Risk of obstetric anal sphincter injury in women having a vaginal birth after a previous caesarean section: A population-based cohort study.

OBJECTIVE: Caesarean section is increasing in prevalence and with it the proportion of women going into their next pregnancy with a scar on their uterus. For women considering vaginal birth after caesarean (VBAC), accurate information about the associated risks is required. STUDY DESIGN: The cohort comprised 192,057 women who had a vaginal delivery of a singleton, term, cephalic infant between the 1st April 2013 and the 31st March 2014 in England: 182,064 women who were having their first baby, and 9993 women who were having a second baby after a previous caesarean delivery. Their risk of an obstetric anal sphincter injury (OASI) was compared using a mixed-effects logistic regression model, adjusting for maternal age, use of instrument, episiotomy, prolonged labour, shoulder dystocia, and demographic factors. RESULTS: The OASI rate was 5.0% in primiparous women, 5.8% in secondiparous women undergoing VBAC after previous elective caesarean, and 7.6% in secondiparous women undergoing VBAC after previous emergency caesarean. Women having a VBAC for their second baby following an emergency caesarean section in their first delivery had a higher rate of OASI than primiparous women (adjusted OR 1.31; 95% CI: 1.20, 1.43), For women with a previous elective delivery, the rates are similar to those for primiparous women. CONCLUSION: Women having a VBAC after emergency caesarean have a higher rate of OASI than primiparous women. This is important in the counselling of women considering VBAC.

Fetal skin possesses the ability to regenerate completely: complete regeneration of skin.

Until a certain developmental stage, cutaneous wounds in mammalian fetuses heal rapidly without scars with complete regeneration of the skin. In the process of fetal wound healing, inflammatory responses, granulation proliferation, and scar formation that are observed in adults are not seen. Numerous studies have reported the causes of fetal scarless cutaneous regeneration, including reduced expression of TGF-ß1 and higher levels of hyaluronan in the extracellular matrix, from the viewpoints of molecular biology and cellular biology, but the mechanisms are not completely understood. Although a variety of substances that inhibit scar formation have been investigated, currently it is almost impossible for adult cutaneous wounds to heal completely without scars. Except for a few animal species, perfect regeneration after wounding can occur only during the gestation period. By strictly comparing the stages before and after the transition from the regeneration of skin to scarring, it will be possible to investigate the mechanisms of cutaneous regeneration.

Analysis of interdigital spaces during mouse limb development at intervals following amniotic sac puncture.

A spectrum of limb abnormalities ranging from adactyly, syndactyly, acrosyndactyly to nail hypoplasia was encountered in mouse embryos subjected to amniotic sac puncture at the corresponding gestational stage when human chorionic villus sampling (cvs) would normally be performed clinically. Previous skeletal studies revealed that, apart from the occasional incidence of fusion of 2 distal phalanges, syndactyly usually only affected the soft tissues within the interdigital spaces. A similar situation was also observed in cases of adactyly; while the skeletal elements of the digits were present, the soft tissues in the interdigital spaces failed to separate. A transient period of bradycardia is induced, possibly secondary to compression of the embryo by the extraembryonic membranes and uterine muscles following amniotic sac puncture. These factors, we believe, produce temporary hypoxia/ischaemia of the distal extremities, and may lead to the modification of the interdigital mesenchymal tissues within the autopods. In order to investigate the mechanism(s) underlying soft tissue syndactyly, limbs recovered at 0.5, 4, 8, 12, 24, or 36 h following amniotic sac puncture (ASP) were examined histologically. Vascular disruption in the form of localised areas of haemorrhage, vascular dilatation and congestion and the presence of fluid-filled cavities occurred in relation to the marginal vein and vascular plexus in the interdigital spaces. It is hypothesised that this interfered with the normal equilibrium of the preset programs of mitosis/cell death and apoptosis within the mesenchymal cells of the interdigital spaces. Apoptosis in these areas was inhibited in the majority of the experimental limbs analysed 4 h after ASP. Instead of undergoing necrosis/apoptosis, increased mitotic activity was usually observed from 8 h following ASP at the sites where apoptosis would normally be expected to be seen. The aberrant fate of the interdigital mesenchyme following ASP and the underlying mechanism(s) involved are discussed, as is the critical importance of an adequate vascular supply to the interdigital spaces during the morphogenesis of the autopod. We believe that this report contributes to understanding the mechanism(s) which lead to syndactyly following ASP, and the limb defects occasionally seen following cvs when this is undertaken during early gestation.