| Background and objectiveBudd-Chiari syndrome(BCS) refers to post-hepatic portal hypertension and/or inferior vena cava (IVC) hypertension caused by obstruction of blood flow in outlet of hepatic veins(HV) and/or post-hepatic inferior vena cava. The first case was reported by Lambron in 1842, then Budd and Chiari described it from different ways, so it was named BCS. Most cases are HV type in western countries, but IVC type in China and Japan. Complex pathological types, different pathologic positions and degrees of HV and IVC, the formation of portal hypertension(PHT), compensatory ability of blood flow and the formation of collateral branches in and out liver contribute to complex hemodynamic changes of BCS. Obstruction of hepatic blood outlet leads to liver congestion, hepatic cell degeneration, inflammatory cell infiltration, connective tissue proliferation, even to congestive cirrhosis. The pathological features of liver may be related with many factors. In this study, we performed biopsies to learn the pathology of liver, usedthe color Doppler ultrasonography to measure the hemodynamic parameters of portal vein(PV) and hepatic artery(HA), used the color Doppler and angiograph to learn the circumstances of HV and IVC; and collected the clinical data. We investigated the relationship between pathology of liver and these factors in BCS. Patients and methods27 cases included 16 males and 11 females and mean age was 38.04 years old(ll-70). 12 cases were HV type, 5 cases were IVC type and 10 cases were HV combined IVC type. The biopsies were performed under digital subtractionangiography during interventional therapy. We performed 28 biopsies in 27 patients, used disp franseen biopsy needle(DFBN) 12 times, quick-core biopsy needle(QCBN) 15 times. The specimens were studied by pathologists with light microscopy.We measured vessel diameter, mean flow speed, direction of blood flow and counted the flood flow volume of PV and HA before interventional therapy. The blood flow volume was calculated with the flowing equation: QVmean X (D/2)2 X 760(Q: flow volume per minute, V: mean blood flow velocity, D: vessel diameter). The measurement point of PV was 1.5-2cm under the cross of left and right main branches. The measurement point of HA was at the hepatica propria in hepatic hilum. Results1. 28 biopsies were performed in 27 patients, 26 specimens were satisfactory (diameter: O.lcm, length: l-4cm). The technical success rate of biopsy with DFBN was 83.3% and the technical success rate of biopsy with QCBN was 100%. The pathologic features of liver were as follows: cellular swelling or ballooning degeneration; congestion in the central vein of hepatic lobule and hepatic sinusoid, even hemorrhage in Disse's spaces; proliferation of connective tissue in the center of hepatic lobule and portal area; and inflammatory cell infiltration. 1 patient happened hematoma after biopsy.2. The degree of liver fibrosis had correlation with age and course of disease(p < 0.05). The age in slight and moderate fibrosis group were significantly lower than that in serious fibrosis group, and the course of disease in slight fibrosis group was significantly lower than those in moderate and serious fibrosis group. The degree of liver fibrosis had no correlation with gender and age of disease onset(p > 0.05).3. The degree of hepatic cell degeneration had no correlation with gender, age, age of disease onset and course of disease(p > 0.05).4. The degree of hepatic sinusoid dilated had no correlation with gender, age, age of disease onset and course of disease(p > 0.05).5. The degree of liver fibrosis, hepatic cell degeneration and hepatic sinusoiddilated had no correlation with the type of vessel lesion(p > 0.05).6. The degree of liver fibrosis had no correlation with the degree of vessel obstruction > 0.05). But moderate and serious fibrosis group was mainly occlusive type and slight fibrosis group was mainly narrow type. The degree of vessel obstruction in moderate and serious fibrosis group was significantly higher than t...
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