Abstract
n majority of healthy preterm neonates, ductusarteriosus closes spontaneously by 3-7 days afterbirth [1]. However, three-fourth of very pretermneonates with respiratory distress may continue tohave a patent ductus arteriosus (PDA) at end of first weekof life. Persistent patency of ductus arteriosus increasesblood flow through pulmonary vascular bed anddecreases blood flow through cerebral, mesenteric andrenal vascular beds. PDA has been associated withdecreased survival and increased incidence of pulmonaryhemorrhage and bronchopulmonary dysplasia. Ever sinceinitial reports of effect of indomethacin in inducing ductalclosure were published in 1970s, impact of prophylacticand therapeutic administration of prostaglandininhibitors on short- or long-term outcomes of pretermneonates has been an active research issue [2]. During thelast decade, acquisition of basic echocardiographic skillsby neonatologists has led to earlier recognition andtreatment of PDA before the associated clinical featuresmake their appearance. However, questions on selectingappropriate biomarker of hemodynamic significance,optimal timing (prophylactic, pre-symptomatic orsymptomatic) of administration of prostaglandininhibitors, and even necessity of inducing PDA closureremain largely unanswered.In this issue of
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