Williams I A, Kleinman C S
Columbia University College of Physicians & Surgeons, Morgan Stanley Children's Hospital of New York, New York, NY, USA.
Ultrasound Obstet Gynecol. 2008 Jan;31(1):96-9. doi: 10.1002/uog.5238.
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.
胎儿水肿是多种胎儿心血管疾病的最终共同血流动力学途径,包括与胎儿贫血或动静脉瘘相关的高输出状态,以及心脏结构和节律异常。继发于心血管失代偿的胎儿水肿通常伴有胎儿体静脉压升高,静脉多普勒血流速度改变可证明这一点。我们报告了两例严重胎儿主动脉狭窄伴左心室纤维弹性组织增生和二尖瓣反流,以及卵圆孔在宫内闭合或狭窄,尽管体静脉多普勒血流图谱正常,但仍有严重胎儿水肿的病例。这些病例促使我们重新考虑左心室泵功能严重受损和继发性二尖瓣反流胎儿中基于心血管的胎儿水肿的假定病因。我们假设,肺静脉压升高,而中心静脉压仅轻度升高,可能会对肺淋巴流动产生负面影响,降低血清胶体渗透压,增加静脉静水压,并导致胎儿水肿。