The effect of a PDA in the etiopathogenesis of BPD was studied during a double blind trial of early dexamethasone (D) therapy in surfactant(S) treated infants with RDS. D (0.5 mg/kg, 0.3 mg/kg, 0.2 mg/kg, 0.1 mg/kg each for three days) or saline P were given b.i.d. starting 7.3 ± 3 hrs (mean ± SD). Infants who survived neonatal period were studied (32 placebo P, 32 D). P and D were comparable in BW (1022 ± 226 vs. 1097 ± 234 g), GA(28.2 ± 2 vs. 28.8 ± 2), sex, race, Apgar and pulmonary status at time of starting study. The diagnosis of PDA was made clinically and was confirmed by cardiac ultrasound. (*<0.05,**<0.01; §<0.05, D vs P) Table

Table 1
Full size table

PDA significantly increased (1) the number of days on ventilator in infants with RDS, (2) the number of days on supplemental oxygen and supplemental oxygen ≥0.4 in D infants. However, D as compared to P significantly reduced the number of days on ventilator in babies with No PDA and the number of days on supplemental oxygen in both PDA and No PDA infants. In conclusion, PDA has a sig. role in the etiopathogenesis of BPD; D reduces the risk of BPD even in babies with PDA.