Reduced fetal movement (RFM) is commonly defined as any reduction in maternal perception of fetal activity. Perceived fetal activity may be movement of limbs, trunk or head movement, but excludes fetal hiccoughs (as this is involuntary movement). The perception of fetal movement by an expectant mother is the first, and ongoing, non-sonographic indicator of fetal viability. The “normal” pattern of fetal movements varies from pregnancy to pregnancy, and often does not become established until 28 weeks’ gestation. Many babies have particularly active periods of the day, usually corresponding to periods of maternal rest and inactivity (which may in itself reflect increased maternal awareness of fetal movement). A variable percentage of sonographically observed fetal movements are perceived by prospective mothers (commonly 30–40%, although some studies report rates as high as 80%).

Full autopsy. A combination of external examination, radiological investigations, evisceration, dissection and subsequent full organ examination with detailed histological evaluation. This is the current “gold standard” of care against which other approaches are compared.

I thank Steve Robson and his team of Editors for their very hard work over the previous years in establishing Fetal and Maternal Medicine Review (FMMR) as a reference point for authoritative reviews in the field of perinatology. I am delighted that Steve is staying on as an Associate Editor, and am very pleased to welcome Professor Neil Sebire (UK) and Professor Jimmy Espinoza (USA) as Associate Editors for 2013 issues onwards. Amanda Johns has taken over from Jean Birtles in the Editorial Office and can be contacted by email at fmr_editorial_office@cambridge.org.

Delivery of the infant at the limits of viability is a complex challenge for the obstetrician. Despite the best efforts of obstetricians to prolong gestation beyond 23–24 weeks, there may be compelling reasons to intervene in an ongoing pregnancy for maternal benefit (for example in severe pre-eclampsia or placental abruption) or delivery may be considered for foetal reasons. However, the majority of deliveries at the limits of viability will be the consequence of spontaneous pre-term labour, leaving the obstetrician with the difficult and time-pressured decisions regarding which, if any, interventions may be of benefit to foetal or maternal outcome. In most European countries, the rate of pre-term birth continues to rise, making such clinical scenarios increasingly common.

In the European Union, it is estimated that 36,000 children are born every year with congenital heart disease and that a further 3000 who are diagnosed with congenital heart disease die as a result of termination of pregnancy, late fetal death or early neonatal death. In a normal population, the risk of a woman having a child with a congenital heart malformation is of the order of 0.8–1%, the risk rising to 2–3%, if a previous pregnancy was affected by heart disease and approaching 6% if the mother herself has a congenital heart defect. There is great variation between countries in the antenatal detection of heart defects, being lowest in those countries without ultrasound antenatal screening programmes (8–11%), but in Western Europe the detection rates vary between 19% and 48%. High-resolution echocardiography enables assessment of precise structures during the second trimester or even earlier.

Significant advances in the field of regenerative medicine have intensified the search for novel sources of stem cells with potential for therapy. Although embryonic and adult tissues can be used for the isolation of pluripotent stem cells, significant limitations including ethical concerns, complexity of isolation/culture and tumorigenicity have hindered translation of laboratory findings to clinical practice.

It is our opinion that the evidence from epidemiological observations, clinical trials and biological studies is strong enough to support the view of different origin and phenotypes of pre-eclampsia: placental, which usually occurs (but not exclusively) early in pregnancy and is associated with poor early placentation of different severity with subsequent restriction of foetal growth, at different stages of gestation; and maternogenic, which generally occurs late in pregnancy and it is not related to placental insufficiency and foetal growth restriction.

Third stage practice, including the timing of cord clamping and its impact on neonatal health, has been comprehensively reviewed previously by Downey and Bewley, and this opinion will focus on the evidence about neonatal transition which has been published since. Many professional organisations and experts recommend at least a 30-second delay before clamping the umbilical cord, especially after preterm births.

Thyrotoxicosis affects approximately 1:500 women of reproductive age. Untreated or poorly controlled thyrotoxicosis in pregnancy is associated with significant maternal and perinatal morbidity. Recognition and diagnosis of new onset thyrotoxicosis in pregnancy can be challenging as many of the symptoms can be misattributed to physiological adaptation of normal pregnancy. Women with hyperemesis gravidarum (HG) often have biochemical, but not clinical evidence of thyrotoxicosis, which does not need treatment with anti-thyroid drugs (ATDs). For women with clinical thyrotoxicosis, uncertainty regarding the risks of teratogenicity due to ATDs has led to new guideline recommendations for their use in pregnancy. Women with autoimmune diseases such as type I diabetes and who have thyroid peroxidase antibodies (TPOAb) are at an increased risk of developing postpartum thyroiditis, which can result in permanent hypothyroidism. This review summarises the management of thyrotoxicosis in pregnancy and highlights controversial areas for which conclusive evidence is still lacking.

The venous system is considered the main capacitor of the human body. Approximately 70% of the total blood volume resides in the venous bed, half of which circulates as venous return whereas the other half functions as reserve volume in the splanchnic veins. These veins are richly innervated and highly compliant, and communicate with the systemic circulation via capillaries (entrance) and portal vein and liver (exit). This constitution allows the venous compartment to balance circulating and stored blood volumes, and thus control cardiac output. Clinical conditions with reduced cardiac output are often associated with hampered venous return, resulting in visceral oedema, ascites or organ dysfunction. Organ dysfunction or failure may also result from (sub)obstructed venous outflow, as is illustrated in renal vein thrombosis or in the Nutcracker syndrome. Recently, the application of Doppler ultrasonography in the study of the maternal venous system illustrated that preeclampsia is another cardiovascular disorder with dysfunctional venous haemodynamics. In this opinion paper, we summarise results from Doppler studies of the maternal venous compartment, illustrating that performing venous haemodynamics function tests is to become a fundamental part of an integrated cardiovascular assessment of women with hypertension in pregnancy, facilitating an individualised diagnostic and therapeutic approach for every woman at risk for gestational hypertensive disease.

Healthy pregnancy is characterised by progressive physiological adaptation of the maternal cardiovascular (CV) system that facilitates optimal fetal development. The adaptations that constitute a healthy or normal progression are not always evident, and, in particular, CV adaptation to pregnancy is highly individualised. Some women develop pregnancy-related CV dysfunction such as pre-eclampsia (PE). Typically, PE is diagnosed by the development of hypertension and proteinuria after 20 weeks of pregnancy and is the leading cause of maternal and perinatal mortality and morbidity. Despite continued efforts to improve the understanding of the aetiology, pathophysiology and subsequently treatment for the disease, CV changes in PE are not well understood. PE before 34 weeks (early onset PE) is believed to differ in pathogenesis from late onset PE (>34 weeks) and can be characterised by a haemodynamic profile of increased systemic vascular resistance (SVR) and lower cardiac output (CO). Early onset PE is more often associated with uteroplacental insufficiency and significant adverse maternal and perinatal outcomes. In contrast, late onset PE (>34 weeks) involves an increased CO and lower SVR and is less likely to be associated with uteroplacental insufficiency and adverse perinatal outcomes. It is not known if PE develops secondary to the CV maladaptation in pregnancy or if a preexisting CV dysfunction predisposes some women to develop PE. Screening, diagnosis and disease management would be vastly improved if more were known about the onset of the maladaptive process associated with PE. To date, a combination of maternal factors including medical history, body mass index, age, parity and blood pressure (BP) have been used to predict the development of PE. In the first trimester, arterial stiffness is significantly increased in women who develop PE. Current hypotheses speculate that CV dysfunction is evident very early in pregnancy in PE and precedes the clinical manifestation at a later stage but whether CV dysfunction is present before pregnancy remains to be elucidated.

From a scientific point of view, the answer to the question might be quite straightforward in favour of routinely screening all pregnant women for pre-eclampsia (PE) during the first trimester of pregnancy. However, irrespective of the large amount of good evidence and expert opinion favourable for universally screening for obstetric syndromes, such as PE, public health policies do not always align with pure clinical science.