Neonatal morbidity in a low volume forceps practice.

BACKGROUND: Currently, the use of FE is decreasing and neonatal adverse outcomes following FE are underreported. We aimed to evaluate the rate of neonatal adverse outcomes in current obstetric practice at two university hospitals with a low FE volume. METHODS: A multicentre retrospective study. All singleton pregnancies delivered by forceps extraction between 2011 and 2020 were analyzed. The characteristics of the deliveries with a composite neonatal adverse outcome (CNAO) were analyzed and compared with those without. RESULTS: The study cohort included 861 neonates delivered by FE. The CNAO was recorded in 131 (15.2%). Women in the CNAO group gained less weight during pregnancy (mean 13 kg vs. 15 kg, p = .014). Factors found to be associated with CNAO were preterm delivery (gestational age < 37°/7) (26 (19.8%) vs. 44 (6.0%), OR [95% CI]: 3.86 (2.28-6.52), p < .001), low birth weight (23 (17.6%) vs. 44 (6.0%), OR [95% CI] 3.32 (1.92-5.71), p < .001), and smaller head circumference (329 vs. 331 mm, OR [95% CI] 0.79 (0.67-0.93), p = .035). In a multivariate analysis, gestational age (adjusted OR [95% CI] 0.672 (0.546-0.826), p < .001) and maternal weight gain during pregnancy (adjusted OR [95% CI]: 0.950 (0.904-0.998), p = .042), were both negatively associated with CNAO. Among term deliveries, the only factor found to be independently associated with CNAO was maternal weight gain during pregnancy (adjusted OR [95% CI]: 0.951 (0.910-0.994), p = .025). CONCLUSIONS: In the setting of low volume FE, this mode of delivery is associated with a relatively low rate of neonatal morbidity. SYNOPSIS: Performance of forceps extraction in the setting of low volume practice is associated with a relatively low rate of neonatal morbidity.

Low volume forceps practice and anal sphincter injury rate.

PURPOSE: While the increased rates of high degree perineal tears were previously associated with the use of forceps, in the current era of low volume of forceps practice, factors associated with the occurrence of this potential complication remain understudied. We aim to evaluate factors associated with obstetric anal sphincter injury (OASIS) in obstetric units with a low volume forceps practice. METHODS: A retrospective cohort study was conducted at two tertiary medical centers. All singleton pregnancies delivered by forceps extraction between 2011 and 2019 were analyzed. Women who experienced anal sphincter injury were compared to those who did not. RESULTS: The study cohort included 764 forceps deliveries. There were 19 (2.5%) cases of OASIS. Women with anal sphincter injury had higher rates of gestational diabetes mellitus (21% vs. 5.6%, OR [95% CI] 4.46 (1.41-14.04), p = 0.02). Birth weights and the rate of macrosomia did not differ between groups. Induction of labor was more common among the OASIS group (68% vs. 41.7%, OR [95% CI] 3.0 (1.1-8.0), p = 0.02). Sequential use of forceps (after failed vacuum attempt) was associated with OASIS (8 (42%) vs. 76 (10.2%), OR [95% CI] 6.4 (2.5-16.4), p < 0.001). In a multivariate logistic regression, sequential forceps was the only factor independently associated with OASIS (OR [95% CI] 4.7 (1.3-18.2), p = 0.02). CONCLUSIONS: Rate of OASIS was relatively low in the current cohort. Sequential use of forceps was found to be the most important determinant in OASIS occurrence.

Induction of apoptosis in granulosa cells by TNF alpha and its attenuation by glucocorticoids involve modulation of Bcl-2.

Tumor necrosis factor alpha (TNF alpha) plays a role in mammalian ovarian follicular development, steroidogenesis, ovulation, luteolysis, and atresia, but the exact mechanism of TNF alpha action is not completely understood. Induction of apoptosis and suppression of steroidogenesis by TNF alpha in primary preovulatory rat and human granulosa cells, as well as, in human granulosa cells immortalized by mutated p53, were characterized in the present work. Dexamethasone (Dex) and hydrocortisone efficiently suppressed TNF alpha-induced apoptosis in granulosa cells. TNF alpha dramatically reduced intracellular levels of Bcl-2, while Dex abrogated this reduction. TNF alpha reduced considerably intracellular levels of StAR protein, a key regulating factor in steroidogenesis. This reduction can be explained only in part by elimination of cells through apoptosis, since loss of steroidogenic capacity was much higher and faster than the rate and extent of loss of cell viability induced by TNF alpha, suggesting independent mechanisms for TNF alpha-induction of apoptosis and TNF alpha-suppression of steroidogenesis.