Minimal-access fetal surgery for twin-to-twin transfusion syndrome.

BACKGROUND: Laser ablation of placental vessels effectively halts severe twin-to-twin transfusion syndrome (TTTS), but fetal surgery remains a dangerous approach. The authors present the technical aspects of endoscopic fetal surgery in their initial clinical experience. METHODS: Altogether, 11 women underwent endoscopic fetal surgery for severe TTTS. Access to the recipient's sac was obtained by the Seldinger technique via minilaparotomy. A 12-Fr peel-away introducer was used as a cannula to accommodate a custom-curved 9-Fr sheath containing a 1.9-mm semirigid fiber endoscope. Laser ablation was performed on all unpaired vessels crossing the intertwin membrane using a 400- micro m neodymium: yttrium-aluminum-garnet (Nd: YAG) fiber. The cannula was removed over a gelatin sponge plug. RESULTS: The median operating time was 65 min (range, 45-105 min). No patient experienced amniotic leak postoperatively. The length of hospital stay was 2.8 +/- 1.6 days. Immediate improvement of the TTTS was noted in all but two patients. Pneumonia developed, in one mother leading to premature labor. There were no other major surgical complications. Fetal survival at 2 weeks was 73%. CONCLUSIONS: The safety and efficacy of endoscopic fetal surgery for severe TTTS can be optimized with the application of current minimal-access techniques. The superiority of this approach over less invasive means is still being evaluated through prospective studies.

Inhibition of placental 11beta-hydroxysteroid dehydrogenase type 2 by catecholamines via alpha-adrenergic signaling.

The placenta expresses high levels of 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) that converts cortisol into inactive 11-keto metabolites and effectively protects the developing fetus from maternal cortisol during pregnancy. Impairment of this glucocorticoid barrier has adverse effects on fetal outcomes. A similar spectrum of adverse fetal effects is induced by antenatal stress during pregnancy. To examine the hypothesis that physiological stress may regulate placental 11betaHSD2 gene expression, we examined the effects of the catecholamines norepinephrine (NE) and epinephrine (E) on 11betaHSD2 expression in human trophoblastic cells. With the use of Northern blotting and semiquantitative RT-PCR, we determined that NE and E rapidly downregulate 11betaHSD2 steady-state mRNA levels in early- and late-gestation human trophoblasts and BeWo trophoblastic cells. Experiments using different adrenoceptor subtype-selective agonists and antagonists demonstrated that this catecholamine suppression of 11betaHSD2 mRNA expression is mediated via both alpha(1)- and alpha(2)-adrenoceptors and is independent of beta-adrenergic stimulation. To examine transcriptional regulation, BeWo cells were transiently transfected with a reporter construct in which an 11betaHSD2 human promoter sequence was inserted upstream of the luciferase gene. Treatment with 10(-7) M NE decreased luciferase activity by ~60% (n = 3, P < 0.01). These results suggest the NE/E-mediated decrease in placental 11betaHSD2 gene expression is an instance of alpha-adrenoceptor-specific rapid transcriptional inhibition of an adrenergic target gene. This molecular mechanism may be involved in the deleterious effects of antenatal physiological stress on fetoplacental growth and development.

Rhesus isoimmunization.

Rh isoimmunization is a potentially preventable condition that occasionally is associated with significant perinatal morbidity or mortality. Disease severity may be assessed using the modalities described above and frequently, invasive techniques are required to determine the risk of severe disease. Doppler flow studies appear to offer accurate, noninvasive means of evaluating fetal risk, which may allow for a decrease in invasive diagnostic procedures. The Rh isoimmunized patient, managed by an experienced team, can anticipate a favorable pregnancy outcome.