Topic Highlight
Copyright ©2007 Baishideng Publishing Group Co.
World J Gastroenterol. Apr 7, 2007; 13(13): 1912-1927
Published online Apr 7, 2007. doi: 10.3748/wjg.v13.i13.1912
Table 1 Definition, etiology and histology of VOD, BCS, and CH
VODBCSCH
Site of venous obstructionHepatic sinusoids and terminal venulesFrom hepatic veins to the superior end of IVCHeart
EtiologySinusoidal endothelial injury due to HSCT, chemotherapy, abdominal radiotherapy, and pyrrolizidine alkaloidsHepatic vein thrombosis, IVC webs, compression of hepatic veins or IVC by tumor, cyst, or abscessIncreased right atrial pressure due to CHF (CAD, cardiomyopathies, valve abnormalities), cor pulmonale (COPD, ILD, pulmonary HTN), and pericardial disease (constrictive pericarditis, pericardial tamponade)
HistologyChanges predominantly in perivenular areasPredominantly in perivenular areas except in presence of concomitant PVT.Predominantly in perivenular areas Sinusoidal congestion and hepatocellular necrosis
Gaps in SEC barrier leading to subendothelial edemaSinusoidal congestion followed by ischemic cell necrosis and bridging fibrosis between central veinsBridging fibrosis between central veins leading to cardiac fibrosis in chronic cases
Narrowing of central veins and sinusoids with sinusoidal congestion and hepatocellular necrosisCaudate lobe hypertrophy, with fibrosis and atrophy in the rest of liver
Collagen accumulation in sinusoids and veins leading to bridging fibrosis between central veins