Regulation of fetal growth: consequences and impact of being born small

The first trimester of pregnancy is the time during which organogenesis takes place and tissue patterns and organ systems are established. In the second trimester the fetus undergoes major cellular adaptation and an increase in body size, and in the third trimester organ systems mature ready for extrauterine life. In addition, during that very last period of intrauterine life there is a significant increase in body weight. In contrast to the postnatal endocrine control of growth, where the principal hormones directly influencing growth are growth hormone (GH) and the insulin-like growth factors (IGFs) via the GH-IGF axis, fetal growth throughout gestation is constrained by maternal factors and placental function and is coordinated by growth factors. In general, growth disorders only become apparent postnatally, but they may well be related to fetal life. Thus, fetal growth always needs to be considered in the overall picture of human growth as well as in its metabolic development.

Maternal factors implicated in fetal bradycardia after combined spinal epidural for labour pain

BACKGROUND AND OBJECTIVE: Combined spinal epidural analgesia is effective for fast relief of severe labour pain but has been associated with worrisome decreases in fetal heart rate. Since the reasons for this phenomenon remain elusive, some anaesthesiologists may abstain from using this technique. We postulated that factors unrelated to the neuraxial technique could play a role in the decrease in fetal heart rate. To our knowledge, no prospective study has previously looked into this possibility. METHODS: We collected prospective data on 223 consecutive patients who received combined spinal epidural analgesia (123) or epidural analgesia (100). Maternal blood pressure, analogue pain scores, exogenous infusion of oxytocin, cervical dilatation, maternal age, parity and ethnicity were collected and correlated with the occurrence of decreases in fetal heart rate post combined spinal epidural. RESULTS: Univariate analysis showed a correlation between the incidence of fetal bradycardia and higher maternal pain scores, older maternal age, and combined spinal epidural analgesia. Multivariate analysis revealed that only pain scores and maternal age were independent predictors of fetal bradycardia post neuraxial blockade. CONCLUSIONS: Maternal pain scores and older maternal age are factors unrelated to the neuraxial technique that are independent predictors of fetal bradycardia after neuraxial analgesia for labour.

Calcium channel TRPV6 is involved in murine maternal-fetal calcium transport

Maternal-fetal calcium (Ca(2+)) transport is crucial for fetal Ca(2+) homeostasis and bone mineralization. In this study, the physiological significance of the transient receptor potential, vanilloid 6 (TRPV6) Ca(2+) channel in maternal-fetal Ca(2+) transport was investigated using Trpv6 knockout mice. The Ca(2+) concentration in fetal blood and amniotic fluid was significantly lower in Trpv6 knockout fetuses than in wildtypes. The transport activity of radioactive Ca(2+) ((45)Ca) from mother to fetuses was 40% lower in Trpv6 knockout fetuses than in wildtypes. The ash weight was also lower in Trpv6 knockout fetuses compared with wildtype fetuses. TRPV6 mRNA and protein were mainly localized in intraplacental yolk sac and the visceral layer of extraplacental yolk sac, which are thought to be the places for maternal-fetal Ca(2+) transport in mice. These expression sites were co-localized with calbindin D(9K) in the yolk sac. In wildtype mice, placental TRPV6 mRNA increased 14-fold during the last 4 days of gestation, which coincides with fetal bone mineralization. These results provide the first in vivo evidence that TRPV6 is involved in maternal-fetal Ca(2+) transport. We propose that TRPV6 functions as a Ca(2+) entry pathway, which is critical for fetal Ca(2+) homeostasis.

Imaging structural abnormalities in the hip joint: instability and impingement as a cause of osteoarthritis

Osteoarthritis is thought to be caused by a combination of intrinsic vulnerabilities of the joint, such as anatomic shape and alignment, and environmental factors, such as body weight, injury, and overuse. It has been postulated that much of osteoarthritis is due to anatomic deformities. Advances in surgical techniques such as the periacetabular osteotomy, safe surgical dislocation of the hip, and hip arthroscopy have provided us with effective and safe tools to correct these anatomical problems. The limiting factor in treatment outcome in many mechanically compromised hips is the degree of cartilage damage which has occurred prior to treatment. In this regard, the role of imaging, utilizing plain radiographs in conjunction with magnetic resonance imaging, is becoming vitally important for the detection of these anatomic deformities and pre-radiographic arthritis. In this article, we will outline the plain radiographic features of hip deformities that can cause instability or impingement. Additionally, we will illustrate the use of MRI imaging to detect subtle anatomic abnormalities, as well as the use of biochemical imaging techniques such as dGEMRIC to guide clinical decision making.