2015 Volume 42 Issue 6 Pages 725-730
Premature constriction of the ductus arteriosus (PCDA) has a comparatively good prognosis if diagnosed early in utero and appropriately treated. If patients whose ductus arteriosus has closed completely are treated at the incorrect time, however, blood flow to the fetal lungs increases and thickening the smooth muscle layer of the pulmonary artery occurs, as well as potentially fatal complications such as fetal right heart failure, fetal hydrops, and persistent pulmonary hypertension of the newborn (PPHN). We report a case of serious atypical PCDA complicated by PPHN in which fetal diagnosis proved lifesaving. A 27-year-old gravida 1, para 1, who had not experienced any complications during her previous pregnancy and delivery underwent a non-stress test at 36 weeks gestation that revealed mild variable deceleration. Fetal echocardiography showed that on three-vessel view and three-vessel trachea view, compared to the aorta, the ductus arteriosus was dilated and blood flow was absent; therefore, the patient was transferred to a tertiary care facility at 38 weeks 4 days of gestation. This case resembled a regular PCDA in that the right ventricular lumen was dilated and the right ventricular ejection fraction (24%) and the right ventricular fractional area change (3.6%) were both low; in addition, the Tei index was high at 1.16, but was atypical in terms of the thinning of the ventricular wall and low right ventricular pressure. The development of this state, despite the fact that the ductus arteriosus had not completely closed, cannot be explained solely in terms of “afterload mismatch” of the right ventricle; although other possibilities such as impaired coronary perfusion must be considered, there were no findings that directly explained the condition, and many points remain unclear. It is conceivable, however, that atypical thinning of the right ventricular myocardium and low right ventricular pressure may be indicative of increased severity of PCDA.
