No abstract

Prophylactic closure of the patent ductus arteriosus (PDA) has been recommended as a means of decreasing early respiratory distress, and thereby chronic respiratory sequelae in the very low birth weight (VLBW) neonate. This study was undertaken to evaluate some possible mechanisms for the observed failure of early indomethacin therapy to achieve such improvement. 24 VLBW infants with échocardiographie evidence of PDA were randomized to receive either indomethacin or placebo at 48 h of life; and then they were studied for clinical, metabolic and laboratory signs of ductal constriction and/or reopening. Early indomethacin conferred no improvement in respiratory sequelae. However, this was not secondary to a short-term therapeutic failure. Prophylactic indomethacin, even in the VLBW infant, was successful in decreasing dilator prostaglandin production, and probably in closing the PDA and in decreasing the number of recurrences. The implications are that even with effective ductal constriction, overall morbidity is not affected.

We hypothesized that the feeding difficulties experienced by premature infants are related to immature peristaltic activity and that a bowel accelerant might promote feeding in prematures. We administered metoclopramide (Meto) to 14 infants admitted to the Intensive Care Nursery at The University of Chicago between January 1, 1984, and January 1, 1987. Each infant had failed enteral feeding on at least two separate occasions. At the time of initiation of Meto, the group of infants tolerated only 11.7 ± (SEM) 3.6 cm^3/kg/day enterally. Feeding tolerance improved steadily after Meto was initiated, and by 29 days the infants tolerated 134 ± 12.6 cm^3/kg/day enterally. The average slope of the post-Meto feeding regression lines was +4.21 ± 0.94 cm^3/kg/day/day, significantly greater than -0.67 ± 0.59 cm^3/kg/day/day pre-Meto. The percentage of feedings followed by significant gastric residual volumes was 33.1 ± 4.6% pre-Meto, compared to 6.9 ± 2.5% post-Meto. No child receiving Meto developed any extrapyramidal neurologic symptoms, worsening of hepatic function, or necrotizing enterocolitis. Meto may have a role in the treatment of premature infants with enteral feeding intolerance.

No abstract

Maintaining patency of the ductus arteriosus pending surgical intervention can be critical to the survival of the neonate with ductal dependent congenital heart disease. Spontaneously delayed ductal closure has been observed clinically and experimentally in newborns with critical pulmonic stenosis. Infants with ductal dependent congenital heart lesions were therefore studied to ascertain whether there was an endogenous increase in dilator prostaglandins prolonging ductal patency. Six neonates with cyanotic lesions (group 1) and six with left ventricular obstructive lesions (group 2) were studied. Circulating PGE2 was not increased in either group. The levels of plasma 6 keto PGF1 alpha, a stable hydrolysis product of prostacyclin, were found to be elevated, but only in the cyanotic group (3143 +/- 1844 vs 404 +/- 250 pg/ml; p less than 0.05; normal less than 500 pg/ml). As expected, PaO2's were also different (36 +/- 15 vs 72 +/- 34 mmHg; p less than 0.05). It is speculated, therefore, that increased synthesis and/or release of prostacyclin, possibly mediated by the hypoxia of the cyanotic ductal dependent lesion, contributes to persistent patency of the ductus arteriosus.