Pre-eclampsia (PE) remains the leading cause of maternal and fetal mortality in the developed world and parts of the developing world. Morbidity and mortality from PE is increased in the developing world compared to the developed world, as availability and access to antenatal care and pathology services are limited.

Pre-labour premature rupture of membranes (PPROM) is defined as rupture of membranes more than 1 hour prior to the onset of labour at <37 weeks gestation. PPROM occurs in approximately 3% of pregnancies and is responsible for a third of all preterm births. Once membranes are ruptured prolonging the pregnancy has no maternal physical advantage but fetal morbidity and mortality are improved daily at early gestations: 19% of those infants born <25 weeks develop cerebral palsy (CP) and 28% have severe motor disability. Those infants born extremely pre term (<28 weeks) cost the public sector £75835 (95% CI £27906–145508) per live birth not to mention the emotional cost to the family. To prolong gestation is therefore the suggested goal: however how and why might we delay birth in those at risk?

Pregnancy is a physiological condition that affects all organs. Diseases unrelated to pregnancy may present coincidentally during pregnancy or may be exacerbated by pregnancy, and may increase maternal and/or fetal morbidity or mortality. Compared with many other systems, the changes within the biliary tree and pancreas are relatively minimal. However, pregnancy is associated with an increased likelihood of cholelithiasis, which can have significant implications for the parturient.

The development of effective anticoagulant drugs available for use in pregnancy has resulted in dramatic improvements for a number of potentially life-threatening conditions. These include the treatment and prevention of venous thromboembolism and the thrombotic complications of antiphospholipid antibody syndrome, as well as the management of pregnant women with mechanical heart valves. The most commonly used class of drug includes heparin, a highly-charged macro-molecule that does not cross the placenta, in contrast to the potentially teratogenic and fetotoxic oral drug warfarin. This review will focus on our current lack of understanding of the wider actions of heparin and examines the possibility that large numbers of pregnant women are presently being treated inappropriately with heparin.

Normal fetal growth and development depends on multiple molecular mechanisms that coordinate both placental and fetal development. Efforts to better understand fetal/placental growth dysregulation and fetal growth restriction (FGR) are now being driven by several findings that highlight the longterm impact of FGR on susceptibility to disease. The association of poor fetal growth to perinatal medical complications is well accepted but more recent data also show that FGR is linked to common, serious adult health problems. Several large-scale human epidemiological studies from diverse countries have shown that conditions such as coronary heart disease, hypertension, stroke, type 2 diabetes mellitus, adiposity, insulin resistance and osteoporosis are more prevalent in individuals with a history of low birthweight.

Since Robinson and Gregory demonstrated the need to administer analgesia to preterm infants and the safety of such anaesthestic techniques in this specific patient population, pain in neonates and adequate analgesia have drawn more and more attention. Thanks to the outstanding work by Anand et al, it became increasingly clear that premature infants experience stress during invasive procedures and that as a consequence long-term neurodevelopmental status may be affected. Fetuses also demonstrate a stress response. Fetal analgesia can be administered efficiently, eliminating the fetal stress response. However, it remains unclear whether this results in improved neurodevelopment and improved long term outcome.

Women with epilepsy constitute about 0.6% of pregnancies. The potential for major structural malformations following gestational exposure to anti-epileptic drugs (AEDs) is well known and causes concern as how best to manage epilepsy during pregnancy. In this review we focus on the structural and functional effects on the developing brain to complement other recent reviews. We do not cover neural tube defects which have been reviewed elsewhere. Suffice to say that carbamazepine, lamotrigine and, in particular, valproate exposure are associated with them. We discuss studies based on animal models as well as those that have followed-up children exposed to AEDs in-utero. Careful longitudinal human research can document the cognitive and behavioural effects, but the long time scales required and inability to rule out confounding variables, both genetic and environmental, are serious limitations. Animal studies are based on the assumption that many developmental processes are conserved between the animals used in the models (most often rodents) and humans. However, the hugely expanded cortex and cognitive and behavioural repertoire of humans implies that there are aspects that can not be well modelled. In addition, due to differences in how susceptible different species are to various teratogens, studies always need to be done in man as well. Nevertheless, an understanding of the molecular mechanisms of neuro-teratogenesis derived from animal models will help us predict which anti-epileptic drugs are likely to cause fewer neuro-developmental problems in humans.

Hepatitis B and its complications are one of the major global health problems. Around 2 billion individuals are infected by hepatitis B virus (HBV) worldwide, more than 350 million are chronically infected, and approximately 15 to 40 percents of them will develop serious complications such as liver cirrhosis, hepatic failure, or hepatocellular carcinoma (HCC). The worldwide prevalence of chronic HBV infection ranges from 0.1 to 20 percent and varies widely in different geographic areas. According to the prevalence rate, WHO has classified countries into 3 levels: high areas (>8%) such as Africa, Asia, Western Pacific and Middle East; intermediate areas (2–8%) such as South America and Eastern Europe, and low areas (<2%) such as Western Europe, North America, and Australia.

Invasive prenatal testing, amniocentesis and chorionic villus sampling, has been used for over four decades to identify fetal genetic disorders. The most common test after obtaining fetal tissues is chromosome analysis, performed for a variety of medical indications including abnormal ultrasound findings, advanced maternal age and an abnormal screen for Down syndrome. About 2% of pregnancies in women over the age of 35 will show a chromosome abnormality, with trisomy 21 being the most common. In addition to Down syndrome, the most commonly observed trisomies are those of chromosomes 13 and 18. Numerical abnormalities of the sex chromosomes are also relatively common, as well as triploidy.

Approximately 12%–27% of cerebrovascular disease in women of childbearing age is associated with pregnancy. The reported incidence of stroke in pregnancy ranges from 0.01%–0.05%. While these events are uncommon, they are often clinically devastating. The Center for Disease Control's (CDC) review of death certificates in all 50 states and the District of Columbia found that neurologic or neurovascular problems are one of the leading causes of mortality in pregnancy.

Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder that affects multiple organ systems, primarily the cardiovascular, ocular and skeletal. It is the most common inherited condition affecting the heart and the aorta, occurring in 1:5000–1:9800 people. There is no ethnic or gender predisposition; 20 to 35% of cases arise from de novo mutations.

Cystic Fibrosis (CF) is the most common life-shortening recessive genetic disease in the UK. Far from being a condition managed exclusively by paediatricians with sufferers dying in early childhood, CF is now a condition in which adults outnumber children with the condition, and the death of a child in a paediatric centre is rare. As increasing numbers of young people grow up relatively healthy it is unsurprising they begin to ask about relationships, sex, fertility and the possibility of having a child. This paper briefly describes the genetics, pathophysiology and clinical features of CF with an emphasis on how it pertains to female reproduction. The management of women with CF considering having a baby including contraception, preparation for pregnancy, the pregnancy itself, delivery and the post natal period will be discussed. Contraindications to pregnancy, method of termination, and pregnancy after transplantation will also be considered. Much of the detailed management is given in the European Guidelines for the Management of Pregnancy in Women with CF on which this paper is based.

Neonatal encephalopathy has been defined as “a clinically defined syndrome of disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal level of consciousness and often seizures”. It occurs in about 2–3 per 1000 births in developed countries. In developing countries, neonatal encephalopathy accounts for the largest number of deaths in infancy and childhood – approximately 1 million per year worldwide. Neonatal encephalopathy is associated with significant morbidity and mortality and is an important predictor of long term neurodevelopmental disability in near- and full-term newborn infants. Fifteen to 20 percent of infants with neonatal encephalopathy die in the neonatal period, and a further 25 percent have permanent neurologic deficits.

The term congenital ‘bladder outlet obstruction (BOO)’ describes the collection of conditions in which the normal, urethral egress of urine from the fetal bladder is impaired. The term is interchangeable with fetal ‘lower urinary tract obstruction’, as used by other authors. After considering normal urinary tract embryology, we describe the epidemiology of congenital BOO and the primary anatomical disorders associated with it. We then proceed to describe its fetal and postnatal clinical manifestations and then consider therapies and interventions which have been used to manage the condition. We not only focus on urethral and bladder disease with constitutes BOO itself, but also describe associated kidney disorders which, via chronic renal excretory failure, are important causes of morbidity. Rather than provide an exhaustive review, we emphasise studies published in the last decade, and therefore readers are referred to other reviews citing numerous earlier references.

Glomerulonephritis (GN) may be manifest clinically in several ways. It may be asymptomatic and associated with only minor urinary dipstick abnormalities, GN may present with one of the classic renal nephritic or nephrotic syndromes, or may be associated with progressive chronic kidney disease with hypertension and the gradual development of uraemia, or it may present with fulminating life threatening illness with severe acute kidney injury. The development of GN may indicate a primary renal limited disease, or may be secondary in association with systemic diseases such as systemic lupus erythematosus (SLE), myeloma, infections or diabetes. Although immunological abnormalities underlie the development of many forms of GN, precise pathogenic mechanisms remain unclear and diagnostic labels may simply reflect a description of the glomerular histological changes observed (Table 1).

The World Health Organisation (WHO) has estimated that 1500 women die every day from preventable complications of pregnancy and childbirth. While barriers to accessing healthcare are undoubtedly multi-factorial, studies have repeatedly shown that providing skilled healthcare workers can result in untold benefits for women and babies in developing countries. The phenomenon of preventable maternal and fetal morbidity and mortality is not limited to the developing world. The Confidential Enquiries into Maternal Deaths (CEMD) and Stillbirths and Infant Deaths (CESDI) in the UK have repeatedly identified substandard care as a major contributor to maternal and neonatal mortality. In 2008 The King's Fund published Safe Births: Everybody's business, an independent enquiry into the safety of maternity services in England. This recommended that simulation-based training to assess clinical, communication and team skills should be available to all maternity staff, and that training should form a core activity. Many hospitals in the UK have been running in-house courses for staff for over a decade with measurable improvements in neonatal outcomes. The value of these training schemes is recognised and rewarded through reduced insurance premiums for participating hospital trusts as part of clinical negligence schemes. Gaining competence in managing obstetric emergencies presents particular challenges for trainees. Most emergencies are, thankfully, uncommon but some constitute life-threatening events where management naturally falls to the most experienced available clinician. The skills required are often particular to emergencies and therefore novel to trainees. Utilising emergencies as training opportunities is further complicated by the presence of a conscious patient.