Pathophysiology of major hepatic resection and benefits of preoperative portal embolization in preventing hepatic failure

Abstract

The mechanism whereby hepatic failure after hepatectomy can be prevented by previous portal embolization (PE) was reviewed. To overcome the surgical stress of hepatectomy, adenosine triphosphate (ATP) energy-dependent protein synthesis of hepatic acute phase proteins and of intrahepatocytic protein is necessary for regeneration. To prevent hepatic failure after hepatectomy. ATP synthesis must exceed ATP consumption, a circumstance achieved by increasing the former or decreasing the latter. PE induces atrophy of the ipsilateral lobe and hypertrophy or hyperplasia of the contralateral lobe by hepatocyte regeneration. It also induces a partial shift of function, much as biliary excretion of indocyanine green (ICG) and bilirubin, from the ipsilateral to the contralateral lobe. The course and rate of the hypertrophy depend upon the patient's age, the extent of the area affected by the PE, the embolization material, and the degree of hepatic fibrosis of the contralateral lobe. In other words, PE may be regarded as atraumatic hepatectomy. Preliminary PE decreases the surgical stress of a hepatectomy by causing atrophy of the ipsilateral lobe and hepatocyte regeneration of the contralateral lobe in the interim, with a resulting decrease of ATP consumption during surgical hepatectomy. This two-stage procedure can prevent hepatic failure after hepatic resection and extends the range of indications for hepatectomy. Levels of the cytokines regulating hepatic regeneration after PE should be examined to determine whether hepatic regeneration is completed and hepatic resection can be performed without complication.