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International Children's Heart Foundation, Hospital Infantil Manuel de Jesus Rivera, Managua, Nicaragua
(Email: kathleennf{at}msn.com).
The earliest attempts to perform fetal cardiac bypass were met with two main problems: (1) size-related difficulties with venous drainage and (2) death from respiratory insufficiency (ie, placental dysfunction) after bypass. The placental dysfunction was subsequently found to be due to a vasoconstrictive response, which appears to be multifactorial, but a large contributor seems to be a previously ill-defined fetal "stress response."
Lam and colleagues [1] studied the hemodynamic and stress-hormone (ie, vasopressin, cortisol, and beta-endorphin) responses to fetal surgery and cardiac bypass in two thirds gestation fetal lambs, an age chosen to correlate with anticipated clinical fetal cardiac surgery. They used study groups with and without bypass, and with and without sternotomy in an attempt to distinguish the effects of surgical stress from those of bypass. Bypass resulted in a profound rise in vasopressin, which strongly correlated with placental dysfunction and poor outcome. The fact that sternotomy did not cause a higher stress response is interesting, but it should not be misconstrued as a lack of surgical stress; the stress of mere hysterotomy and line placement is evident when one notes that there was already a respiratory acidosis with lower than normal placental blood flow when the first samples were taken. In addition, as noted, bypass caused a more severe and prolonged stress response than surgery alone. Had the study been done in chronically instrumented fetal sheep, it is likely that the results noted would have been even more profound. The findings of the study are similarly limited by the "partial" cardiac bypass that was used (ie, a pump flow of 200 cc/kg/minute represents only approximately half of normal fetal cardiac ["combined ventricular"] output), and the substantial contribution of the fetal heart to cardiac output during bypass is evidenced by the fact that placental blood flow (see Fig 1B) was often higher than pump flow. The problems of adequate venous drainage in the small fetus and of maintaining appropriate distribution of blood flow on bypass (particularly to the placenta and away from the lungs) remain to be solved.
This article is an important contribution to the overall understanding of this stress response, to what causes it, and to how it sometimes results in fatal placental dysfunction. As such, it is likely to be a key step in the development of a technique that will one day lead to successful prenatal treatment of congenital heart defects, and in the short term it provides information that can also be used to improve management of other fetal surgery patients.
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