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.

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 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.

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.