Fetal growth restriction (FGR) is defined as the failure of a fetus to attain its full genetic growth potential. It is a leading cause of stillbirth, prematurity, cerebral palsy and perinatal mortality. Small size at birth increases surviving infants’ lifelong risk of adverse health outcomes associated with the metabolic syndrome. The pathophysiology of abnormal fetal growth is extremely complex and incompletely understood, with a plethora of genetic, signalling and metabolic candidates under investigation, many of which may result in abnormal structure and function of the placenta. In contrast to, or maybe because of, the underlying complexities of FGR, the strategies clinicians have for identifying and managing this outcome are conspicuously limited. Current clinical practice is restricted to identifying pregnancies at risk of FGR, and when FGR is detected, using intensive monitoring to guide the timing of delivery to optimise fetal outcomes. Abnormal Doppler indices in the umbilical artery are strongly associated with poor perinatal outcomes and are currently the “gold standard” for clinical surveillance of the growth-restricted fetus.

Congenital cytomegalovirus (CMV) infection is now the commonest infective cause of neurological handicap. Arguably, there is no other single contributor to developmental disability where a greater opportunity, and imperative, exists to improve outcomes than CMV. CMV is the most common intrauterine infection and congenital CMV is the leading non-inherited cause of sensorineural deafness. The public health impact of CMV is significant: the overall birth prevalence of congenital CMV is estimated at 0.64%, with 11% of live born infants displaying symptoms.

Preterm birth may be spontaneous or medically indicated for maternal or fetal reasons. Around 20–25% of preterm births (PTB) follow preterm premature rupture of the membranes (PPROM), however the cause of preterm labour is often unknown. It may represent early maturation and activation of the normal labour process or it may be precipitated by pathological causes. The normal process of labour has a diurnal variation with more deliveries occurring at night. Evidence demonstrating that the diurnal variation persists in preterm deliveries suggest that at least a proportion are due to early maturation of the normal process and the logical assumption is that these may be amenable to prevention or effective treatment. Whatever the cause of preterm delivery, there appears to be a common pathway resulting in activation of inflammatory processes. It is important to distinguish the physiological and pathological causes of preterm labour and not to assume that all inflammation is pathological. The distinction is clinically important since pathological causes may be associated with an adverse intrauterine environment, which would be a contraindication to delaying delivery.