Neonatal jaundice in Greek immigrants.
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Biomedical subjects
Publications and source records attributed to T Valaes.
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The bilirubin titration point--the lowest bilirubin concentration at which loosely bound bilirubin could be demonstrated by Sephadex gel filtration--was determined in samples collected before, during, and on completion of 17 exchange transfusions as well as in the discarded and donor blood. The bilirubin titration point expressed either as bilirubin concentration or as bilirubin/albumin molar ratio failed to be increased by the exchange transfusion and, in each case at the end of the procedure, the titration point was below the expected level, assuming that the donor albumin was going to retain its binding properties in the infant's circulation. The bilirubin titration point was also depressed in the discarded blood, and the depression was inversely related to the amount of bilirubin removed by the exchange transfusion (expressed as mg/kg of body weight/mg of initial bilirubin concentration). These results are interpreted as an indication that interfering substances are responsible for the decreased binding of bilirubin in newborn, particularly preterm, infants. In practical terms the criteria for a repeat exchange transfusion should be the same as for the initial one, as no change in the bilirubin binding properties of the serum is likely to occur following exchange transfusion.
Development of rickets in association with parenteral nutrition is described in four premature infants having gestational ages of 26-31 wk. In the first two infants there was a documented deficiency of vitamin D, but in the second two adequate supplementation was achieved. Vitamin D, whose primary action is to facilitate intestinal absorption of calcium, may also be a hormone of prime necessity in infant bone formation. Conversion of precursor cholecalciferol to the active form of hormone, 1,25-DHCC, requires intermediate hydroxylation by the liver. The premature infant liver may be deficient in its ability to carry out this step of metabolism, and in normal intrauterine existence the fetus may receive 1,25-DHCC, the active metabolite, from the mother. Calcium intake in these infants was far below that achieved by fetuses of comparable age in utero, even though in excess of that provided by usual premature infant oral formulas. Although calcium deficiency has not been incriminated as a cause of rickets in the past, it is possible that in very tiny premature infants rapid growth requirements lead to a relative calcium deficiency which may be manifested as uncalcified osteoid. Until the mechanism of the formation of rickets in small premature infants is clarified it is recommended that supplemental calcium and vitamin D be given to all premature infants receiving parenteral nutrition, and that periodic x-rays be obtained to detect the development of rickets.
Carboxyhaemoglobin levels were measured in 250 consecutive, normal, term newborns and in a group of 75 severely jaundiced infants in an effort to assess the role of haemolysis in non-specific neonatal hyperbilirubinaemia--"Physiologic jaundice"-as well as in severe jaundice of various etiologies. In normal newborns a significant correlation (r=0.3293, p less than 0.001) was found between third-day carboxyhaemoglobin and serum bilirubin levels. Significant correlations were also found between the cord and third day values for carboxyhaemoglobin (infants of non-smoking mothers) for reticulocyte count, and for serum bilirubin. Third day haemoglobin showed no correlation with any of the other parameters including cord haemoglobin. Of the infants with third day carboxyhaemoglobin up to 0.75%, 1.7% had third day serum bilirubin values above 16.0 mg/100 ml. The corresponding percentage for the infants with carboxyhaemoglobin above 0.75% was 6.1%. It is concluded that increased rates of haemolysis due to as yet unspecified caused play an important role in the non-specific hyperbilirubinaemia of normal term newborns. As expected, high levels of carboxyhaemoglobin were found in infants with severe jaundice due to Rhesus and ABO haemolytic disease and glucose-6-phosphate dehydrogenase deficiency but also in jaundiced prematures and in Greek infants with severe jaundice of unknown cause.
A simple modification to the standard 'in-out' exchange transfusion technique is described which requires cannulation of the umbilical vein only, yet provides many of the theoretical and practical advantages of a 2-catheter arteriovenous technique. The advantages include a reduction of cardiovascular disturbance; a reduction of the inevitable pressure changes in the portal venous system (probably important in the pathogenesis of complicating necrotizing enterocolitis); administration of alkali or drugs diluted in donor blood; accurate assessment of balance; a more efficient exchange; and general ease of management allowing better clinical observation of the infant.
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Clinical experience with Sephadex gel filtration for evaluation of the bilirubin binding affinity of serum in neonatal jaundice is reported. In serum specimens from 362 jaundiced neonates the results of the test were in most cases in good agreement with the independently determined decision to perform exchange transfusion. In all relevant cases of the 24 with bilirubin encephalopathy the Sephadex test was strongly positive. The test was positive at lower bilirubin levels and bilirubin:albumin molar ratios in preterm as compared with term neonates, especially those in poor clinical conditions. Among term infants the test indicated an increase in bilirubin binding affinity after the fifth day of life. The Sephadex test appears to be of practical value in supplementing and refining existing criteria for exchange transfusion.
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