Vitamin E supplementation and the retinopathy of prematurity.

The effect of high-dosage E treatment (Rx) initiated at the stage of 3-plus active disease (target serum E levels, 5-6 mg/dl) was evaluated by a standardized scoring system of visual morbidity at the one to two year eye exam among infants cared for in the University of Pennsylvania Neonatal Complex (1976-1978). The incidence of legal blindness in both eyes or worse was decreased from 71 to 40% in E Rx (n = 10) as compared to non-E Rx (n = 14) infants, and the number of infants with minimal visual morbidity was increased. Pilot studies (1972-76; target serum E level, 1.5 and 3.0 mg/dl) of the prophylactic effect of E Rx from birth on showed a decrease in mean severity of acute stage disease and a decrease in sequelae at one to two years. A strikingly difference in visual morbidity following resolved low-grade ROP was seen when prestudy infants (1968-72) who were fed early iron supplements and given formulas with low E:PUFA ratios were compared to non-E Rx as well as to E Rx 1972-76 infants. Vitamin E seems to exert a beneficial effect at all stages of ROP, perhaps because of its broadly based regulatory role.

A classification of retrolental fibroplasia to evaluate vitamin E therapy.

A refined classification of the stages of the retinopathy of prematurity (RLF) based on the experience of over 7500 examinations during the past decade is presented. We have been using the basic elements of this classification since 1972 in order to evaluate the influence of vitamin E on retrolental fibroplasia (RLF). It is our impression that it provides a more accurate clinical method of following the course of the retinopathy and a tool for assessing the factors other than prematurity and hyperoxia that may play a subtle role in the development of RLF.

Adrenocortical response to ACTH stimulation in postmature newborns.

Diminished total plasma cortisol levels have been demonstrated in postmature neonates, suggesting that fetal glucocorticoids may be involved in the cause of postmaturity. This hypothesis was tested by adrenocortical stimulation in 32 newborns: 12 were postmature; 12 were postterm, but not postmature; and 8 were normal term neonates. The mean pre- and poststimulation total plasma cortisol levels were 3.9 and 50.9 microgram/100 ml, respectively, for the postmature newborns, 9.7 and 44.0 microgram/100 ml for the postterm, but nonpostmature newborns, and 9.8 and 37.1 microgram/100 ml for the normal term newborns. The differences in the poststimulation rise in plasma cortisol between the postmature and merely postterm infants or between the postterm and normal term infants were not statistically significant. The mean poststimulation cortisol rise in the postmature group exceeded that of the normal term group (P less than 0.05). The adequacy and promptness of response to adrenocortical stimulation eliminate the likelihood of adrenal insufficiency in postmature infants.

Toxicity to bilirubin in neonates: infant development during first year in relation to maximum neonatal serum bilirubin concentration.

Neurologic and developmental performance during the first year of life was correlated with maximum neonatal serum bilirubin levels for 27,000 infants in the Collaborative Perinatal Project. The infants were grouped by race and by five birth weight/gestational age categories to control for the effect of these factors on hyperbilirubinemia and developmental outcome. Low mean eight-month motor scores and delayed one-year motor development were associated with serum bilirubin levels in the range of 10 to 14 mg/dl and above. This relationship was strongest for low-birth-weight/short-gestational-period infants. A persistent association of developmental outcome with hyperbilirubinemia was found over and above the variation of maturity within the birth weight/gestational age categories.

Skin lesions in association with beta-hemolytic Streptococcus group B.

A full-term male infant delivered by caesarean section following a prolonged rupture of the amniotic membranes of 30 hours' duration manifested peculiar skin lesions at the time of birth consistent with the healing phase of bullous impetigo. He was colonized with beta-hemolytic Streptococcus group B that was also cultured from the mother's cervix. It is possible this infant became infected in utero since the healing stage of the lesions suggest that they were present sometime before birth.

Possible adrenocortical insufficiency in postmature neonates.

Total plasma cortisol in cord and neonatal blood was measured by a radioassay method in neonates resulting from (1) term vaginal delivery following uncomplicated labor (control group), (2) term vaginal delivery following fetal distress during labor, (3) postterm, postmature vaginal delivery following fetal distress during labor, and (4) postterm, postmature emergency cesarean section performed because of signs of severe fetal distress during labor. Comparison of the mean peripheral plasma cortisol values showed that whereas the mean level (plus or minus S.E.) of the distressed term neonates (22.2 plus or minus 5.3 mug per 100 ml.) use 180 per cent of that of the control group (12.3 plus or minus 1.1 mug per 100 ml.; P smaller than 0.01) the mean level for the vaginally delivered postmature group (7.5 plus or minus 1.8 mug per 100 ml.) was only 61 per cent of that of the control group (P smaller than 0.05). Furthermore, in the postmature group with sufficient intrapartum distress to warrant emergency cesarean section the mean level (4.6 plus or minus 1.5 mug per 100 ml.) was found to be only 37 per cent of that of the control group. No differences were observed among the cord plasma cortisol values. These results are strongly suggestive of a relative adrenocortical insufficiency in postmature neonates. Such insufficiency could result from a defect in any portion of the adrenal-pituitary-hypothalamic axis. Effort is under way to further define such a defect.

Possible role of the fetal adrenal glands in the etiology of postmaturity.

Plasma cortisol levels were studied in the cord blood and neonatal blood of the following vaginally delivered groups: (A) postmature; (B) postterm (but not postmature); and (C) term neonates. Significantly lower levels of 8 A.M. neonatal plama cortisol were found in postmature neonates when compared with term neonates (P LESS THAN 0.02) or merely postterm neonates (P LESS THAN 0.02). No difference was found in the cord blood cortisol levels in all three groups. Contrary to the traditional belief that postmaturity results from placental aging, our findings appear to indicate that postmaturity represents a specific fetal disorder. Fetal adrenal insufficiency may be a characteristic of this disorder. Prolonged pregnancy in these cases may be reflected inability of the affected fetus to initiate labor.

Early neonatal pneumoperitoneum from progressive massive tension pneumomediastinum.

Three cases of early neonatal pneumoperitoneum as a result of progressive massive tension pneumomediastinum are described. The important roentgenographic features include massive pneumomediastinum located both above and behind the heart, absence of free peritoneal fluid, pneumothorax, and air in the stomach. Laparotomy should be avoided in this condition.