Risk is defined as the probability of an untoward event. In fetal medicine this event is one or more of the outcomes listed in Table 1. The aim of antenatal care is to predict these events and thereby, hopefully, to avoid them.

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.

Human and ovine fetuses produce and absorb prodigious amounts of water and electrolytes daily. As will be described, fetal fluid exchange approximates to 300–400ml/kg per day near term. On a per kilogram basis, this is equivalent to an adult ingesting and secreting 15–20 litres per day. Upon delivery, the newborn rapidly adjusts to a much reduced rate of fluid exchange. In this respect, the fetus resembles an amphibian during development: an aquatic phase of in utero gestation and a comparatively arid state following delivery. Although the amphibian-like pattern of development may be partly an example of ‘ontogeny recapitulates phylogeny’, the remarkable volume of fetal fluid exchange suggests an important physiological role for amniotic fluid.

In pregnancy the uterus and its contents constitute a growing mass of tissue with an increasing need for oxygen and substrates. Muscle activity is associated with an even more dramatic increase in metabolic demands. One might question if the physiological adaptations are adequate to provide for the combined demands of exercise and pregnancy.

The detection of an intrauterine fetal death or the delivery of a stillborn infant often initiates a futile and haphazard series of investigations set against a background of parental anxiety and clinical discomfort. The changes of successful diagnosis of the cause of intrauterine or intrapartum death are better served by the adoption of a prompt and co-ordinated approach to laboratory and other investigations. The purpose of this review is to examine the ways in which the laboratory can aid in the management of fetal death. Some of the more common causes of fetal death will be outlined, with particular emphasis on the lupus anticoagulant, fetomaternal macrotransfusion and specific infections such as Listeria and parvovirus, as these are all attracting current interest and debate. The problem of the macerated stillbirth is given some prominence in order to put to rest the notion that examination of the fetus in the presence of autolysis is worthless. None of the details are comprehensive but key references to reviews have been included in order to help the perinatologist on the spot.

During nine months of pregnancy, a woman who smokes 20 cigarettes each day will inhale nicotine, tar and carbon monoxide more than 50 000 times. This smoke contains chemicals known to be mutagenic and carcinogenic and will interfere with the normal growth and development of her child. Recent studies have revealed disturbing long-term consequences for the offspring. This article reviews the constituents of cigarette smoke, the effects of tobacco usage on the pregnancy, child and placenta, and strategies by which smoking during pregnancies may be prevented.

The newborn baby draws its first postnatal breath either during or within seconds of delivery. Within minutes, a regular breathing rhythm is established and this remains virtually continuous for the remainder of postnatal life. The mechanisms responsible for these sudden, dramatic and vital changes in the respiratory system at birth are only partially understood. Since fetuses make intermittent breathing movements long before birth, understanding the control of the fetal respiratory system may be essential to understanding the rapid onset of respiratory efforts at delivery. In this review the stimuli present at birth will be considered and, based on our current understanding of the fetal and neonatal respiratory control systems, those factors which are likely to play an important role in the initiation of lung ventilation at this time will be examined. Normal respiratory events in the early postnatal period will be concentrated on, but it is important to recognize that in some cases problems occur: a neonate may fail to initiate breathing efforts rapidly, or an apparently healthy premature neonate may suddenly stop breathing a few days after birth. In both cases, clinical intervention may be required to maintain adequate gas exchange and to prevent brain damage or death. Clearly, greater knowledge of respiratory control during this critical time of life would assist in the development of more appropriate and successful treatments for these life-threatening disorders.

Preterm labour, defined as delivery before 37 weeks of completed pregnancy, continues to present a major problem in clinical obstetrics and remains the major contributory factor to the perinatal mortality and morbidity statistics. While it is now possible, with recent advances in neonatal care, to take infants delivered very prematurely and provide them with the lifelines that will ensure their ultimate discharge from the neonatal intensive care nursery, the cost of this form of management – in terms both of health care funds and of emotion – is extraordinarily high. Hence there remains a strong rationale for attempting to understand the underlying biochemistry and physiology of labour in order to develop methods of recognizing the patient in true preterm labour, and of developing better strategies to prevent or to manage this condition. In the best of our neonatal intensive care settings, survival of the infant born at 28–30 weeks’ gestation, or greater than 1500 grams, may be greater than 90%. Thus, the clinical management strategy may be directed more towards sustaining intrauterine life for 4–6 weeks in those patients presenting in preterm labour before this time in order to gain time for intrauterine maturation of these fetuses before they are delivered to the tertiary care NICU setting.

It is now 21 years since active management of labour was first reported in the British Medical Journal. Whether one agrees with Professor O'Driscoll or not, there is little argument that his views on the care of women in labour have had a major impact on obstetrics worldwide. As active management comes of age, it is appropriate to review the literature on this subject.

Products of arachidonic acid metabolism (eicosanoids, e.g. some prostaglandins and leukotrienes) have important roles in the maintenance of pregnancy, and certain diseases of pregnancy such as pregnancy-induced hypertension and the machanism(s) of parturition both at term and before term. The volume of literature describing these last relationships dictates that the present review has to be focused rather than global in nature. Only studies of preterm labour in women and the use of human tissues will be discussed in detail despite the limitations in experimental designs that are imposed on such studies. Emphasis will be placed on studies of cyclo-oxygenase and to a lesser extant lipoxygenase pathways of arachidonic acid metabolism mentioning only briefly the pathways for catabolism of these eicosanoids. It should be noted also that eicosanoids from the epoxygenase pathways and those not derived from arachidonic acid will not be discussed here. The review of literature will not be comprehensive but rather selective in order to focus on specific issues of importance or controversy. In developing concepts of regulation I have emphasized studies with amnion since this tissue has received most attention experimentally. The significance of the eicosanoids in the mechanisms of labour at term and before will be described primarily in a section in which I have attempted to deleneate those regulatory mechanisms that are considered most significant in, or specific to, pregnancy and parturition. Studies of labour at term will be freely interspersed with studies specific to preterm labour since the latter are limited, and we need a ‘strandard’ for comparison; moreover, results from one series of studies helps the development of concepts for the other. Finally, the reader is directed to several excellent reviews that concentrate on areas not emphasized in this review.1–7

The mammalian uterus is composed of a preponderance of small smooth muscle cells usually aligned in two layers. The number of muscle cells in the human uterus at term is estimated at 200 billion, each minute fusiform cell measuring about 5–10μm in diameter and about 200μm in length. The main function of the uterus is to harbour the developing fetus during pregnancy and then to contract vigorously during labour to expel the products of conception. In order for the uterus to contract rhythmically and forcefully, a mechanism must exist to allow interaction between muscle cells in order to achieve synchronous activity. Phasic or cyclical patterns of contractile activity of the uterus cannot be accounted for by stimulation or inhibition from the nervous or endocrine systems. Since myometrial cells are dependent upon action potentials for their contractile processes, some system must be present between the muscle cells for the propagation of action potentials between them. The observation that gap junctions occur in large numbers between myometrial cells during parturition is thought to be significant in this regard and they are considered to play an essential role in parturition and in the control and co-ordination of uterine contractility. In this brief review, we will discuss the role of gap junctions in the modulation of myometrial contractility and the mechanisms that regulate their synthesis and permeability.

The growth-retarded fetus is susceptible to intrauterine death, perinatal asphyxia and subsequently neonatal morbidity. Recent technical advances have only moderately increased the obstetrician's ability to recognize the fetus with intrauterine growth retardation (IUGR) prior to delivery, compared with two decades ago when less than one-third of such infants were identified before labour and delivery.

In 1981 De Bold and colleagues demonstrated that when extracts of atrial tissue were given intravenously to rats a large diuresis and natriuresis occured promptly. The structure of the hormone concerned, atrial natriuretic peptide (ANP), was elucidated in 1983. Since then, ANP has received attention as a potentially important mediator in the homoeostasis of sodium and fluid volume.