The present study demonstrated that Doppler parameters could identify different stages of hepatic fibrosis, and these Doppler parameters correlated closely with ICG retention rate (percentage of total injected ICG dose) at 15 min (ICG 15), which is considered to be one of the most valuable and reliable tests for assessing hepatic functional reserve and predicting post-hepatectomy liver failure in cirrhotic patients.
The assessment of hepatic functional reserve of patients with cirrhosis is critical for predicting prognosis, postoperative outcome in those who are candidates for nonhepatic surgery or liver resection for hepato-cellular carcinoma (HCC), or for determining the timing of liver transplantation in patients with advanced cirrhosis . Quantitative assessment of hepatic function reserve before the occurrence of liver cirrhosis has been paid much attention in clinical practice in recent years. Though liver biopsy is the gold standard for diagnosing and staging liver fibrosis, its clinical application is limited because of its invasiveness. Exploring non-invasive methods for evaluating hepatic reserve function of liver fibrosis is of significance. Present study showed that ALT concentration was increased significantly after modeling, and remained at a high lever during the fibrosis stage. However, no significant difference in ALT was found between all experimental groups, indicating that the conventional hepatic function parameters are not sensitive in reflecting the hepatic reserve function changes at different stages of liver fibrosis. ICG retention rate at 15 min (ICG R15) is considered to be one of the most valuable and reliable tests for assessing hepatic functional reserve and predicting post-hepatectomy liver failure in cirrhotic patients. The present study also showed that with the development of liver damage, ICG R15 was increased while clearance ratio of indocyanine green decreased, and there was significant difference in ICG R15 among experimental groups. This might be related to the fact that the liver blood flow resistance was increased due to increased liver fiber tissue and hepatic sinusoidal endothelium capillarization, resulting in the decreased effective hepatic flow volume. These results suggest that ICGR15 could better reflect the severity of the liver fibrosis compared to the conventional hepatic function parameters.
Though ICG R15 is considered to be one of the most valuable and reliable tests for assessing hepatic functional reserve and predicting post-hepatectomy liver failure in cirrhotic patients, the measurement of ICG R15 is relatively complicated. The liver fibrosis is a pathological process of abnormal proliferation of hepatic fiber connective tissue in response to various kinds of liver-damaging factors, which is mainly characterized by the excessive deposition of extracellular matrix and hepatic sinusoidal endothelium capillarization. Advanced liver fibrosis results in the change of hepatic vascular structure and the increase of the hepatic vascular resistance, and even develops into portal hypertension. Actually in human, there is development of portal hypertension even in pre-cirrhotic stage. After development in portal hypertension, there are changes in the hepatic circulation. Thus, the hepatic hemodynamic parameters by US might change with the development of liver fibrosis. Although there was no significant difference in blood flow velocity of hepatic artery and portal venous system between the experimental group and the control group, HCI, a parameter that combines both the hepatic arterial and portal venous measurement, was decreased gradually with the development of fibrosis. Moreover, HCI has significant negative correlation with portal venous pressure and ICG R15, indicating that the liver and its peripheral organs were in high-resistance state since HCI could overall reflect the liver blood flow perfusion profile that correlated with hepatic reserve function . These results indicate that HCImight be an alternative parameter of ICG R15 that could sensitively reflect the gradually-decreased hepatic reserve function during the course of different degree of liver fibrosis and portal hypertension.