In 3 (9 %) of 34 children with biliary atresia, US revealed gallbladde
r contraction following an oral feed, given on admission, but not with
subsequent feeds. Surgery revealed a Kasai type IIIa biliary atresia
with a patent communication between the gallbladder and duodenum. We p
ropose that the bile ducts may initially have been patent, but then gr
adually became obliterated secondary to inflammation. These cases may
explain the development of one type of biliary atresia.