Oxygen tox1c1ty and barotrauma from mechanical ventilation are considered to be the most important factors contributing to lung injuries in premature infants with RDS 1 . Various evidences suggest that inflammatory changes following lung injuries may occur very early in the course of RDS and may play an important role for the subsequent development of chronic lung disease (CLD) 2 • 3 • Previous studies using dexamethasone (D) in infants with CLD have shown a short-term benefit of improving lung compliance and facilitating extubation 4• 5 • 6• However, the majority of these studies were done on infants aged one week or older, who might already have well established lung injuries. None of these studies demonstrated improvement in CLD morbidity 4• 7• We believe that if steroid is to be beneficial in preventing lung injury, it may have to be administered very early after birth. Our previous study 8 and recent study by Sanders et al. 9 strongly indicated this possibility. Based on this hypothesis, a double-blind multicenter collaborative study was undertaken. The purposes of the study were: 1) does early D therapy, given within 12 hours after birth and appearing during the first 28 postnatal days, improve pulmonary status in premature infants with severe RDS? 2) does improvement of pulmonary status increase survival or decrease the incidence of CLD?3) what are the mechanisms responsible for the improvement of pulmonary status? 4) what are the associated side effects?Premature infants with B.W. <2000 gm and with severe RDS requiring mechanical ventilation shortly after birth were included in the study. They were randomized into two groups: Placebo (saline control, C) and D treated group. The dosages of D given (I.V.) were: 0.25 mg/kg/dose q.l2h. (day 1-7)~ 0.125 mg/kg/dose q.l2h. (day 8-14)~ 0.05 mg/kg/dose q/12h. (day 15-21); 0.025 mg/kg/dose q.12h. (day 22-28). During the first part of the study, surfactant was not given because it was not commercially available. During the 2nd part of the 1997 Wiley-Liss, Inc.study, one dose of surfactant (survanta) was giVen routinely to all infants. RESULTS (PART 1)262 infants were included: 130 in the C and 132 in the D treated group. The first dose ofD was given at 7.4 ± 4.1 hrs. Infants in the D group required lower mean airway pressure and had lower PC0 2 values than infants in the C group. Among the survivals, more infants in the D than in the C group were extubated at 28 postnatal days (p<0.05). The incidence of CLD judged at 28 postnatal days among the survivals was significantly lower in the D group (21%) than in the C group (44%). There was no difference between the groups in mortality, duration of 0 2 and IMV therapy. Infants in the D group had transient higher blood pressure, glucose, parathyroid hormone, cardiac septal hypertrophy than infants in the C group during the first 2 weeks after study. There was no · difference between the groups in incidence of intraventricular hemorrhage (> Grll), retinopathy of immaturity and necrotizing enterocolitis. The D group had ...

The effect of indomethacin on the control of breathing was simultaneously evaluated in 10 premature infants who had significant patent ductus arteriosus and received indomethacin therapy. In an attempt to maintain high plasma level in these infants of advanced postnatal age (≥ 6 weeks), indomethacin was administered intravenously at a dosage of 0.3 mg/kg, at 8-hour intervals, for a total of three doses. Following indomethacin therapy, there was a significant increase in tidal volume, minute ventilation, tidal volume/inspiratory time and in airway pressure (P(0.1), P(max)) generated during airway occlusion. Seven infants required lower ventilatory rates after study. In spite of desirable plasma indomethacin level, there was no significant improvement in echo left atrium/aortic root dimension ratio, cardiovascular dysfunction score and in blood pH, PO(2) and PCO(2). None of the infants showed clinical evidence of ductus closure. The results of the study suggested that indomethacin may stimulate respiration and that endogenous prostaglandin may play a role in the regulation of breathing.

manager 5.2 (statistical significance with two-sided p-value of 0.05). Results Nine trials were included from 1622 non-duplicate records. The meta-analysis results were shown in a table with pooled risk ratios (RR) and 95% confidence interval (CI).

Simultaneous administration of one dose of indomethacin (0.3 mg/kg, i.v.) and furosemide (1 mg/kg, i.v.) was given to 8 consecutive premature infants who had patent ductus arteriosus (PDA), and oliguria because of prerenai failure. Four infants responded with ductus closure and 2 infants showed improvement in echocardiogram and clinical distress. There was a significant increase in U/O, GFR, FE(Na) and FE(C1) following drug administration. This study suggests that simultaneous administration of indomethacin and furosemide can be safely used in infants with PDA and oliguria.

The effects of dexamethasone therapy on calcium homeostasis and bone growth were evaluated in 49 infants (24 placebo and 25 dexamethasone) who participated in a double-blind trial of early dexamethasone therapy for the prevention of chronic lung disease. Dexamethasone (0.25 mg kg −1 b.i.d. on d 1-7; 0.12 mg kg −1 b.i.d. on d 8-14; 0.05 mg kg −1 b.i.d. on d 15-21; 0.02 mg kg −1 b.i.d. on d 22-28) or saline placebo was given i.v. Serum calcium (Ca), phosphorus (P) and parathyroid hormone (PTH), and the corresponding urinary excretion of calcium (FE Ca ) and phosphorus (FE P ) were measured on d 2, 3, 7, 10, 14, 21 and 28 after starting the study. Radiographic evaluations of bone growth were also evaluated. Infants in the dexamethasone group had significantly higher PTH on d 2 ( p Ͻ 0:01), 7 and 14 ( p Ͻ 0:05) than infants in the placebo group. The dexamethasone-treated infants also had significantly higher FE P on d 2, 7 and 14 ( p Ͻ 0:05) and lower FE Ca on d 7 and 14 ( p Ͻ 0:05) than control infants. There was no significant difference between the groups in bone growth during the study. It was concluded that early dexamethasone therapy causes a transient elevation in PTH without apparent change in bone growth. The long-term effect remains to be evaluated further. ٖ Calcium homeostasis, dexamethasone, parathyroid hormone, preterm infant