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An in-vitro model was set up to study a possible causal relation between bacterial colonisation of extraplacental membranes and spontaneous preterm labour. When amnion cells in tissue culture were exposed to bacterial products, their prostaglandin E output rose considerably. The degree of response varied with the organism. These findings support the theory that bacterial products may be responsible for the premature onset of labour.

Ritodrine 0·05 mg/min gave a mean scrum level of 3·6ng/ml and 0·55mg/min gave a mean level of 204 ng/ml, when infused intravenously into women in spontaneous preterm labour. Oral administration of ritodrine, 5 mg 3 hourly, gave a mean serum level of 0·3ng/ml; 10 mg 2 hourly gave 1·3ng/ml. The drug crosses the placenta and umbilical vein cord serum levels were higher than maternal levels when it was continued until delivery. Ritodrine was detected in such a baby 24 hours after birth.

One hundred and forty-six infants of 34 weeks' gestation or less were repeatedly scanned by means of real-time ultrasound to diagnose the presence of intraventricular haemorrhage (IVH), its severity, and the timing of onset of the condition. We describe a new method for grading the extent of the IVH which does not depend on ventricular size. IVH was clearly present in 52 (36%) of the 146 infants and in 32 (50%) of the 64 infants of 30 weeks' gestation or less. Repeated scans accurately timed the onset of IVH in 41 infants, and 32 (78%) had the first sign of IVH before 72 hours of age. Thirty-two clinical factors were analysed for possible correlation with the development of IVH: outborn compared with inborn, administration of sodium bicarbonate, hypothermia, intermittent positive pressure ventilation, continuous positive airways pressure, hypercapnia, severe acidosis, and respiratory distress syndrome all reached statistical significance. Analysis of variance showed that respiratory distress syndrome was the most important factor, but severe acidosis had some independent action on the development of IVH. Seventeen (81%) of 21 infants with hypercapnia (PCO2 greater than 6 kPa) together with severe acidosis (pH less than 7.1) developed IVH, of which more than half was moderate or severe in degree.

The outcome of two hundred and twelve infants transferred in utero and delivered in the regional neonatal intensive care center is compared with one hundred and sixty-six infants born elsewhere and transferred neonatally to the same unit, during the same period of time. The mean birthweight (+/- 1 S.D.) was 1391 g (+/- 415 g) for the infants transferred in utero, and 1398 g (+/- 415 g) for the infants transferred neonatally. The mean gestational age of the two groups was 29.9 completed weeks for both groups. Survival was defined as discharge from the neonatal unit and intraventricular hemorrhage was diagnosed ultrasonically. The survival rate was 83% for the group transferred in utero and 70% for the group transferred postnatally (p = less than 0.01). The incidence of intraventricular hemorrhage was 30% and 45% respectively (p = less than 0.01). Using birthweight specific perinatal mortality rates and intraventricular hemorrhage rates of the neonatally transferred group for standardisation, it can be calculated that 27 infants survived and 31 were protected from intraventricular hemorrhage because of in utero transfer. It is concluded that infants likely to require neonatal intensive care have decreased mortality and morbidity if transferred in utero to a center with these facilities rather than being transferred neonatally.

During a 2-year period, 56 infants of less than 34 weeks gestation were delivered from 53 pregnancies complicated by severe hypertension and proteinuria. In the first part of the study 32 infants were delivered whose mothers did not receive antepartum glucocorticoids; subsequently 24 infants were born whose mothers did receive antepartum glucocorticoids. The severity of maternal disease, gestational age at delivery, birthweight and obstetric management was similar in both groups. In the group receiving glucocorticoids 88% of the infants were discharged live from the neonatal unit compared with 72% in the group who did not receive corticosteroids. It is concluded that in pregnancies complicated by severe hypertension and proteinuria requiring delivery before 34 completed weeks of pregnancy, the administration of antepartum glucocorticoids to the mother does not carry an increased risk to the fetus, and may be of benefit by reducing the risk of idiopathic respiratory distress syndrome and subsequent intraventricular haemorrhage.

Preterm labour is a major cause of perinatal mortality and morbidity. The aetiology is multifactorial and attempts to predict preterm labour are unsuccessful. At the present time prophylaxis is unhelpful and the obstetrician must manage preterm labour as it arises. The management of preterm labour remains controversial because of the difficulty in conducting good clinical trials. Antepartum glucocorticoids are effective in reducing the incidence and severity of respiratory distress syndrome. The effect is dependent upon a number of factors such as race, fetal sex, gestational age, state of the membranes, fetal asphyxia and timing of delivery in relation to therapy. Tocolytics are effective in stopping contractions but this does not produce a significant prolongation of pregnancy or reduce perinatal mortality or morbidity. It is because they can suppress contractions and delay delivery for a short time that great care should be taken that this short delay is used beneficially, e.g. in-utero transfer, or steroid therapy. It is also important that this suppression does not result in an inappropriate delay where early delivery is indicated because of infection or fetal distress. Steroids, tocolytics and antibiotics are potentially hazardous although all may benefit the fetus. The particular risks versus benefits of each form of therapy should be carefully considered for the particular presentation of each individual patient. While all these agents given antenatally are of potential benefit to the fetus and neonate, prolongation of pregnancy for its own sake or for the sake of allowing time to administer such agents is no substitute for delivery of an infant in optimum condition.

Eleven pregnancies were studied in which i.v. hydralazine was given within 24 hours of delivery. Hydralazine (with its active metabolites, the hydrazones) was measured in maternal, cord and neonatal blood and in breast milk by high performance liquid chromatography (HPLC). Cord venous hydralazine concentrations Were approximately equal to maternal venous concentrations. Hydralazine was detectable in breast milk and concentrations were about half those in maternal blood taken simultaneously. Concentrations of hydralazine Were 557 nmol/l and 293nmol/l in the serum of two babies after breast feeding. Boiling expressed breast milk destroyed hydralazine. One other infant, with coarctation of the aorta, required 6 mg/kg/day of hydralazine to lower his blood pressure and his plasma concentration exceeded 8000 nmol/l. We conclude that the transfer of hydralazine across the placenta and into "reast milk is unlikely to subject neonates to pharmacological effects.