The aim of this study was to determine the feasibility and safety of hysteroscopic metroplasty in cases of diethylstilboestrol-exposed and hypoplastic malformed uterus. Twenty-four patients were referred for primary infertility (n = 9), secondary infertility (n = 1) or infecundity (n = 14). Fifteen had been exposed to diethylstilboestrol in utero. All patients had a hypoplastic uterus and/or uterine deformity as seen by hysterosalpingography and each served as their own control. All patients underwent hysteroscopic metroplasty. Outcome measures included postoperative hysterosalpingography and the ability to conceive and to carry pregnancy to live birth. Postoperative hysterosalpingograms revealed improvement in 23 cases; the final result was considered excellent in 15 cases and 11 pregnancies occurred. The abortion rate decreased from 88% in previous pregnancies to 12.5%, and the rate of term deliveries increased from 3% to 87.5%. Ten patients were delivered after 30 weeks' gestation of healthy infants and one delivered more prematurely. Six deliveries were normal and four required a Caesarean section. We conclude that hysteroscopic metroplasty gives good results. This technique can be used in women with diethylstilboestrol-exposed or hypoplastic malformed uterus, suffering from severe infertility, recurrent pregnancy loss or implantation failures in an in-vitro fertilization programme.
In 228 patients, fetal blood pH, pCO2 and lactic acid were measured in two distinguishable parts of the second stage of labor. The 'first' part begins at full cervical dilatation and ends when the mother starts her first voluntary bearing down efforts. In our study, the fetal acid-base status did not change in this part, regardless of a late developing hypoxia. In contrast, higher levels of lactic acid and pCO2 and lower pH values were observed in the 'final' part of the second stage, indicating increasing acidosis. In this 'final' part, the fetuses with clinical signs of distress, as defined by an ominous Apgar score at birth, showed quicker and larger acid-base shifts than did the normal fetuses. Thus the two parts of the second stage of labor actually differ in their potential to stimulate fetal acidosis. Since such fetal acidosis may develop especially during the 'final' part of labor, we have concluded that special particular attention should be devoted to this part.
This study evaluates the prognostic value of uterine Doppler performed on the day of embryo transfer in an in vitro fertilization program. Patients were divided into two groups according to the type of ovarian stimulation. The Doppler investigation was carried out using vaginal sonography. The pulsatility index was used to evaluate the uterine blood flow pattern. The hormonal profile (estradiol, luteinizing hormone (LH) and progesterone) was correlated to Doppler results and to the pregnancy rate. The comparison between patients treated with analogs and those who were not shows a significant difference in their hormonal profile. In the first group, we found a higher estradiol and progesterone serum concentration. The LH level and the pulsatility index were statistically lower. The endometrium was thicker in patients treated with gonadotropin releasing hormone agonists. In the group of patients treated with analogs, the statistical analysis showed no significant difference in the mean pulsatility index value in women who achieved a pregnancy and in those who failed. In the group of patients who received no agonists, only one variable was significantly different: the mean age was lower in women who became pregnant. We observed no ongoing pregnancy in women who had a pulsatility index value higher than two standard deviations (pulsatility index = 3.55). We therefore suggest the use of this value as a threshold. Thus, if a patient has a high uterine artery impedance, cryopreservation should be used and embryo transfer should be postponed to a subsequent cycle, or embryo transfer delayed for a few days using co-culture. This study clearly shows the impact of hormonal response on the Doppler value and on the pregnancy rate. However, the use of a threshold value for uterine artery pulsatility index might have a clinical impact in the future management of patients attending an in vitro fertilization program.
The purpose of this study was to investigate whether maternogenic fetal acidosis can occur at the time of labor and delivery and to evaluate the extent of the possible maternal contribution to fetal acidosis. We have therefore determined fetal and maternal lactate concentrations and acid-base status under various conditions in 589 women at the end of gestation and during labor. The results show that metabolic acidosis develops in all fetuses because of increased production of lactic acidosis is primarily of fetal origin: 1) the umbilical arteriovenous lactate differences were positive and large in steady-state conditions as well as in depressed newborns; 2) the conditions that could produce a net transfer of lactate from the mother to the fetus, namely a positive maternofetal gradient of lactate and proton, were rarely observed; and 3) the correlation between fetal and maternal lactate levels was very weak, with regression coefficients decreasing from near steady-state conditions to acute stress conditions, indicating that the increase in lactate in the fetus and mother occurs independently. This correlation indicates also that increased maternal lactate production under conditions of labor and delivery can make a contribution by affecting the rate of net transfer from fetus to mother. This is possible in approximately 6% of the fetuses.
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