Caesarean section rates in the United Kingdom continue to be a topic of importance in both the medical and lay press. In previous years most of the discussion has been about what the correct caesarean section rate should be. More recently the debate has focused on whether a woman has the right to choose to have her baby delivered by caesarean section in the absence of a medical indication. This has medical implications, in terms of short and long term complications for the woman, but also carries a financial burden that the National Health Service can ill afford.

The fetus mounts a coordinated cardiovascular response to an insult of acute hypoxaemia which involves neural and endocrine components. During acute hypoxaemia in late pregnancy there is a transient bradycardia, a gradual increase in arterial blood pressure and an increase in heart rate variability. In addition, there is a redistribution of the combined ventricular output favouring the cerebral, myocardial and adrenal circulations by shunting blood away from the peripheral circulations. A component of the increase in peripheral vascular resistance and the increase in arterial blood pressure during acute hypoxaemia is mediated via increases in plasma concentrations of vasoconstrictor hormones such as vasopressin, angiotensin II and neuropeptide Y. Whilst an increase in plasma ACTH and cortisol is also seen during acute hypoxaemia, their contribution to cardiovascular control in fetal sheep is less clear.

Evidence has been presented to suggest that a number of these cardiovascular and endocrine responses to acute hypoxaemia are chemorefiex in nature, mediated principally by carotid chemoreceptor afferents. In addition, this reflex may be modifiable in terms of changes in magnitude and gain: first, by an influence of the intrauterine environment during chronic hypoxaemia and second, through genetic influences, in animals adapted to life at high altitude.

Recent studies have shown that babies who are small for dates at birth, or who fail to grow in infancy, have, in adult life, raised blood pressure, impaired glucose tolerance, abnormal serum lipids, raised fibrinogen and high death rates from coronary disease, stroke and obstructive lung disease. This has led to the hypothesis that these diseases are ‘programmed’ in utero in response to an adverse environment.

Within the human placenta the villous trophoblast represents the epithelial covering of the chorionic villi. This layer of trophoblast actively participates in transport processes between mother and fetus and is the surface of the barrier separating maternal and fetal blood. It represents the main site of metabolic and endocrine activities of the placenta. It is comprised of an outer continuous layer without cell borders, the syncytiotrophoblast, beneath which resides a population of proliferating cytotrophoblast cells. Daughter cytotrophoblast cells fuse into the syncytium, while aged nuclei inside syncytial fragments are shed into the maternal circulation (Figure 1). Any process disturbing the balance between proliferation, syncytial fusion or shedding will alter the integrity and function of the layer as a whole, which in turn may impair gas and/or nutrient transfer to the fetus as well as endocrine activities. Trophoblast turnover is thus tightly regulated to ensure normal fetal development.

The management of children with cleft lip and palate presents many challenges but also many rewards. Our involvement with these children and their families often begins before birth and can extend into late adulthood. Affected individuals present a multiplicity of problems and effective management involves a wide range of specialists.

Although significant advances to patient care have been made in various branches of obstetrics and gynaecology, the incidence of preterm birth has not changed in the past 40 years. Indeed there are signs that factors such as low socioeconomic status of some inner city populations, the tendency for women to choose to start a family at an older age and the impact of fertility treatments are leading to an increase in the incidence of preterm delivery. Improved neonatal care over this period has significantly reduced the mortality rate due to prematurity, although it remains the primary cause of neonatal death. The morbidity rate in preterm infants, however, has not substantially changed due largely to the resuscitation of neonates at or close to the limits of gestational age viability. This has inevitably had a tremendous economic impact upon health care systems and upon society in general. Neonatal care in the USA alone cost over $5 billion annually in the 1980s – the vast majority of which was due to prematurity. When one adds the costs of chronic care for some of these infants with major motor and/or mental handicaps as well as the loss of potential earnings, prematurity ranks as one of the most costly of medical complications.

It is now over half a century since Arthur Hertig first reported vascular pathology in the uterine arteries supplying the placenta in women suffering from preeclampsia. His pioneering histological studies have been validated and extended by many others, leading to the general concept that placental perfusion is compromised in these patients. More recent Doppler ultrasound studies have confirmed reduced intervillous blood flow in vivo, and so gradually a consensus has emerged that the placental lesions associated with preeclampsia arise from a state of chronic hypoxia. Whilst hypoxia may undoubtedly play a significant role in the generation of placental pathology, there is considerable evidence that another feature of the intervillous circulation, namely the constancy of the blood flow, may be a more important factor. In this review we propose that hypoxia-reoxygenation, secondary to intermittent perfusion of the intervillous space, is a more physiological approach to take to understanding the pathophysiology of both normal pregnancies, and those complicated by preeclampsia. We further propose that chronic reduction in placental perfusion alone may lead to fetal growth restriction, and that if the two phenomena are superimposed then preeclampsia with growth restriction will result.

The developmental origins of the ability to hear have been the subject of much debate and speculation. Since time immemorial, there has been much anecdotal evidence that the fetus responds to sound. In contrast, until the late 19th Century, scientific evidence and opinion held that the newborn was deaf and only developed the ability to hear in the first weeks after birth. At the beginning of the 20th Century the prevailing scientific and clinical view changed and it was accepted that the newborn was able to hear at birth. This led to much speculation about, and limited experimental study of, when the individual first started to hear. Detailed study of the ontogency of auditory abilities had to wait until the 1980’s when scientific opinion regarding the abilities of the newborn changed and the ultrasound technology with which to observe the fetus in utero became widely available. Research thus commenced in earnest to investigate the response of the fetus to sound. Despite this increased interest in fetal hearing, experimental studies have concentrated upon the responsiveness to sound in late pregnancy and not on the developmental origine of auditory abilities. It is the aim of this review to examine the ontogenesis of hearing in the fetus.

Eclampsia is defined in the obstetrical literature as the occurrence of unexplained seizure during pregnancy in a woman with preeclampsia. In the Western world, the incidence of eclampsia is ~1 per 2000 to 1 per 3000 pregnancies, but the incidence is 10-fold higher in tertiary referral centers and undeveloped countries where there is poor prenatal care, and in multi-fetal gestations. Nearly 1 in 50 women with eclampsia die as do 1 in 14 of their offspring, and mortality rates are considerably higher in undeveloped countries. Eclampsia is also associated with significant life-threatening complications, including neurological events. Seizure acutely can cause stroke, haemorrhage, oedema and brain herniation and thus lead to epilepsy and cognitive impairment later in life.

From the moment of implantation until delivery some 37 weeks later, the human embryo or fetus is surrounded by fluid. Initially this fluid is a transudate from maternal and embryonic tissues which provides nutrients for the growing embryo. Starting in early pregnancy, the fetal kidneys begin to contribute substantial quantities of urine to the amniotic fluid volume. At mid pregnancy, when the skin becomes keratinized, the kidneys become the main source of amniotic fluid. Fetal swallowing is the main route of amniotic fluid removal. Although fetal urine production and swallowing have been studied in both human pregnancy and animal models, the knowledge from these investigations is not sufficiently extensive to explain overall amniotic fluid volume regulation. None the less, it is clear that the amniotic fluid is in a dynamic, ever-changing state. The production rate of the fetal urine in the human fetus at term (800–1200ml/day) is sufficient to replace completely the entire amniotic volume every 12–24 hours1. While the fetus is producing large volumes of urine, the volume of amniotic fluid is normally maintained within a very narrow range. Deviations from the normal range are often associated with significant perinatal morbidity and mortality.

In the absence of any prenatal screening, some two percent of babies will be born with a structural anomaly; a further 1 in 700–800 will be born with Down's syndrome, with similar numbers having other chromosomal and serious genetic disorders. The prevalence of abnormalities in early pregnancy is higher because abnormal fetuses are more likely to miscarry than normal ones. A small number of women enter pregnancy at increased risk of conceiving a baby with an abnormality. They may have a maternal condition such as diabetes, need medication for conditions such as epilepsy, or have a family history of a genetic disorder (www3.ncbi.nlm.nih.gov/Omim/searchomim.html). Most abnormalities, however, occur in healthy, low-risk women.

This year marks the 250th anniversary of the discovery by William Hunter of the existence of two distinct circulations within the human placenta. Until relatively recently the placenta has been viewed with “respect” – a passive structure which occasionally elicited fear and anxiety if implanted either too low or too deep. More recently our understanding of perinatal physiology, blood flow regulation and epidemiological data linking prenatal events with adult disease has created renewed interest in the placenta. This review will focus on the regulation of fetal blood flow in the placenta, the possible mechanisms whereby it may be deranged and why this might be relevant to adult disease.

All pregnancies are at some risk of adverse fetal and neonatal outcome. The risk increases, however, if the pregnancy ends too soon (preterm), or if it ends too late (postterm).

Early this century, the term cytomegalic inclusion disease (CID) was used to designate the cellular changes characterized by enlargement and typical intranuclear inclusions observed in tissues of fetuses and infants with a fatal illness. In 1957, Smith and Weller et al, identified the causative agent of CID, which was named cytomegalovirus (CMV) by Weller in 1960. By 1971, it was clear that congenital human CMV (HCMV) infection was an important health problem. Since then, many advances have been made in the diagnosis, therapy, and knowledge of the epidemiology of congenital HCMV infection. However, most of these improvements, particularly those concerning diagnostic technologies and development of antiviral drugs, have been the result of the powerful effort to reduce the devastating impact of HCMV infections in AIDS and transplanted patients. Indeed, it is disappointing to observe that in the year 2000 CID does still occur, that HCMV is still recognized as the leading cause of congenital infection and the leading infectious cause of mental retardation and deafness, and, most important, that no active prevention is available for seronegative women. Moreover, because of the limited possibilities of prophylaxis and treatment, and the misuse of the currently available serologic assays, the issue of whether the determination of HCMV antibody status for women of childbearing age is justified has become a matter of debate.

Obstetric caregivers must deal with a wide range of emergencies, some of which are quite uncommon, and many believe they have achieved a high level of expertise based on study rather than experience. Yet a growing body of work demonstrates that simulation training can sharpen the skills of all caregivers and promote the development of efficient teams capable of reducing the morbidity of these rare events. This paper outlines current recommendations for emergency and teamwork training in obstetrics and reviews different training methods and their effectiveness.

Preeclampsia (PE) is a common disease of pregnancy that affects women particularly in their first pregnancies. Current estimates suggest that between 7 and 10% of pregnancies may be complicated by PE. Despite considerable research and medical efforts, the incidence of the disease has not changed substantially in the last century. In severe cases the disease may be life-threatening and is associated with high neonatal mortality and morbidity. Furthermore, therapy is often ineffective and at best treats the disease symptoms rather than the aetiology. One reason for the lack of progress may be that while the disease is generally agreed by most to be due to abnormal implantation and development of the placenta (events which happen in the first trimester) most research efforts have focused on managing and understanding the maternal disease. Since the disease typically appears in the last trimester, many weeks after the likely start of the pathology, it has been difficult to understand the progression of events. However, this picture has improved recently. The purpose here is to review how placental development is affected in PE and describe new insights into the causes. It is hoped that an understanding of the pathogenesis of the placental defects in PE will lead to new efforts towards early diagnosis, before the onset of clinical symptoms, as well as new treatments for these lesions.

Intrauterine growth restriction (IUGR) remains a major cause of perinatal morbidity and mortality and, as yet, there is no effective treatment. Most fetuses with ultrasound evidence of moderate to severe IUGR do not grow better out of the womb than in, despite early enteral feeds and subsequent calorie supplementation. Research into possible therapies for growth restricted babies has thus also been directed towards the fetus. Major advances have been made in recent years in the understanding of the physiology of fetal growth, and it has become clear that fetal nutrition is the determining factor.

Thyroid hormones are important for normal development of the human central nervous system (CNS). It is well established in children with congenital hypothyroidism that neonatal thyroid hormone deficiency significantly impairs subsequent neurodevelopment. In these children, the period of thyroid hormone insufficiency, which can begin in utero and extend until thyroid status is restored to normal in the neonatal period, determines the severity and type of defect manifested. While prompt and optimal thyroid hormone supplementation, following newborn screening is associated with far improved outcome and near normal development, subtle specific neurodevelopmental differences are still detectable compared to euthyroid controls. Because the particular impairments reflect the exact period of thyroid hormone insufficiency postnatally, as well as during gestation, this implies that brain development is not only thyroid hormone dependent in the neonatal period, but also prior to birth.

Iron deficiency and iron supplementation are well known but unresolved issues of perinatal care. Approximately one thousand articles listed in Medline® over the last ten years focus on iron and pregnancy. Clearly, there are many unresolved questions regarding perinatal iron deficiency and iron supplementation.