AbstractThe effect of early furosemide‐induced diuresis was prospectively evaluated in 39 neonates less than 24 hr of age with clinical respiratory distress syndrome (RDS) who received either four doses of furosemide (1 mg/kg) or no diuretic. Measurements of Fio2alveolararterial oxygen gradient (PA‐aO2), peak inspiratory pressure (PIP), and urine output as a fraction of intake (O/l) were averaged for every 8 hr. The furosemide group overall showed a significant decrease (P<0.01) in Fio2, PA‐aO2, and PIP with an earlier (32 hr vs 52 hr) and more pronounced diuresis (35 greater O/l) when compared to the controls. This effect was accentuated in the subgroup with 1,000–1,500 g birth weight (significantly lower Fio2and P(A‐a)o2from 16 to 48 hours), while no increase in urine output was observed for the infants weighing less than 1,000 g. A significant reduction in supplemental oxygen and need for ventilatory support at 96 hr of age was observed in the furosemide‐treated, less than 1,500‐g infants. The incidence of patent ductus arteriosus was not increased following furosemide therapy, and no significant difference in echocardiographic parameters was observed in 21 infants from both groups, who were followed daily during the first week of life. This study suggests that early furosemide‐induced diuresis, particularly in infants weighing 1,000–1,500 g at birth, promotes improvement in pulmonary functions in RDS and leads to faster reduction in oxygen and ve
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