The risk of hepatic artery embolization in the presence of obstructive jaundice

Rhesus and cynomolgus monkeys were used as experimental subjects to determine the extend to which the presence of biliary obstruction increases the risk of hepatic necrosis following hepatic artery embolization. It was found that peripheral hepatic artery embolization without biliary obstruction resulted in acute hepatic swelling and dysfunction and chronic focal infarction with bile cyst formation. However, massive hepatic necrosis and bile lakes were not seen. Distal common bile duct obstruction unaccompanied by arterial occlusion did not seriously damage the liver, although it was found that distal common duct obstruction in monkeys is not strictly comparable to distal common duct obstruction in humans. When peripheral hepatic artery embolization was performed following ligation of the right or left hepatic ducts at the point of their emergence from the porta hepatis, total infarction of the obstructed segment occurred and a massive bile lake formed. The pathophysiologic explanation is probably the decreased portal venous inflow that accompanies biliary obstruction; hepatic artery inflow reciprocally increases and the liver become critically dependent upon an intact arterial system. Clinical evidence suggests that a liver with a recently decompressed biliary tree may also be more susceptible to infarction and abscess formation following hepatic artery ligation or embolization.