It is quite clear that pre-eclampsia is not simply pregnancy-induced hypertension; rather, it is a multisystem disease with pathophysiological changes secondary to reduced organ perfusion. This reduction can be explained by vasospasm secondary to increased sensitivity of the vasculature to usual circulating pressors, and vascular occlusion secondary to activation of the coagulation cascade. Although pre-eclampsia becomes clinically evident late in pregnancy, pathological and pathophysiological changes antedate the clinical syndrome by weeks to months. The syndrome occurs only in pregnancy and is cured by the removal of fetoplacental tissues.

Based on these findings, we have proposed that the inciting pathophysiological change of preeclampsia is reduced trophoblastic perfusion, which produces an agent that perturbs endothelial cells. The altered endothelial functions associated with this insult increase sensitivity to pressors, activate the coagulation cascade and produce the clinical and pathological findings of preeclampsia. Although we feel this hypothesis could explain pre-eclampsia, it is possible that its major value will be to stimulate others to approach this disorder by considering all facets of its pathophysiology rather than merely its hypertensive component.

The appreciation of pre-eclampsia as a disease present from early pregnancy and the potential role of vasodilator prostaglandins have already stimulated therapeutic trials of aspirin in women at very high risk with encouraging results. At present, information is insufficient to determine the risk/benefit ratio of this therapy in lower risk patients, and aspirin therapy should not be used in these women. Another potential modification of therapy, the substitution of phenytoin for magnesium sulphate, does not seem warranted on the basis of either currently available data or on theoretical grounds.

Fruitful directions for research in the near future will be the explanation of the abnormal trophoblastic invasion of pre-eclampsia and the determination of how reduced perfusion translates into a multisystem disease. In addition, aspirin therapy or other potential prophylactic therapies would be greatly aided by the development of new tests with reasonable positive predictive values, in order to identify preeclampsia prior to clinically evident disease.

Preterm birth remains a paramount problem in health care worldwide. In the USA, approximately 6–10% of births occur preterm.1–3 Gestational age at birth is the most important determinant of an infant's morbidity and mortality. Preterm infants account for approximately 75% of neonatal deaths,3–5 as well as incalculable direct and indirect financial costs and morbidity.6–9

Autoimmune thrombocytopenia (ITP)

1) The risks to mother and fetus have previously been overstated.

2) There is no maternal test which will accurately determine fetal thrombocytopenia.

3) The only reliable test for fetal thrombocytopenia is cordocentesis – this carries a higher morbidity than that of fetal intracerebral haemorrhage from ITP.

4) Contrary to received wisdom, there is no evidence that, even for the most severely thrombocytopenic infant, abdominal delivery protects against intracranial haemorrhage.

5) Management therefore involves keeping the maternal platelet count above 50 × 1091 and choosing the route of delivery on normal obstetric grounds.

Alloimmune thrombocytopenia

1) Alloimmune thrombocytopenia is commoner than hitherto believed (0.15% all neonates).

2) The fetal risks are considerable: intracranial haemorrhage occurs in 4% of cases antenatally and in 10% in labour. The risks are virtually confined to those with a platelet count of less than 30 × 109l−1.

3) Cordocentesis is justified for the ‘at risk’ fetus; fetal immunoglobulin or platelet therapy can be given.

4) When the fetal platelet count is below 50 × 109l−1, abdominal delivery should be planned.

5) A maternal screening test for neonatal alloimmune thrombocytopenia exists (lack of P1A1 antigen).

The behavioural response of the neonate to stimuli is an essential part of neurological examination in the newborn infant in order to measure the integrity and function of the central nervous system. Different sensory channels, such as auditory, vibrotactile or olfactory, have been used to elicit a response. With use of real-time ultrasound, Nijhuis et al. observed that human fetuses of 36 weeks gestation had developed behavioural states (1F–4F) that were, in their organization, fully comparable to the states originally described by Prechtl et al. in neonates. Three variables are used to identify human fetal behavioural states: fetal heart rate (FHR) pattern (A-D), fetal eye movements and fetal body movements.

Subspecialization in fetal medicine has expanded the scope for obstetricians to investigate the fetus and its surrounding environment in greater detail. Of the advances in technology that have made this possible, ultrasonography is the most important. A high degree of skill is required if it is to be applied to the performance of invasive diagnostic techniques. These should be performed only in specialized centres with appropriate facilities and an adequate referral base. However, it is important for obstetricians to know what is possible in the field of prenatal diagnosis and therapy in order to give patients the best advice.

Not only does the placenta function as an organ of exchange between mother and fetus, it also has an endocrine role, producing a number of hormones necessary for the maintenance of pregnancy and the initiation of parturition. There is a large amount of information available which describes the synthesis and secretion of steroids, prostaglandins, human chorionic gonadotrophin (hCG)and placental lactogen by the placenta and fetal membranes. However, the placenta also contains a number of counterparts of hypothalamic-releasing factors and pituitary peptides. Why the human placenta should be the site for the synthesis and secretion of these hypothalamic and pituitary factors is something of a mystery. In man and other vertebrates the nervous system is derived from embryonic ectoderm. In particular, the hypothalamus and pituitary are in part derived from the neural plate and in part from the neural crest. Embryonic ectoderm in the early stages of embryonic development is intimately related spatially to trophoblast, and it is therefore possible that the cells of the ectoderm and trophoblast may be similarly programmed. It is unclear, however, why the trophoblast cells assume similar endocrine functions to those of the pituitary and hypothalamus rather than of other regions of the brain. Furthermore, whether the pituitary and hypothalamic-like peptides are of physiological importance or serve only as an evolutionary and embryological residue remains to be determined.

The ductus arteriosus is a large vessel which connects the pulmonary trunk with the aorta. During fetal life it serves together with the foramen ovale as a shunt at cardiac level. Due to a complex regulatory mechanism it is capable of maintaining patency during fetal life and of rapid closure after birth. However, in premature neonates ductal patency frequently persists, an occurrence which may even be favourable in some situations. Recent investigations on the ductus arteriosus have provided new information about the regulatory mechanisms involved with its function. Initially, most studies on the fetal ductus arteriosus were conducted in animals. With the introduction of the combined use of two dimensional real-time and Doppler ultrasound systems the opportunity became available to study blood flow within the ductus arteriosus in the human fetus and neonate in a noninvasive manner. The increasing use in obstetric care of cyclo-oxygenase inhibitors for tocolysis and for prevention of the development of pregnancy induced hypertension and pre-eclampsia justifies the re-evaluation of the potential adverse effects of these drugs on the ductus arteriosus.