care unit from January 1971 to December 1974 was 44 in 1,000 infants who survived to age 28 days. This rate is approximately ten times that of the general population. Congenital malformations (59%), infections (12%), sudden infant death syndrome (10%), and asphyxial brain damage (10%) were the most common causes of death. One third (26) of the infants remained in the hospital whereas two thirds (52) had been dismissed prior to death. All who remained in the hospital plus 36 who had been dismissed died of severe illnesses that were incompatible with prolonged survival. The remaining PNIM was 10 in 1,000 neonatal survivors. This rate is still twice that of the general population. These deaths occurred in infants who were apparently well at the time of dismissal and subsequent examinations. Sudden infant death syndrome and infections constituted the largest portion of this mortality. Factors contributing to mortality in this group were poor socioeconomic status and low birth weight. Maternal age, race, marital status, and neonatal illnesses including apnea were not significantly related. Factors that appear to be important in the birth of high-risk infants continued to be operative in the postneonatal period, and contribute to a high mortality in apparently normal infants dismissed from the neonatal intensive care unit.

Glucose disappearance in infants of diabetic mothers. III. Relationship of spontaneous glucose disappearance to glucose tolerance, neonatal hypoglycemia and lowest blood glucose.

Spontaneous glucose disappearance in the first 90 min of life and glucose disappearance following an intravenous injection of 1 g/kg dextrose were measured in 23 infants of insulin-dependent diabetic mothers. Spontaneous disappearance was log-linear in 12/23 infants, providing for calculation of an endogenous Kt which correlated significantly (P < 0.01) with the exogenous Kt determined after the dextrose injection, r = 0.74. Hypoglycemia < 20 mg/dl occurred in 4/23 infants, and was identified during the spontaneous glucose disappearance (3 infants) and/or predicted by an endogenous Kt greater than or equal to 3.0%/min (2 infants). There was also a significant inverse correlation (P < 0.01) of the lowest blood glucose obtained within the first 24 h of life with the endogenous Kt, r = 0.61. There was no correlation of the endogenous or exogenous Kt, lowest blood glucose or hypoglycemia with White's classification of the maternal diabetes, diabetic control during pregnancy, the maternal blood glucose at delivery or the cord blood glucose. These data indicate that determination of spontaneous glucose disappearance within the first 90 min of life is useful in identifying infants of diabetic mothers with hypoglycemia or those who will subsequently develop hypoglycemia.

Postasphyxial lung disease in newborn infants with severe perinatal acidosis.

The pulmonary course and respiratory management of 65 asphyxiated infants with at least one arterial pH less than or equal to 7.00 within the first 2 hours of life was determined. Asphyxia in the preterm and term infants in the absence of respiratory distress syndrome or meconium aspiration syndrome was associated with a transient respiratory insufficiency requiring assisted ventilation which markedly improved in the first 24 hours of life. In contrast, infants with asphyxia complicated by respiratory distress syndrome or meconium aspiration syndrome developed profound lung disease including pulmonary hemorrhage and persistence of the fetal circulation. The course of their illness was significantly worse than control infants without asphyxia. Ineffective neonatal resuscitation allowing for the development of meconium aspiration syndrome and persistent respiratory acidosis contributed to the severity of illness in more than 50% of the infants. Central nervous system pathologic conditions were present in asphyxiated infants with and without severe pulmonary disease. We conclude that severe asphyxia in the absence of underlying lung disease results in a predictable postasphyxial transient respiratory insufficiency, with marked improvement in the first 24 hours of life.

Etiologic factors in rickets of very low-birth-weight infants.

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.

Cerebrospinal fluid lactate dehydrogenase in infants with perinatal asphyxia.

Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.

Hyperbilirubinemia in breast-versus formula-fed infants in the first six weeks of life: relationship to weight gain.

Bilirubin determinations were obtained at weekly intervals from 1 to 6 weeks of age in 27 breast-fed and 12 formula-fed term, average size infants. Mean bilirubin levels were significantly higher in breast-fed infants at each age studied. The highest mean bilirubin level in each group was present at 1 week of age, 10.6 (+/- SD 4.6) mg/dl in breast-fed and 4.7 (+/- SD 3.0) mg/dl in formula-fed infants. Thereafter, values gradually fell in both groups. Mean birthweight was not different between the two groups; however, breast-fed infants lost significantly more weight (4.8%) by the time of discharge than formula-fed infants (2.2%). Breast-fed infants remained significantly lighter in weight at 6 weeks of age. Analysis of variance and covariance revealed no significant correlation between body weight, weight change in grams or percent weight change, and bilirubin levels in either group. These data indicate that mean bilirubin levels are significantly higher in breast-fed infants compared with formula-fed infants from 1 to 6 weeks of age. Breast-fed infants also have a significantly greater weight loss during the first four days of life and remain lighter at 6 weeks of age; however, there is no relationship of weight loss to bilirubin levels.

Postnatal diuresis and respiratory distress syndrome in infants receiving mechanical ventilation.

Measurements of body water homeostasis and pulmonary function were obtained in 24 infants with respiratory distress syndrome requiring mechanical ventilation during the first five days of life to determine the relationship of diuresis to improvement in pulmonary function. Initial diuresis (output intake ratio greater than 0.8) occurred at 24 hours, maximum diuresis (output intake ratio greater than or equal to 1.6) at 40 hours, and initial improvement in pulmonary function (fall in AaDO2 greater than 50 mm Hg) at 48 hours. Urine flow rates over four-, eight-, or 12-hour periods were quite variable and correlated poorly with improvement in pulmonary function. Reduction in body weight was a more accurate indicator of total changes in body water than urine output, output intake ratio, or fractional excretion of sodium. Although there was a temporal relationship of loss of body water and improvement in pulmonary function by analysis of means, no cause-and-effect relationship could be found on a case-by-case analysis. Five of 24 infants demonstrated improvement in pulmonary function prior to diuresis or reduction in body weight. Nine infants had a diuresis more than 24 hours prior to pulmonary improvement, and two infants had a diuresis without pulmonary improvement during the five-day study period. These data indicate that factors other than body water are associated with improvement in pulmonary function in infants with respiratory distress syndrome.

Comparison of calcium- and phosphorus-supplemented soy isolate formula with whey-predominant premature formula in very low birth weight infants.

In a random, controlled study of very low birth weight (VLBW) infants from 3 to 8 weeks of age, 17 infants were fed soy isolate formula supplemented with calcium (92 mg/kg/day), phosphorus (44 mg/kg/day), and vitamin D (500 IU/kg/day), and 15 were fed a new whey-predominant, low osmolality formula designed for small preterm infants. Mean birth weight (1,206 g, SD 178) and gestational age (30 weeks, SD 1.9) of the soy-fed group were not significantly different from the whey formula group (1,143 g, SD 158, and 30 weeks, SD 1.8, respectively). Caloric and protein intakes were not different between the formula groups throughout the study period. However, mean weight gain in g/kg/day was significantly greater for the whey formula group: 15.3 g, SD 2.5, vs. 11.3 g, SD 2.3, p less than 0.0001. Serum protein and albumin were higher in the whey formula-fed group during the latter 2 weeks of the study (p less than 0.05). The incidence of vomiting, gastric residual, abdominal distension, diarrhea, and constipation was low and not different between the two groups. No infant developed necrotizing enterocolitis. Serum calcium, phosphorus, alkaline phosphatase, 25-hydroxy vitamin D and parathyroid hormone were similar in both groups, and no infant developed radiographic evidence of rickets. Although soy isolate formula supplemented with calcium, phosphorus, and vitamin D was not associated with rickets, no fewer complications were observed with this lactose-free, low solute formula.(ABSTRACT TRUNCATED AT 250 WORDS)