Establishing a porcine model of “Small for Flow Syndrome”

Abstract

Introduction The concept of "Small for Flow Syndrome” (SFFS) arises from the observation that the determining factor of the appearance of the “Small For Size Syndrome” (SFSS) and the posthepatectomy liver failure is the increase of portal inflow against a reduced hepatic mass. The criteria that define the SFFS are intraoperative and determined by: a portal pressure >20mmHg or a portal flow >250mL/min/100g. They indicate that we must take measures to prevent the development of the SFSS, as a consequence of the structural alterations caused by this inflow. Materials and Methods An experimental study (10 minipigs) of 24-hour survival was carried out. An hyperextended hepatectomy (90%) was performed. It consists on resecting the lateral and medial left lobes, and lateral and medial right lobes. Blood tests, hepatic and systemic hemodynamics, hepatic function (PDR), histology, and volumetry were assessed before and after the surgery. Intracranial pressure (ICP) and hepatocyte proliferation were evaluated. Results In all of the swines the surgery was completed with success and hemodynamic stability to start the postoperative observation period. The percentage of hepatic volume remaining after surgery was 8.85±2.59% (volumetry by CT). Hemodynamic data were measured at the beginning, after the hepatectomy, and 24 hours after. There was an increase in portal pressure after surgery, 20.90±4.50mmHg. Portal flow varies from 68'38±23’54ml/min/100g to 245’02±115’62ml/min/100g. This increase in portal flow through a reduced sinusoidal volume is reflected in the increase in the portosystemic pressure gradient, going from 1.11±1.90 to 13.20±7.16mmHg. PDR values went from?? 12.30±5.47 to 4.54±1.82 and R15 from 17.53±10’86 to 52’12±13'00 after surgery. There are significant histological damages, oscillating the score from 0.75±1.16 to 5.62±2.55. After surgery 75% of the animals had a Ki-67<2%. The ICP was monitored, observing a gradual increase in it. Discussion After the resection there is a deterioration in the liver function (decreases the PDR and increases the INR), similars to hepatic transplant models with reduced grafts. The histological disorders are compatible with those described in the literature in relation to the SFSS. Above 20 mmHg of portal pressure all animals showed histological damage. Since the aim of establishment of an animal model of SFFS is a better understanding of this clinical syndrome as well as studying the possible preventive and curative methods, we strongly believe that, in a porcine model with normal parenchyma, 90% liver resection can be considered as ideal model. Following 90% hepatectomy, we can render the hemodynamic, histological, and biochemical changes of the SFFS. Conclusion Hyperextended hepatectomy in porcine model is a feasible, reproducible and appropriate model to study the pathophysiology, prediction, prevention, diagnosis and management of SFFS.