Abstract
The occurrence of minor cerebral deficit in the absence of gross neurologic demage as a result of neonatal hyperbilirubinemia has been suspected for some time [Day and Haines, Pediatrics 00: 000, 1954]. Recently Odell (J.Pediat. 00:000, 1970] has documented the presence of such demage by means of pyschometic and neurologic evaluations at age 5 to 6 years in a group of jaundiced infants treated with exchange transfusion. Demage was found to correlate with degree of saturation of the serum proteins with bilirubin (as measured by his salicylate saturation index). We are confirming these result in a similar study using our HABA technique (program SPR 1966, Coleman as a mesure of serum binding reserve.
Analysis of the first group of infants being recalled at age 4 years for detailed psychometric, speech and hearing and neurologic examinations suggests that jaundiced infants whose HABA binding levels fall below 50% are likely to suffer some degree of measureable damage which infants whose binding levels remain above this level will escape (Chi square = 6.04, p = 0.014, n = 41). Correlation of damage with bilirubin/albumin molar ratio was good. As in the study of ODELL, correlation with serum bilirubin concentration was poor.
The data clearly indicate that if minimal as well as major cerebral damage as a consequence of neonatal jaundice is to be prevented more exchange transfusions will have to be done or some alternative or additional form or therapy will have to be used. Phototherapy in conjunction with exchange transfusion gives promise of providing increased protection without increased therapeutic risk. Its ability to do so should be subjected to the scrutiny of long-term follow up studies.
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Johnson, L., Boggs, T. Failure of Exchange Transfusion to Prevent Minimal Cerebral Damage When Employed so as to Maintain Serum Bilirubin Concentrations Below 18 and 20 mg/ 100 ml. Pediatr Res 4, 481 (1970). https://doi.org/10.1203/00006450-197009000-00185
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DOI: https://doi.org/10.1203/00006450-197009000-00185