In a consecutive sample of all preterm infants < 1500 gms (76) admitted to our premature nurseries from July 1995 to June 1996, 13 patients (19%) demonstrated peak levels of direct bilirubin ranging from 2.0≈12.5 mg/dl(mean 6.9 ± 2.8 SD). There were 11 deaths. Significant differences were observed between the total and affected populations in sex (M/F), gestational age (GA), birthweight (BW), days to full enteral feeding (FE), duration of total parenteral nutrition(TPN), and discharge or death (D/C).Table

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Sixty-three infants (92%) of all infants <1500gms were treated with antibiotics and TPN. All 13 infants with elevated direct bilirubin levels received TPN & antibiotics. Twenty-nine control infants (46%) had positive blood cultures. Eleven of the thirteen patients (85%) with elevated bilirubin had positive blood or CSF cultures, temporally related to their increased bilirubin levels. Importantly, one patient developed bilirubin elevation, several days after TPN was discontinued. In four additional patients, changes in alkaline phosphatase levels did not support a hepatocellular or cholestatic operant mechanism. These data suggest that TPN itself may not be the sole cause of direct hyperbilirubinemia and other factors such as: time of TPN treatment, concurrent bacterial infection, or other hepatocellular processes such as failure of excretion of bile acids, should be further evaluated as increasing risk for cholestasis.