Portal and splanchnic hemodynamics after partial splenic embolization in cirrhotic patients with hypersplenism.

To assess the acute effects of partial splenic embolization (PSE) on portal and splanchnic hemodynamics in patients with cirrhosis. Ninety-five patients with hypersplenism were included in the study. Duplex examinations were performed before and 3 and 7 days after PSE. Portal and splanchnic hemodynamics including vessel cross-sectional area (CSA), mean flow velocities (cm/s), blood flows (mL/min), Doppler indices as portal congestion index (CI), liver vascular index, hepatic artery and superior mesenteric artery (SMA) pulsatility and resistive indices (PI and RI), were performed before and after PSE. In our study, 69 of 95 patients were males (72.6%) and 26 females (27.3%). Chronic hepatitis C virus infection was the main cause of cirrhosis (81.1%). PSE failed technically in six patients (6.3%). After PSE, both CSA and CI significantly decreased (p < 0.05 and <0.01). The portal vein velocity significantly increased (p < 0.01). The portal flow volume (892.4 ± 151 mL/min) did not show significant changes. The hepatic artery RI and PI showed a steady increase that became significant 7 days post-PSE (p < 0.05). The RI and PI of SMA increased significantly after 7 days of PSE (p < 0.05). PSE has an immediate portal decompression effect in patients with portal hypertension without reduction in portal flow. This effect on portal pressure should be investigated in future studies as a potential tool for management of acute variceal bleeding when other medical procedures fail.

Predictors of hepatic decompensation after TACE for hepatocellular carcinoma.

AIM: To study predictive factors for hepatic decompensation after transarterial chemoembolisation (TACE) for hepatocellular carcinoma (HCC). METHODS: Between November 2009 and August 2010, of 254 patients with HCC who presented to our multidisciplinary HCC clinic for evaluation, 102 (40%) were amenable for TACE. In this prospective study, there were 102 patients with compensated cirrhosis with HCC and Child-Pugh Class A cirrhosis who underwent TACE at the National Liver Institute, Menoufiya University, Egypt. We excluded all patients with prior locoregional therapy, systemic therapy and/or surgical intervention. At baseline and at 1 month postprocedure, laboratory criteria, tumour criteria (size, number) and Child-Pugh score were recorded. Patients were classified into group 1 (no Child-Pugh point increase after TACE) and group 2 (one or more added Child-Pugh points after TACE, defining hepatic decompensation). Univariate and multivariate analyses were performed to identify factors predictive of hepatic decompensation. RESULTS: Patients were mostly males (82.4%) of mean age 58.4±8.1 years. The only significant changes in laboratory findings at 1 month after TACE were increased international normalised ratio, serum total bilirubin, alanine transaminase and aspartate transaminase and decreased serum albumin and α-fetoprotein (AFP). The statistically significant predictive factors for hepatic decompensation using univariate analysis were found to be baseline lower serum albumin, higher serum α-fetoprotein, more advanced Barcelona Clinic Liver Cancer (BCLC) stage, larger tumour size and a greater number of tumour nodules; with logistic regression, multivariate analysis found that at baseline larger tumour size (p=0.004 at 95% CI), higher serum AFP (p=0.046 at 95% CI) and lower serum albumin (p=0.033 at 95% CI) predicted decompensation; BCLC stage, number of tumour nodules and pre-TACE bilirubin did not predict changes in liver function. CONCLUSIONS: Lower serum albumin and increased tumour burden (larger tumour size/more nodules and higher α-fetoprotein) at baseline may help predict post-TACE decompensation.