Reproductive failure is relatively common in humans compared with other mammalian species that have been studied. In young couples that are trying to conceive, the fecundity rate, (probability of achieving a clinically recognised pregnancy within a monthly cycle) is about 25%. The major cause of implantation failure in humans after both in vivo and in vitro fertilisation is now thought to be the high incidence of chromosomal abnormality.

The purpose of this article is to provide an ethical framework for fetocide in the practice of obstetrics. Ethically responsible clinical management of pregnancy and its complications requires ethical justification: the giving of reasons that derive from an ethical framework and that together support a conclusion about what ought or ought not to be done in the care of pregnant patients. An ethical framework provides an account of the concepts that are relevant to clinical practice and identifies the clinical implications of these concepts. In this chapter we will present an ethical framework for fetocide based on the ethical concepts of moral status and of the fetus as a patient and identify the clinical implications of this concept for fetocide both before and after fetal viability.

Cytomegalovirus (CMV) is the most frequent cause of congenital viral infection,1 with a prevalence of 0.5 to 1% of all live births, and the leading infectious cause of sensorineural deafness and mental retardation.1 As other Herpesviridae, CMV fetal infection can develop following both primary and recurrent maternal infection. Vertical transmission rate is around 30% following primary infection and 2 to 3% following recurrent infection.2 Effects on the unborn as well as on the newborn are widely variable. It is estimated that only 5 to 10% of infected newborns have symptoms at birth, whereas around 90% of congenitally infected infants are asymptomatic although 5–15% of these infants will develop some degree of sensorineural hearing loss.3

Obesity and type 2 diabetes are serious health issues in the developed world and are becoming increasingly important on a global scale. Furthermore, the marked increases in both childhood obesity and type 2 diabetes will translate to further increases in adult obesity, diabetes and associated co-morbidities in the near future; as such it has been ranked as a critical public health threat. It is a widely held view that the primary cause of obesity is the development of an obesogenic environment, due to ease of access to highly calorific food and reduced energy expenditure in work and leisure activities. In addition there is strong evidence for a genetic component to human obesity with the identification of a number of genes associated with human obesity. However, on its own the genetic component of this condition cannot account for the dramatic increase in the prevalence of obesity in recent years. Of relevance and as highlighted by epidemiological and experimental studies, is the relationship between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity. The terms “developmental programming” and the “Developmental Origins of Adult Health and Disease” are preferentially used to describe these relationships. Despite initial controversy when these relationships were first suggested, both prospective clinical and experimental studies have clearly shown that the propensity to develop abnormalities of cardiovascular, endocrine and metabolic homeostasis in adulthood are increased when fetal development has been adversely affected. This pathogenesis is not based on genetic defects but on altered gene expression seen as a result of fetal adaptation to an adverse intrauterine environment. The relative role of genetic versus environmental factors and the mechanisms underlying developmental programming remain speculative. It is generally argued that in response to an adverse intrauterine environment, the fetus adapts its physiological development to maximise its immediate chances for survival. Owing to the plasticity of the fetus, these adaptations may include resetting of metabolic homeostasis and endocrine systems and the down-regulation of growth, commonly reflected in an altered birth phenotype. It is thought that whilst these changes in fetal physiology (i.e. the prenatal environment) may be beneficial for short term survival in utero they may be maladaptive in postnatal life, contributing to poor health outcomes when offspring are exposed to catch-up growth, diet-induced obesity and other factors. The “predictive adaptive response” hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is a major determinant of subsequent disease. This review will address recent work in animal models and observations in the clinical and epidemiological settings on in utero adaptations and subsequent development of obesity and type 2 diabetes.

Preterm birth and its subsequent consequences continue to be a major challenge worldwide. In the United States in 2004, 12.5% of infants were born preterm, making the annual societal economic burden associated with preterm birth in excess of $26.2 billion (and this is a modest estimate). Spontaneous preterm birth accounts for about 75% of all preterm births; however, at earlier gestations iatrogenic preterm birth accounts for a greater proportion of all preterm births; at 27–28 weeks 50% are iatrogenic. The proportion of babies transferred to the neonatal unit is more than 90% for those born before 33 completed weeks of gestation compared with 31% at 36 weeks; delivery between 33 completed weeks and 36 completed weeks has a relatively low morbidity and mortality. Nonetheless, 1 in 3 children born preterm but beyond 32 weeks have educational and behavioural problems at the age of 7, with 1 in 4 children born between 32 and 35 weeks requiring support from non-teaching assistants at school. Although more than 40% of babies at 35 completed weeks show signs of maturity, some still need ventilation at 38 completed weeks. Almost one-fifth of all infants born at less than 32 weeks gestation do not survive the first year of life.

The aetiology of hypoplastic left heart syndrome (HLH) is complex and involves both genetic and environmental factors. Hypoplastic left heart syndrome accounts for 1.4–3.8% of all congenital heart defects but up to 25% of neonatal deaths. As well as having a high mortality, HLH is a very significant cause of morbidity and therefore justifies aetiological investigation.

Placentas from different species differ not only in their cellular structure and normal trajectory of growth but also in the architecture of their placental vasculature and the transport and exchange mechanisms that determine nutritional transfer from mother to fetus and waste disposal from fetus to mother.1 Many maternal and fetal hormonal and nutritional factors, as well as placental paracrine and autocrine systems affect placental growth and development throughout gestation.2 Nutrients delivered from the maternal circulation are as important for placental growth as they are for fetal growth. In addition to passing across the placenta to provide the building blocks for fetal growth, amino acids, carbohydrate and lipids are incorporated into the placenta.

Mechanical heart valves pose a particular challenge in pregnancy, as the primary agent used to prevent valve thrombosis, coumadin (warfarin), is a known teratogen. Alternatives to coumadin, such as unfractionated heparin (UFH) and low-molecular weight heparin (LMWH) are safer for the fetus, particularly during the first trimester of pregnancy, but expose the mother to potential valve failure. This review will examine these controversies and the complex literature regarding management in pregnancy.

Breakthroughs in the management of sick newborns, including exogenous surfactant therapy, advance ventilation techniques, inhaled nitric oxide, and use of antenatal corticosteroids have led to substantial improvements in the survival of vulnerable preterm infants. Neonatal clinicians now have access to an ever increasing armament of antimicrobial agents to help combat infections. However, even with the support of such advanced therapeutic modalities, strict infection control measures and low thresholds for use of broad-spectrum antibiotics, the threat of bacterial infections especially in the most susceptible group of preterm, very low birth weight (VLBW) infants have persisted. A recent survey suggests that a significant proportion of VLBW infants (21%) have at least one episode of late-onset culture proven sepsis during their stay in the neonatal unit. Infected infants require longer hospital stay and have higher risk of developing complications, such as bronchopulmonary dysplasia and adverse long-term neurodevelopment. Neonates with infection often present with subtle and non-specific signs of sepsis. Some may be asymptomatic at the initial stages of infection. Even those infants with signs may not be clinically distinguishable from patients suffering from transient tachypnoea of the newborn, respiratory distress syndrome, apnoea of prematurity or acute exacerbation of bronchopulmonary dysplasia, during early phases of the disease. Such presentations can lead to both delayed treatment of genuinely infected infants and indiscriminate use of antibiotics in non-infected cases, resulting in acceleration of emergence of bacterial resistance, alteration of patterns of bacterial infection, and inefficient treatment of septicaemia. Both early and late-onset infections are important causes of neonatal morbidity and mortality. Methods to assist neonatal clinicians diagnose infants in the early stages of infection are, therefore, highly desirable.

One of the most important stages of pregnancy is the activation of uterine contractions that result in the expulsion of the fetus. The timely onset of labour is clearly important for a healthy start to life but incomplete understanding of the precise mechanisms regulating labour onset have prohibited the development of effective and safe treatments for preterm labour. This review explores the activation of the myometrium at labour onset, focussing on mechanisms of uterine contractility, including those proteins that play an important role in smooth muscle contractility. The review primarily focuses on human work but in the absence of human data describes animal studies. A broad overview of myometrial contraction mechanisms is provided before discussing more detailed aspects and identifying areas where uncertainty remains. Also discussed is the recent application of ‘omics’ based approaches to parturition research, which has facilitated an increase in the understanding of myometrial activation.

Fetal bradycardia may herald fetal demise. This article highlights arrhythmic fetal bradycardia rather than bradycardia caused by perinatal distress. We briefly examine the embryonic conduction system's development and physiology and we review the classification, aetiology, evaluation, and approach to fetal bradycardia. Our aim is to provide the clinician with practical information about fetal bradycardia that enlightens causative conditions and aids management.

Traditionally, the maternal mortality ratio has been used as a measure of the quality of maternity care and review of individual cases of maternal death has provided information for professional learning in order to improve patient care. In the United Kingdom, this process of multidisciplinary review has been carried out for over 50 years in the form of the Confidential Enquiry into Maternal Deaths (CEMD). The Confidential Enquiry is well respected internationally and has been used as a model for confidential enquiries in other countries, such as South Africa.

In this review, we are concerned primarily with pyrexia (hyperthermia; increased maternal temperature in labour) as hypothermia is rare and usually iatrogenic (as in hypothermia for cardiac bypass surgery). We start by reviewing the factors determining maternal temperature, and how it can be measured. We move on to the effects of the commonest cause of maternal pyrexia in labour in modern obstetric practice in developed countries, epidural anaesthesia. We then discuss the most feared cause of maternal pyrexia in labour, chorioamnionitis.

Although three-dimensional ultrasound (3DUS) was already being used in the early 1980's and the first commercially available three-dimensional scanner was presented in 1989 in Paris at the International Radiology Congress, it has only been in the recent decade that the technology has found its way into clinical applications. This rapid development is mainly due to the equally rapid development of computer processor technology, essential for three-dimensional ultrasound. Originally used as a tool for creating a surface mode showing the face of the fetus and gender abnormalities, its application has become much broader nowadays. The technique is now becoming ever more important in obstetrics and gynecology, but also in many other fields such as cardiology, surgical applications and urology. Three-dimensional ultrasound is an easy, quick and cheap imaging technique without any known adverse effects on the mother or developing fetus as has been stated by the American Institute of Ultrasound in Medicine (AIUM). In addition, it has been reported by numerous authors to be very accurate in assessing volumes. Recently, it has been suggested that both two- and three-dimensional ultrasound, especially in the 1st and 2nd trimester, are of positive influence in initiating the bonding between mother and infant.

Morbid adherent placenta (MAP), also known as placenta accreta, increta or percreta, is one of the main causes of maternal morbidity and mortality. Its incidence has noticeably increased in the last few decades, a fact directly related to the increase in caesarean sections. There is a close relation between iterative caesarean sections and MAP. This connection is of vital importance, since caesarean rates have risen worldwide, especially in the countries where there is the possibility of caesarean section on demand.

Obstetric haemorrhage has been recognised as a major cause of maternal death as long as physicians have studied and written about childbirth. Until the 20th century, however, little was possible in the way of effective treatment. Postpartum haemorrhage (PPH) is still a frequent cause of death in many parts of the world. Even in developing countries, it remains the 3rd biggest killer of women in childbirth, despite considerable advances in medical care in the last half-century. The modern management of PPH may include a team of anaesthetists, haematologists, vascular surgeons, gynaecologists and radiologists.1 Clearly, this change represents an advance which has saved and will continue to save countless lives, not only in the developed world where such teamwork is routine, but also in developing nations that are desperately looking for ways to reduce maternal mortality as part of their efforts to comply with the United Nations Millennium Development Goals by the year 2015.2