V. Zanardo et al., SILENT PATENT DUCTUS-ARTERIOSUS AND BRONCHOPULMONARY DYSPLASIA IN LOW-BIRTH-WEIGHT INFANTS, Journal of perinatal medicine, 23(6), 1995, pp. 493-499
We conducted a clinical study on the antecedents of bronchopulmonary d
ysplasia (BPD) in 290 premature RDS infants with less than or equal to
1.75 kg birth weight (BW). They were enrolled in a prospective trial
of indomethacin treatment for ''silent'' patent ductus arteriosus (PDA
), screened by 2-D echocardiographic and pulsed Doppler evaluation on
the third day of life. The trial took place at the NICU of the Pediatr
ic Department of Padua University between January 1987 and December 19
91. Out of 290 infants screened, 96 had evidence of ''silent'' PDA (33
%) and 77 responded to indomethacin treatment (80%). Comprehensively 7
9 (27%) developed BPD, and from thse the incidence of BPD was statisti
cally increased in infants with ''silent'' PDA, 47 out of 96 (49 +/- 9
%), with respect to 32 out of 194 (16 +/- 3%) preterm infants without
PDA. Statistical analysis showed that in preterm infants with ''silent
'' PDA the development of BPD was correlated at 99% C. L. to their low
BWs (mean BW = 1.13 kg): in fact the mean and the mode of BW distribu
tions were statistically lower in the presence of BPD, 1.03 kg versus
1.24 kg, and 0.88 kg versus 1.65 kg respectively. Moreover, the preter
m infants with ''silent'' PDA unresponsive to the first course of indo
methacin and/or submitted later to surgical closure, presented a stati
stically lower BW with respect to the early responders, 1.06 kg versus
1.18 kg, and at the same time a statistically higher incidence of BPD
(63 +/- 20% versus 43 +/- 9%). From these data we conclude that, alth
ough ''silent'', PDA increase per se the incidence of BPD, even if ben
efits from an early induced closure. Furthermore, a lower BW of infant
s affected by ''silent'' PDA represents a contributing factor to the d
evelopment of BPD.