Cytomegalovirus (CMV) is the most frequent cause of congenital viral infection,1 with a prevalence of 0.5 to 1% of all live births, and the leading infectious cause of sensorineural deafness and mental retardation.1 As other Herpesviridae, CMV fetal infection can develop following both primary and recurrent maternal infection. Vertical transmission rate is around 30% following primary infection and 2 to 3% following recurrent infection.2 Effects on the unborn as well as on the newborn are widely variable. It is estimated that only 5 to 10% of infected newborns have symptoms at birth, whereas around 90% of congenitally infected infants are asymptomatic although 5–15% of these infants will develop some degree of sensorineural hearing loss.3

Placentas from different species differ not only in their cellular structure and normal trajectory of growth but also in the architecture of their placental vasculature and the transport and exchange mechanisms that determine nutritional transfer from mother to fetus and waste disposal from fetus to mother.1 Many maternal and fetal hormonal and nutritional factors, as well as placental paracrine and autocrine systems affect placental growth and development throughout gestation.2 Nutrients delivered from the maternal circulation are as important for placental growth as they are for fetal growth. In addition to passing across the placenta to provide the building blocks for fetal growth, amino acids, carbohydrate and lipids are incorporated into the placenta.

Fetal bradycardia may herald fetal demise. This article highlights arrhythmic fetal bradycardia rather than bradycardia caused by perinatal distress. We briefly examine the embryonic conduction system's development and physiology and we review the classification, aetiology, evaluation, and approach to fetal bradycardia. Our aim is to provide the clinician with practical information about fetal bradycardia that enlightens causative conditions and aids management.

Obstetric haemorrhage has been recognised as a major cause of maternal death as long as physicians have studied and written about childbirth. Until the 20th century, however, little was possible in the way of effective treatment. Postpartum haemorrhage (PPH) is still a frequent cause of death in many parts of the world. Even in developing countries, it remains the 3rd biggest killer of women in childbirth, despite considerable advances in medical care in the last half-century. The modern management of PPH may include a team of anaesthetists, haematologists, vascular surgeons, gynaecologists and radiologists.1 Clearly, this change represents an advance which has saved and will continue to save countless lives, not only in the developed world where such teamwork is routine, but also in developing nations that are desperately looking for ways to reduce maternal mortality as part of their efforts to comply with the United Nations Millennium Development Goals by the year 2015.2