laparoscopic exploration showed marked cirrhosis of the liver with nodular surface
The diagnosis of biliary atresia was confirmed by poorly developed gallbladder seen laparoscopically and no normal bile seen by puncture
The incidence of biliary atresia has been on the rise in recent years, with a higher incidence in female than male infants.
Etiology.
In the past, it was thought to be a congenital malformation The current view is that it occurs perinatally, as a result of an inflammatory lesion that causes nasal congestion, atrophy or partial disappearance of the biliary tract.
Pathological typology: It can be divided into three types.
Type I, common bile duct atresia with fair intrahepatic bile duct development, accounts for 5-10%.
Type II, hepatic duct atresia with almost complete absence of extrahepatic biliary structures.
Type III, hepatoportal atresia, where anastomosis with the intestine cannot be done.
Clinical manifestations.
The stools are gray or yellowish in the neonatal period, and jaundice usually begins to show gradually 1 to 2 weeks after birth, with the stools becoming lighter and later grayish, but in more advanced stages, the stools can be slightly yellowish. The color of the urine becomes darker as the jaundice increases. Jaundice deepens, the skin becomes golden yellow or even brown, mucous membranes and sclera are significantly yellow, tears and even saliva are yellow in the late stage, and there are scratches on the skin. Abdominal distension is obvious, the liver is large, the right lobe is prominent, and ascites may be present in the late stage.
Laboratory tests.
Biliary atresia is obstructive jaundice with marked elevation of direct bilirubin.
Definitive diagnosis requires biliary tract exploration and angiography.
Treatment.
Gussy surgery, preferably at an age of no more than three months.
Liver transplantation.
The child has marked generalized skin yellowing, deep yellow urine, enlarged liver with a hard texture
with a tiny gallbladder and no normal extrahepatic bile ducts seen at the hepatic hilum.
The stool was light in color, almost bile-free and close to white clay-like
One year after biliary atresia Gussy, the child recovered well with completely normal bilirubin