Obstructive Jaundice

Introduction Neonatal cholestasis is defined as prolonged elevation of serum levels of conjugated bilirubin beyond the first 14 days of life. Neonatal hyperbilirubinaemia is usually physiologic, unconjugated, and self-limited. Only 2–15% of neonates remain jaundiced past 2 weeks of life, and just 0.2–0.4% have cholestatic jaundice from either intrahepatic cholestasis or structural abnormalities that cause biliary obstruction. Intrahepatic cholestasis may result from numerous infectious or inflammatory causes, as well as from inherited metabolic defects. The major structural diseases include biliary atresia and choledochal cyst. A variable element of hepatocellular dysfunction is common to all of these, thus rendering initial discrimination between medical and surgical cholestatic disease challenging. Obstructive jaundice in infancy presents a surgical challenge, not only because of the difficulty in differentiating those cases that are amenable to surgical correction from those that are not, but also because of the desire to improve the persistently low salvage rate obtained even for correctable cases. Only if surgery is undertaken before 3 months of age, and preferably by 2 months of age, can the ravages caused by prolonged obstruction—namely, cirrhosis, portal hypertension, liver failure, and death—be prevented. Survival of patients whose obstruction is surgically relieved after 3 months of age is rare, and when they do survive, many of them (even those operated on before this time) have a severe morbidity or even mortality caused by cirrhosis and, later, portal hypertension. Thus there is only a short time between the appearance of the jaundice (usually between the ages of 4 and 6 weeks) and the optimal time for surgical intervention.