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.

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.

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.

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.