Drug Closure of a Patent Ductus Arteriosus in an Extremely Low Birth Weight Premature Newborn. A Case Report

Introduction: Patent ductus arteriosus involves maintaining the permeability of the vascular ductus located between the pulmonary artery and the descending aorta, due to the failure of transition from foetal to adult type circulation. This malformation is characteristic to premature newborns with extremely low birth weight. The main pathophysiological factors identified in this pathology are immaturity of the smooth muscles, presence of vasodilator mediators and persistent hypoxaemia. Ductal-dependent cardiac malformations require drug therapy for keeping the permeability of the ductus arteriosus until the time of corrective surgery.
Case presentation: We present the case of an extremely low birth weight premature new-born, derived from twin pregnancy with suspected specific pathology, respectively feto-fetal transfusion syndrome, admitted to the Regional Centre of Neonatal Intensive Care Unit Tîrgu-Mureş.
Premature newborn with gestational age 31-32 weeks, extremely low birth weight, derived from twin pregnancy, with adequate prenatal follow up, was born by caesarean section for severe intrauterine growth restriction secondary to feto-fetal transfusion syndrome suspicion. The newborn developed respiratory distress syndrome by surfactant deficiency, intraventricular-haemorrhage grade I/II, and severe retinopathy. The detection of a systolic murmur in the second week of life, the diastolic theft revealed by trans-fontanellar ultrasound as well as lowered diastolic blood pressure values raised the suspicion of a patent ductus arteriosus and therefore specific treatment with ibuprofen, a cyclooxygenase inhibitor, was initiated. Progressive alteration of the newborn`s condition and the evidence of a coarctation of the aorta imposed the initiation of Prostaglandin E1 therapy and subsequent surgical correction.
Conclusions: Although beneficial, prophylactic or therapeutic closure of persistent ductus arteriosus may worsen the evolution of a newborn with a “silent” cardiac malformation and associated pathology.