RESUMO
We studied the risk of a large group of jaundiced neonates for bilirubin encephalopathy by serial assessment of their reserve serum albumin binding capacity as measured by the saturation index test. In 1271 infants with serum bilirubin concentration greater than 10 mg/dl, 12% had a saturation index (SI) of 7% or greater and therefore were clinically at or near risk for bilirubin encephalopathy. Treatment with glucose infusion (1 gm/kg over one hour) was highly effective in lowering the SI (delta = -3.7%. P less than 0.001). In none of the infants did SI rebound to 7% or greater within 24 hours after the infusion. In a detailed study of 19 infants who received glucose, the highly significant (P less than 0.001) fall in SI (delta = -3.7%) was accompanied by an equally significant rise in serum values for insulin (delta = +21.6 mcu/ml) and fall in serum free fatty acids (delta = -0.51 mEq/L). Many factors in the study, such as prematurity, hemolysis, acidosis, and hypoxemia, could have predisposed the infants to the risk of bilirubin encephalopathy. However, the facility by which most (93%) of the infants with high SI, including those who were premature or had evidence of hemolysis or respiratory insufficiency, responded to infusion of glucose indicates that serum free fatty acids may be the principal factor contributing to the high saturation index and therefore an underestimated factor in bilirubin binding to albumin.