Premature closure of the ductus arteriosus carries wide range of fetal and postnatal presentations; starting from mild asymptomatic disease with transient neonatal tricuspid and pulmonary regurgitation, passing by persistent pulmonary hypertension of the newborn ending by severe perinatal lethal condition (intra uterine death or early postnatal functional pulmonary atresia with consequent neonatal death). Several factors determine the postnatal presentation, the most important of which are fetal hydrops, complete ductal closure and the duration of prenatal ductal closure.Premature ductal closure shows multi-level downstream consequences on different right heart structures (RA, RV, Pulmonary valve, MPA, central pulmonary arteries and peripheral pulmonary vascular bed). The overall pathologic findings are due to prenatal elevation of pulmonary systolic and diastolic pressures. While both fetal lung fields are fluid filled and show high resistive pulmonary vascular flow pattern, most of the RV stroke volume (about 90%) will be ejected through ductus arteriosus into systemic circulation, thus its premature constriction will eventually shift most of the RV output into both lung fields with significant pressure load exerted on the right ventricle. The pressure load on the RV will cause variable degrees of remodeling to overcome the sustained elevation of pulmonary pressures owing to both ductal closure and the high resistivity in fetal pulmonary vascular bed. Initially, adaptive concentric right ventricular hypertrophy will occur then systolic dysfunction (mainly the longitudinal shortening component with concurrent moderate to severe tricuspid regurgitation and consequent RA dilatation), leading to progressive RV dilatation pooling more blood to compensate for rather normal stroke volume till the degree where a decompensated RV failure occurs (elevated RV filling pressure “diastolic pressure” with systolic dysfunction and consequently severe pan systolic tricuspid regurgitation, monophasic filling across tricuspid valve, severe RA dilatation, severe systemic venous congestion and finally hydrops with decline in cardiac output).  This picture is prenatally reflected initially by the reversal of A wave in ductus venosus till reaching pulsatile flow pattern in umbilical vein itself with fetal hydrops carrying very high mortality risk at this stage. Shift of the RV output into the high resistive pulmonary circulation will lead to high volume load on both lungs carrying the risk of pulmonary vascular remodeling and postnatal persistent pulmonary hypertension of the newborn (PPHN) and functional pulmonary atresia. During fetal life, complete ductal closure, duration of closure as well as the progressive pulmonary regurgitation could be key features to define such neonatal risk. Premature ductal constriction also has an impact on pulmonary trunk and central pulmonary arteries with consequent pulmonary regurgitation and changes in pulmonary artery distensibility and degree of dilatation. Preserved good arterial distensibility reflects a favorable prognosis in early neonatal life , while progressive dilatation with poor distensibility carries a risk of neonatal bronchomalacia and air trapping.In absence of fetal hydrops, the preserved RV function, incomplete ductal closure, the absence of pulmonary regurgitation as well as good pulmonary arterial distensibility represent good indicators of fetal and neonatal outcome. In our case, these markers were assessed to evaluate neonatal prognosis. The most important of which is preserved RV ejection capacity manifested by preserved normal Tie index and the early systolic TR (reflecting good systolic ejection capacity despite reduced longitudinal shortening component evidenced by reduced TAPSI compared to MAPSI) and the normal biphasic inflow pattern across tricuspid valve (reflecting still preserved normal filling pressure) with moderate RA dilatation but still no significant elevation of systemic venous pressure (Ductus venosus). The second important one is incomplete closure of ductus arteriosus for short duration reflecting still opened, yet stenotic, pathway for RV stroke volume into systemic circulation. The third one is the ability of pulmonary circulation to accommodate the increased pulmonary flow volume manifested by absence of pulmonary valvular regurgitation and the good distensiblity of main and central pulmonary arteries. According to fetal cardiovascular profile score, our case was given a score of 8 (due to presence of pericardial effusion and mild cardiomegaly) representing a good neonatal outcome.In conclusion, study of all downstream effects of premature ductal constriction is of great importance prior to taking a decision about delivery time to avoid complicated neonatal chest condition and enhance early complete recovery.

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