Hypertensive disorders in pregnancy are a leading cause of maternal and perinatal morbidity and mortality. Overall, hypertension complicates approximately 10% of pregnancies. The incidence is higher in patients with predisposing factors including nulliparity, multiple gestation, preexisting hypertension or diabetes, a previous pregnancy complicated by preeclampsia-eclampsia, familial history of preeclampsia, hydrops fetalis and rapidly growing hydatidiform moles.

The purpose of any form of antenatal fetal surveillance must be to recognize accurately fetal and environmental conditions which adversely influence perinatal mortality and morbidity at an early enough stage to use whatever corrective measures may be available. At booking, risk assessment identifies the woman with social or medical predictors of poor pregnancy outcome from the woman in good health who should have a successful pregnancy. Thus the high-risk patient is a woman in whom the chances of an adverse outcome to herself and/or the baby are greater than the incidence of that outcome in the general obstetric population. The corollary of this definition however, is that the “low-risk” obstetric patient still has the chance of an adverse outcome but the incidence of that outcome is that of the general obstetric population. In the absence of information relating specifically to the fetus, this maternal data is then extrapolated to predict the high or low risk fetus. This system however, does not predict the high risk normally formed stillbirth who is often, but not always, smaller than the gestational age-matched liveborn infant but who is commonly delivered of the low risk woman.

The cardiovascular system undergoes profound changes during pregnancy. Maternal intravascular volume begins to increase in the first trimester rising an average of 45% by term.1 Cardiac output increases similarly2 and is redistributed to organs whose functions are crucial for a successful pregnancy. In the guinea pig, uterine artery (UA) blood flow increases 3500%, while mesenteric and renal artery blood flows increase only 90% and 10% respectively.3 Blood flow to the trunk actually diminishes. The mechanism underlying this redistribution is unknown. Coupled with the rise in cardiac output is a decrease in the systemic pressor response to angiotensin II (AII), norepinephrine(NE), and epinephrine.4–8 There is also a decrease in the contraction response among some but not all vascular beds. For example, contraction of UA to NE and thromboxane is characteristically reduced by pregnancy, whereas the response of the carotid artery is unaltered8–10 Since pregnancy does not alter neuroeffector mechanisms of NE such as release, receptor sensitivity, and accumulation11, changes in sympathetic control during pregnancy must be dependent on alterations at sites other than the neuroeffector junction. We have hypothesized that the mechanisms which alter vascular reactivity during pregnancy also mediate the redistribution of maternal cardiac output.9 We have further hypothesized that many of these mechanisms involve endothelium-dependent factors which are modulated by sex hormones.

Improvements in anaesthetic care and postoperative management over the last two decades have significantly improved survival of neonates with ventral abdominal wall defects, from a dismal 47% in 1971, to 96% for both gastroschisis and isolated omphalocele in two recent series. This increased survival has generally been attributed to result from improvements in the pre and postoperative management of these fragile neonates. Specifically, the routine use of total parenteral nutrition, and staged repairs for cases with severe “viscero-abdominal disproportion” have been implicated in a decreased incidence of sepsis, morbidity and mortality. In addition, an appreciation of the wide spectrum of anomalies uniquely associated with gastroschisis and omphalocele have helped improve survival, as each has unique pathophysiologic features that have prognostic implications for the fetus before, during and after delivery.

Behaviour originally depends on precise and specific interconnections between nerve cells. The nervous system itself develops in a series of appropriately timed steps with a temporal sequence characteristic of each neural structure.

Since the introduction of ultrasound into obstetrics during the 1960s, there has been rapid progress in the detection of genetic and nongenetic defects in utero. With the development of sampling procedures like amniocentesis, chorionic villus sampling (CVS) and fetal blood sampling, the obstetrician has been able to obtain fetal tissue and the parallel improvement in laboratory techniques has allowed the diagnosis of chromosomal anomalies and single gene defects from fetal cells. Amniocentesis and CVS have become well established techniques for routine prenatal diagnosis of chromosomal and metabolic disorders and fetal tissue is now accessible throughout all three trimesters.

Preterm labour and its consequences are the major contributors to perinatal morbidity and mortality worldwide. The prevention of preterm labour and delivery is the single most important challenge to modern obstetrics today. Progress in this area has been hampered by lack of understanding of the basic mechanisms responsible for preterm labour. The implicit paradigm which has governed the study of parturition, is that term and preterm labour are fundamentally the same processes except for the gestational age at which they occur. Indeed, they share a common terminal pathway composed of uterine contractility, cervical dilatation and rupture of membranes. We proposed that while term labour is the result of physiological activation of this common terminal pathway, preterm labour and delivery is the consequence of pathological activation.1 Thus, preterm labour may be considered as the response of the fetomaternal unit to a variety of insults (e.g. chorioamnionitis, ischaemia, fetal growth restriction, etc.) (Fig 1) If these insults cannot be effectively handled in the context of a continuing pregnancy, then labour and delivery may occur.

The unstated aim of preterm fetal welfare surveillance is to enable the obstetrician to delay delivery if a fetus is not at risk of death or permanent damage. Although the penalty for preterm delivery has decreased with advances in neonatal care, the obstetric goals of prolonging pregnancy and minimizing intervention persist. The modern goal of minimizing costs also dictates appropriately timed delivery.

The ultrasound diagnosis of myelomeningocele has been greatly improved by the recognition of associated abnormalities in the fetal skull and brain, potentially leading to an increased number of cases detected during pregnancy. Unfortunately, the counselling of potential parents about the natural history and prognosis of myelomeningocele is frequently based on extrapolations from data in which the diagnosis was made following delivery. Moreover, much of this information predates recent advances in paediatric care. In 1981, Leonard stated “as most children (with myelomeningocele) will grow to be productive, participating adults, then perhaps we should consider myelomeningocele a new disease”1. It is, therefore, appropriate to review recent outcome data for children with myelomeningocele, emphasising those studies where the diagnosis was made before delivery. This review will concentrate on issues of particular concern to the perinatal obstetrician, such as the reliability of sonographic diagnosis, the frequency of karyotypic anomalies, the likely longterm infant outcome and the most appropriate mode of delivery.

Fetal reactivity to acoustic stimulation is a long-recognized phenomenon. Obstetrical interest in this phenomenon is usually considered to have begun with peiper’s report in 1925 of marked fetal movements following a pulsed, loud sound. Occasional attention to the subject was given in the subsequent five decades. Read and Miller are often credited with writing the first comprehensive clinical study of the usefulness of acoustic stimulation in evaluating fetal health. A clear finding in this study was the correlation between an abnormal contraction stress test and faliure of the fetus to respond to stimulation.

The term “dysmorphology” was coined by Dr David Smith in the 1960s to describe the study of human congenital malformations. Literally, it means “the study of abnormal form”, emphasizing a focus upon structural abnormalities in development.2 As a scientific discipline, dysmorphology combines concepts, knowledge and techniques from paediatrics, clinical genetics and embryology.

In pregnancies complicated by severe red cell alloimmunization, fetal haemolytic anaemia can lead to intrauterine demise as early as 17 weeks' gestation. Intrauterine intraperitoneal blood transfusion, introduced by Liley in 1963, proved to be the first successful example of fetal therapy. The use of this complex procedure, involving X-ray guided puncture of the fetal peritoneal cavity, was limited to fetuses with a gestational age ranging from 24 to 33 weeks. When performed below 26 weeks, survival rates were as low as 16%. The need for intrauterine transfusion was mainly based on determination of bilirubin levels in amniotic fluid, and plotting the results in a three-zone chart devised by Liley. This chart was based on correlations of amniotic fluid bilirubin concentrations with the degree of neonatal anaemia, and ranged from 27 to 41 weeks' gestation. In the 1980s, with the introduction of ultrasound-guided intravascular transfusion, treatment became possible from 17–18 weeks' gestation onwards. Consequently, there was a need for diagnostic tests to assess the degree of anaemia in the second trimester fetus. The use of the Liley chart was shown to be unreliable in the prediction of disease severity before 27 weeks' gestation. Ultrasonographic detection of fetal hydrops in these pregnancies reliably indicates severe anaemia, but for reasons that are still unclear, a significant number of severely anaemic fetuses do not show ultrasonographic signs of hydrops. In 1988, Nicolaides et al studied the use of several ultrasonographic parameters to predict anaemia in nonhydropic fetuses. Their results were disappointing, and they concluded that the only reliable diagnostic test to assess the degree of fetal disease was fetal blood sampling.

Deoxyribonucleic acid (DNA) is composed of a deoxyribose backbone, the three position (3') of each deoxyribose being linked to the five position (5') of the next by a phosphodiester bond. At the two position each deoxyribose is linked to one of four nucleic acids; the purines adenine or guanine or the pyrimadines thymine or cytosine. Each DNA molecule is made up of two such strands in a double helix with the nucleic acid bases on the inside. The bases pair by hydrogen bonding, adenine (A) with thymine (T) and cytosine (C) with guanine (G). Deoxyribonucleic acid is replicated by separation of the two strands and synthesis by DNA polymerases of new complementary strands. With one notable exception, the reverse transcriptase produced by viruses, DNA polymerases always add new bases at the 3' end of the molecule. Ribonucleic acid (RNA) has a structure similar to that of DNA but is always single stranded. The backbone consists of ribose, and uracil is used in place of thymine.

Caesarean section (CS) is one of the most common major operations performed around the world, yet operative rates vary considerably. This review will address the variation in caesarean section rates worldwide and changes in these rates over time. In addition we shall try to assess possible explanations for the differences and whether such differences are reflected in outcome.

Shoulder dystocia is an unpredictable obstetrical emergency that results in serious complications especially to the neonate. Such complications include fracture of the clavicle, brachial plexus injury, fracture of the humerus and asphyxia.1-4 The incidence of shoulder dystocia appears to be increasing5 and its unpredictability continues to be the nightmare of the obstetrician. The following is a review of risk factors which are associated with shoulder dystocia, a critical review of the usefulness of antenatal ultrasound in the prediction of the macrosomic fetus and a discussion of the controversies surrounding the management of shoulder dystocia.

Among serious fetal anomalies currently detectable with ultrasound, defects of the central nervous system (CNS) are among the most common. These congenital anomalies are especially likely to burden not only affected children with severely limiting handicaps, but also their families with long-lasting anguish and financial responsibility. It is appropriate that interest in methods for improving prenatal detection of these abnormalities has intensified. Alphafetoprotein screening programmes are now widely available, and many papers have been written describing useful sonographic observations that enhance prenatal diagnosis. As a consequence, the majority of the most common serious neural axis defects including fetal hydrocephalus, anencephaly, myelomeningocele and encephalocele, previously detected almost exclusively at birth, today can be accurately detected prenatally. A few observations in the fetal brain and spine have proven to be especially useful in this task. This article presents a simplified and effective approach to the general sonographic survey of the neural axis in fetuses at average and increased risk for these anomalies. The aim is to improve not only accuracy of diagnosis of CNS malformations, but the efficiency and confidence of the examiner.