Infants with very low birth weights have less need of transfusions if given epoetin beta during the first six weeks of life (250 IU per kilogram three times a week). We recommend early epoetin treatment for all such infants, but further studies of nutrition and iron supplementation during treatment are needed.

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Sixty very low birth weight infants (birth weight 560-1450 g) were studied during the first 28 days of life. The infants were classified as group A (n = 19 infants who never required ventilator support), group B (n = 20 infants mechanically ventilated for minor respiratory problems), and group C (n = 21 infants ventilated for respiratory distress syndrome). Diagnostic blood sampling was measured, infants were checked for clinical symptoms and laboratory signs of anaemia 24 h before and after the transfusion of packed red cells. A total of 7998 punctures (average: 4.8 per infant per day) were performed, the mean blood loss due to diagnostic sampling was 50.3 ml/kg per 28 days (range 7-142) for all infants. A high correlation (rs = +0.91) was found between the blood volumes sampled and transfused. In group A, the mean blood loss was 24 ml/kg, and a total of 29 blood transfusions were administered. The most frequent symptoms of anaemia were poor weight gain and apnoeic spells. In group B, the mean blood loss was 60 ml/kg and a total of 97 blood transfusions were administered. In group C, the mean blood loss was 67 ml/kg and a total of 116 blood transfusions were administered. In both groups B and C, poor weight gain, pallor and distended abdomen were the most frequent symptoms of anaemia. Following the blood transfusion, haematocrit rose and blood pressure remained unchanged. The symptoms that responded most favourably to the blood transfusion were: poor weight gain, oxygen requirement, and distended abdomen. The results emphasize the need for miniaturizing laboratory techniques and monitoring blood sampling.

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Necrotizing enterocolitis (NEC) is not a new disease but one that has been reported since special care units began to house preterm infants. It was observed in foundling hospitals in Paris [Billard, 1828] and Vienna [Bednar, 1850] and, as it occurred in clusters, was regarded as a nosocomial infection in the infant hospitals of Zurich [Willi, 1944] and Berlin [Ylppö, 1931]. Clinical and patho-anatomic characterization was achieved by Schmidt and Quaiser in 1952. The unproven hypothesis of mesenteric hypoperfusion as a major etiological factor arose from animal models and analogous perforating disorders in term infants. Despite similarities between NEC and clostridial infections, few studies employed anaerobic culture techniques. The pathogenesis remains unclear and its distinction from related disorders uncertain. It is unlikely that strategies to prevent NEC will be successful unless the disease is better understood.