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A reference range of fetal haemoglobin concentration (g/dl) was established from umbilical cord blood samples obtained by cordocentesis (n = 200) or at delivery (n = 10). In normal pregnancy the mean fetal haemoglobin increases linearly from 11 g/dl at 17 weeks' gestation to 15 g/dl at 40 weeks' gestation and one standard deviation is approximately 1 g/dl. The haemoglobin was also measured in fetal blood from 154 red cell isoimmunised pregnancies from 17 to 36 weeks' gestation. In 48 fetuses with ultrasound features of hydrops the haemoglobin was 7-10 g/dl below the normal mean for gestation. It is proposed that in pregnancies complicated by red cell isoimmunisation the severity of the disease should be assessed and treated on the basis of the deviation of the fetal haemoglobin from the normal mean for gestation into mild (haemoglobin deficit less than 2 g/dl), moderate (deficit 2-7 g/dl), and severe (deficit greater than 7 g/dl).

Humidified oxygen (55%) was administered continuously through a face mask to 5 patients whose pregnancies (4 singleton and 1 twin) were all complicated by severe intrauterine growth retardation, oligohydramnios, high blood-flow impedance in the fetal aorta and umbilical artery, and low mean blood-velocity in the fetal thoracic aorta. All the fetuses were hypoxic and 2 were acidotic. After maternal hyperoxygenation, the fetal pO2 increased to within or near the normal range, and resulted in a sustained increase in the mean blood-velocity in the fetal thoracic aorta. 5 fetuses survived with minimum neonatal morbidity. The effect of maternal hyperoxygenation on the fetal pO2 in such cases may prove to be a useful method of assessing placental function and guiding management.

Fetal and maternal placental (intervillous) blood samples were obtained by means of an outpatient ultrasound-guided technique from a 33-week pregnancy with symmetrical intrauterine growth retardation. The baby was delivered by emergency caesarean section because blood gas, pH, and lactate measurements showed severe hypoxic acidosis, due to inadequate placental transfer.

Umbilical venous blood pO2, pCO2, pH, erythroblast count, and plasma lactate were measured in twenty-nine fetuses with growth retardation. There were significant negative correlations between the severity of fetal hypoxia, hypercapnoea, acidosis, and hyperlactaemia and the mean velocity of blood in the fetal aorta measured by doppler ultrasound.