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Furosemide in indomethacin-treated infants--systematic review and meta-analysis
1Albert Einstein College of Medicine and Montefiore Medical Center, Weiler Hospital, Bronx, NY 10461, USA. brion@aecom.yu.edu
Insights
Furosemide may increase the risk of patent ductus arteriosus (PDA) closure failure in premature infants receiving indomethacin. Dehydration is a contraindication for furosemide use in these patients.
Area of Science:
- Neonatal research
- Pharmacology
- Nephrology
Background:
- Patent ductus arteriosus (PDA) is common in premature infants.
- Indomethacin is a standard treatment for symptomatic PDA.
- Furosemide's role in modifying indomethacin efficacy and side effects is unclear.
Purpose of the Study:
- To assess furosemide's effect on PDA closure with indomethacin.
- To evaluate furosemide's impact on indomethacin-induced renal and hydromineral side effects.
- To determine if furosemide's renal effects depend on initial hydration status.
Main Methods:
- Systematic review and meta-analysis of controlled trials.
- Included studies compared indomethacin with furosemide versus indomethacin alone.
- Assessed outcomes included ductal closure and renal function.
Main Results:
- Limited evidence exists due to small study sizes and methodological limitations.
- Furosemide increased urine output and sodium excretion post-indomethacin.
- Renal function effects varied: improved GFR in well-hydrated infants, decreased GFR in dehydrated infants.
Conclusions:
- Dehydration is a potential contraindication for furosemide in premature infants with symptomatic PDA treated with indomethacin.
- Further large randomized trials are needed to clarify the risk-benefit ratio of furosemide in well-hydrated infants.
Abstract:
This study was designed to assess: (1) whether furosemide modifies the incidence of failure to close a symptomatic patent ductus arteriosus (PDA) in response to indomethacin in premature infants, (2) whether furosemide decreases renal and hydromineral side effects of indomethacin, and (3) whether the effects of furosemide on renal function depend on initial extracellular volume [assessed by blood urea nitrogen (BUN)/creatinine ratio]. We did a systematic review and meta-analysis of all published controlled trials assessing either ductal closure or renal function after randomized allocation to treatment with indomethacin and furosemide versus indomethacin alone. All of the three studies meeting entry criteria were small and had methodological limitations. The number of patients was too small to rule out a 10% risk increase in failure of ductal closure. After the first dose of indomethacin, patients receiving furosemide had higher urine output, fractional excretion of sodium, and osmolar clearance than controls. Among patients with initial BUN/creatinine ratio <20, those on furosemide had a higher glomerular filtration rate (GFR) than controls. Among patients with initial BUN/creatinine of 20-30, those on furosemide had a lower GFR than controls. Thus, dehydration appears to be a contraindication for furosemide administration in premature infants treated with indomethacin for symptomatic PDA. The risk-benefit ratio of administering furosemide in well-hydrated patients treated with indomethacin for symptomatic PDA could only be assessed by a large randomized clinical trial.