Forty-two of 340 infants dying before 3 months of age had bile stasis in the liver. Statistical comparison of these infants with 81 jaundiced infants and 217 with neither jaundice nor bile stasis demonstrated that bile stasis was associated with hepatitis, galactosemia, erythroblastosis fetalis, prematurity, esophageal atresia with tracheoesophageal fistula, duodenal atresia and lower small intestinal obstruction. High proportions of the infants with bile stasis also had one or more of: infection with gram-negative organisms, significant internal hemorrhage and dehydration. Infants with congenital heart disease were statistically unlikely to have either jaundice or bile stasis, and the transposition complex was associated with a lower incidence of jaundice than was the hypoplastic left heart complex. The data indicate that biochemical dysfunction of liver cells is a cause of bile stasis, as is duct obstruction, and suggest that disturbance of hepatic blood flow is also a causative factor. Statistically, bile stasis in the liver is associated with elevation of conjugated bilirubin in serum, and the causative factors listed are thus relevant to the genesis of the inspissated bile syndrome in infancy. The spectrum of causes of bile stasis in older children differs strikingly from that seen in young infants.