Background-Intramuscular supplementation with vitamin A in large doses may reduce the incidence of chronic lung disease. Aim-To investigate whether oral supplementation with vitamin A would reduce the incidence of chronic lung disease in a group of extremely low birthweight infants. Methods-Infants with birth weight < 1000 g were randomised at birth to receive oral vitamin A supplementation (5000 IU/day) or placebo for 28 days. The primary outcome was oxygen dependency at 28 days of age or death. Results-A total of 154 infants were randomised; 77 received vitamin A (median birth weight (interquartile range) 806 (710-890) g), and 77 received placebo (median birth weight (interquartile range) 782 (662-880) g). Plasma vitamin A concentrations in the supplemented group were significantly higher at 24 hours of age but did not diVer significantly at birth, 12 hours of age, 7 days, or 28 days of life. There were no significant diVerences in the proportion of infants who survived, required oxygen at 28 days, required oxygen at 36 weeks postmenstrual age, survived without chronic lung disease at 36 weeks, survived without significant retinopathy, or who survived without significant intraventricular haemorrhage. Conclusions-Oral supplementation with 5000 IU vitamin A in extremely low birthweight infants does not significantly alter the incidence of chronic lung disease. However, this dose may have been inadequate to achieve optimal serum retinol concentrations. (Arch Dis Child Fetal Neonatal Ed 2001;84:F9-F13) Keywords: chronic lung disease; lungs; preterm; vitamin A; retinol Preterm infants have limited hepatic reserves and lower plasma concentrations of vitamin A and plasma retinol binding protein than term infants because vitamin A is transferred across the placenta mainly during the third trimester.

Cerebral fractional oxygen extraction (FOE) represents the balance between cerebral oxygen delivery and consumption. This study aimed to determine cerebral FOE in preterm infants during hypotension, during moderate anemia, and with changes in the PaCO2. Three groups of neonates were studied: stable control neonates (n = 43), anemic neonates (n = 46), and hypotensive neonates (n = 19). Cerebral FOE was calculated from the arterial oxygen saturation measured by pulse oximetry, and cerebral venous oxygen saturation was measured using near infrared spectroscopy with partial jugular venous occlusion. Mean +/- SD cerebral FOE was similar in control (0.292+/-0.06), anemic (0.310+/-0.08; P = 0.26), and hypotensive (0.278+/-0.06; P = 0.41) neonates. After anemic neonates were transfused, mean +/- SD cerebral FOE decreased to 0.274+/-0.05 (P = 0.02). There was a weak negative correlation with the hemoglobin concentration (n = 89, r = -0.24, P = 0.04) but not with the hemoglobin F fraction (n = 56, r = 0.24, P = 0.09). In the hypotensive neonates, there was no relationship between cerebral FOE and blood pressure (n = 19, r = 0.34, P = 0.15). There was a significant negative correlation between cerebral FOE and PaCO2 within individuals (n = 14, r = -0.63, P = 0.01), but there was no relationship between individuals (n = 14, r = 0, P = 1). Cerebral FOE was not significantly altered in neonates with either mild anemia or hypotension. There were, however, changes in cerebral FOE when physiological changes occurred over a relatively short period: Cerebral FOE decreased after blood transfusion and increased with decreasing PaCO2. As no change in cerebral FOE was seen during hypotension, it was speculated that cerebral oxygen delivery may have been maintained by cerebral blood flow autoregulation.

Aims-To assess whether changes in survival over time in infants of 23 to 25 weeks of gestational age were accompanied by changes in the incidence of disability in childhood during an 11 year period. Methods-Obstetric and neonatal variables having the strongest association with both survival to discharge from a regional neonatal medical unit and neurodevelopmental disability in 192 infants of 23 to 25 weeks of gestation, born in 1984 to 1994, were studied as a group and in two cohorts (1984 to 1989 n = 96 and 1990 to 1994 n = 96). The data collected included CRIB (clinical risk index for babies) scores and cranial ultrasound scan findings. The children were followed up at outpatient clinics. Results-Between 1984 and 1989 (cohort 1) and 1990 and 1994 (cohort 2) the rate of survival to discharge increased significantly from 27% to 42% and the rate of disability in survivors increased from 38% to 68% ; most of this increase was in mild disability. The proportions of survivors with cerebral palsy did not alter significantly (21% vs 18%), but more survivors with blindness due to retinopathy of prematurity (4% vs 18%), myopia (4% vs 15%) and squints (8% vs 13%) contributed to the increased rate of disability. Clinically significant cranial ultrasound findings and a high CRIB score were strongly associated with death. A high CRIB score was most strongly associated with disability. Conclusions-The rise in disability with improved survival was not due to cerebral palsy; rather the main contributors were blindness due to retinopathy, myopia, and squint. The causes of these disabilities seem to be linked to high CRIB scores. A system of regular and skilled retinal examination and access to facilities for retinal ablation should be in place in all neonatal units which undertake the care of such extremely preterm infants. (Arch Dis Child Fetal Neonatal Ed 1998;78:F99-F104)

A measurement of tissue oxygenation may be a better marker of transfusion need than the Hb concentration. Peripheral fractional oxygen extraction, oxygen consumption, and oxygen delivery were measured noninvasively using near infrared spectroscopy in babies, some of whom were given blood transfusions. The above indicators of oxygenation were measured in 96 preterm babies. The decision to transfuse was based on a standard protocol. Transfusions were not considered necessary for babies in group 1 but were given to those in groups 2 (asymptomatic) and 3 (symptoms attributed to anemia). Hb and Hb fraction F (HbF) were measured in each baby. Oxygenation, Hb, and HbF measurements were made again 12-24 h after transfusion, and red cell volume (RCV) was calculated. Fractional oxygen extraction was significantly higher in symptomatic (0.43 +/- 0.06) but not asymptomatic (0.33 +/- 0.05) babies compared with control subjects (0.35 +/- 0.06). Oxygen consumption and oxygen delivery were similar in the three groups before transfusion. After transfusion the mean fractional oxygen extraction fell significantly in symptomatic but not in asymptomatic babies. There was no significant change in either oxygen consumption or oxygen delivery in symptomatic babies. The asymptomatic group had no change in oxygen extraction or oxygen consumption after transfusion, although oxygen delivery increased significantly. Fractional oxygen extraction correlated with HbF (n = 66, r = 0.49, p < 0.001) and RCV (n = 19, r = -0.48, p = 0.04) and there was a weak correlation with Hb (n = 94, r = -0.21, p = 0.04). Peripheral fractional oxygen extraction monitored noninvasively correlated with variables known to determine oxygen availability to the tissues, namely RCV and HbF, and was higher in babies with symptomatic anemia and decreased after transfusion.