Abstract
Furosemide is the diuretic most used in newborn infants. It blocks the Na+-K+-2Cl− symporter in the thick ascending limb of the loop of Henle increasing urinary excretion of Na+ and Cl−. This article aimed to review the published data on the clinical pharmacology of furosemide in neonates to provide a critical, comprehensive, authoritative and, updated survey on the metabolism, pharmacokinetics, pharmacodynamics and side-effects of furosemide in neonates. The bibliographic search was performed using PubMed and EMBASE databases as search engines; January 2013 was the cutoff point. Furosemide half-life (t1/2) is 6 to 20-fold longer, clearance (Cl) is 1.2 to 14-fold smaller and volume of distribution (Vd) is 1.3 to 6-fold larger than the adult values. t1/2 shortens and Cl increases as the neonatal maturation proceeds. Continuous intravenous infusion of furosemide yields more controlled diuresis than the intermittent intravenous infusion. Furosemide may be administered by inhalation to infants with chronic lung disease to improve pulmonary mechanics. Furosemide stimulates prostaglandin E2 synthesis, a potent dilator of the patent ductus arteriosus, and the administration of furosemide to any preterm infants should be carefully weighed against the risk of precipitation of a symptomatic patent ductus arteriosus. Infants with low birthweight treated with chronic furosemide are at risk for the development of intra-renal calcifications.
Highlights
Diuretics increase the rate of urine flow and Na+ excretion and are used to adjust the volume and/or the composition of body fluids
Furosemide may be administered by inhalation to preterm infants with chronic lung disease [10] to improve pulmonary mechanics [11]
Furosemide stimulates the synthesis of prostaglandin E2 which inhibits the closure of the ductus arteriosus
Summary
Diuretics increase the rate of urine flow and Na+ excretion and are used to adjust the volume and/or the composition of body fluids. The basic urine-forming unit of the kidney is the nephron, which consists of a filtering apparatus, the glomerulus, connected to a long tubular portion that reabsorbs and conditions the glomerular ultrafiltration. Furosemide increases the delivery of solutes out of the loop of. Around the year 1960 “loop” diuretics (furosemide, ethacrynic acid and bumetanide) were developed. These block the Na+-K+-2Cl− cotransport system in the ascending limb [4] and inhibit Na+, Cl− and K+ entering the tubular cell. Loop diuretics are highly efficacious, and for this reason, are called “high-ceiling-diuretics”
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