Pathobiochemical Features of Posthepatectomy Liver Failure and Prospects for Its Metabolic Correction

Abstract

We review the current understanding of pathophysiology and pathobiochemistry of conditions following extensive resections of the liver parenchyma and describe potential ways of surgical and metabolic correction, including promising molecular targets for therapy. Reduced residual tissue volume (small-for-size syndrome), parenchymal edema due to hyperperfusion and impaired venous blood outflow, septic complications, organ ischemia-reperfusion, mitochondrial dysfunction, and oxidative stress are considered key pathogenetic factors in liver failure development following extensive resections of the liver parenchyma. Given the above, promising ways of managing posthepatectomy conditions are the use of agents reducing portal pressure (octreotide [somatostatin analogue], terlipressin [vasopressin analogue], and propranolol), energotropic metabolic drugs (combined preparations of succinate and antioxidants, gasotransmitter donors), and antibiotics and synbiotics for prevention of infectious complications. The approaches currently used in clinical practice cannot always effectively manage complications following extensive hepatectomy, so fundamental research should focus on searching and creating effective strategies for prevention and therapy of posthepatectomy liver failure.