Hydrops fetalis is the final common hemodynamic pathway for a variety of fetal cardiovascular pathologies, including high-output states associated with fetal anemia or arteriovenous fistulas, and abnormalities of both cardiac structure and rhythm. Hydrops fetalis secondary to cardiovascular decompensation is usually accompanied by increases in fetal systemic venous pressure as evidenced by alterations in venous Doppler blood flow velocities. We present two cases of severe fetal aortic stenosis with left ventricular fibroelastosis and mitral regurgitation, and in-utero closure or stenosis of the foramen ovale, with severe hydrops fetalis, despite normal systemic venous Doppler flow profiles. These cases have led us to reconsider the presumed etiology of cardiovascular-based hydrops fetalis in fetuses with severely impaired left ventricular pump function and secondary mitral regurgitation. We hypothesize that raised pulmonary venous pressure, with only mildly increased central venous pressure, may impact negatively on pulmonary lymphatic flow, decrease serum oncotic pressure, increase venous hydrostatic pressure, and lead to hydrops fetalis.
Copyright (c) 2007 ISUOG. Published by John Wiley & Sons, Ltd.