Cerebral palsy is the most common neurological disorder in children. Epidemiological evidence suggests that antenatal origins are a major cause. Currently there is no antenatal test for cerebral palsy, no proven preventable measures in late pregnancy, and no known cure. Cerebral palsy affects not only the diagnosed child, but also their family and the community, requiring considerable social and financial resources to assist these children in their daily lives.

Respiratory Distress Syndrome (RDS) is due to immaturity of the lungs, primarily the surfactant synthesising system; hence, the risk of RDS is inversely proportional to gestational age. The incidence of RDS has been reduced by the routine use of both antenatal corticosteroids and postnatal surfactant, but still approximately one per cent of babies develop RDS. Hyaline membranes, formed from plasma proteins which have leaked onto the lung surface through damaged capillaries and endothelial cells, line the terminal airways. Hence, RDS has also been called hyaline membrane disease, but RDS is the preferred name as the presence of hyaline membranes can only be confirmed histologically. The aim of this review is to emphasize the pathophysiology of RDS and the clinical presentation and relevance of diagnostic techniques in the current population of very prematurely born infants, highlighting the differential diagnosis. In addition, the evidence base for prophylactic and management strategies including whether new therapies and techniques of respiratory support have positively impacted on outcomes are discussed. The mortality and long term morbidity associated with very premature birth are described. Our increasing understanding that the so-called new bronchopulmonary dysplasia (BPD) and associated chronic adverse respiratory outcomes in such infants can reflect antenatal events resulting in abnormal lung growth is highlighted.

Despite a plethora of publications existing in the literature, there is still confusion about the definition and management of intrauterine growth-restricted fetuses. Fetal growth restriction (FGR) is defined by the American College of Obstetricians and Gynecologists as estimated fetal weight (EFW) less than that expected for gestational age. Clinically this is applied when the EFW is less than the 10th percentile because perinatal morbidity and mortality is increased in low-birth weight infants. Other investigators have proposed and used a variety of fetal definitions: a fetus with an estimated weight < 2SD (standard deviation) from the mean, the 3rd 5th or 15th percentile and an abdominal circumference 2 SD below the mean. Because of the different definitions, it is understandable why different information has been obtained in growth restricted fetuses and why different management schemes have been proposed. A second source of confusion in FGR lies in the fundamental misunderstanding that all growth restricted fetuses are the same, and all will progress to cardiovascular failure following a similar time frame. We believe that in FGR, 2 concepts are important: the first is to detect those growth restricted fetuses at risk for adverse perinatal outcome; the second is to optimize the timing of delivery for these fetuses.

Gestational diabetes (GDM) is defined as “carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.” The definition is applicable regardless of whether insulin is used for treatment or the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated the pregnancy”. GDM complicates 3–15% of all pregnancies and is a major cause of perinatal morbidity and mortality, as well as maternal long term morbidity. Of all types of diabetes, gestational diabetes (GDM) accounts for approximately 90–95% of all cases of diabetes in pregnancy.