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Based on the knowledge gained from the advances in the aforementioned diagnostic modalities, perinatal management recommendations have been formulated for select fetuses with life-threatening anomalies (Table 3-1). More precisely, the natural history, pathophysiology, associated anomalies, and therapeutic options have become the basis for the multidisciplinary fetal treatment team, which has enabled the approach to the fetus as patient (13:Calan). Prenatal intervention has, in large part, been predicated on those anomalies that result in either low- or high-output cardiac failure resulting in hydrops (skin and/or nuchal edema or fluid accumulation in two of three body cavities (pleura, pericardium, peritoneum)]. Hydrops resulting from a specific lesion results in nearly 100% fetal mortality. Examples include fetuses with hydrops from a CCAM, sacrococcygeal teratoma (SCT:Calan), pericardial teratoma, select heart defects, tension hydrothorax, twin–twin transfusion syndrome (TTTS:Calan), and twin reversed arterial perfusion (TRAP) sequence. Pulmonary and kidney failure can be predicted in a subset of fetuses with urinary tract obstruction (e.g., posterior urethral valves:Calan) and may benefit from US-guided vesicoamniotic shunt placement.

Persistent patency of the ductus arteriosus is a common problem in sick, premature infants and can lead to high-output cardiac failure due to aortic to pulmonary artery shunting. In the fetus, 69% of combined ventricular output is oxygenated blood that travels from the placenta to the fetal right atrium through the umbilical vein, ductus venosus, and inferior vena cava (Fig. 4-1:Calan). A portion of oxygen-rich blood that enters the right atrium from the inferior vena cava is shunted preferentially across the atrial septum through the foramen ovale to the left atrium. This oxygenated blood is pumped into the ascending aorta by the left ventricle and is thus more available to the coronary arteries and subclavian and carotid arteries than to the systemic circulation. Because only about 7% of fetal right ventricular output goes to the lungs, owing to supersystemic pulmonary vascular resistance during fetal life, the right ventricle performs about twice as much work as the left ventricle during fetal life. About 90% of right ventricular output flows to the systemic circulation through the ductus arteriosus. Fetal oxygen tension is usually 25 to 30 mm Hg.