Published online May 28, 2006. doi: 10.3748/wjg.v12.i20.3265
Revised: November 25, 2005
Accepted: December 7, 2005
Published online: May 28, 2006
In this article, we have reviewed the hepatic perfusion disorder (HPD), etiopathogenesis of HPD and corresponding diseases. Review of the literature was based on computer searches (PubMed, Index Medicus) and personal experiences. We considered HPD reflects perfusion differences due to redistribution of arterial blood flow among segments, subsegments and lobes of the liver. The plain CT scan findings of HPD manifests as triangular or wedge-shaped areas of low attenuation. On contrast-enhanced CT scan, HPD manifests multiple (or single) transient wedge-shaped, rotundloid or irregular appearance, homogeneous hyperattenuation (in less cases, hypoattenuation) during the hepatic arterial phase (HAP) and isoattenuated or slightly hyperattenuated areas during the portal arterial phase. Dynamic enhanced magnetic resonance (MR) features are similar to enhanced CT scan. Angiographic findings include non-opacification of portal vein on portograms or wedge-shaped segmental staining in arterial and parenchymal phases on hepatic angiograms. The causes of HPD are arterioportal shunts (APS), intrahepatic vascular compressions and portal vein occlusion, steal phenomenon by hypervascular tumors, vascular variations and any other unknown reasons. It is very important for radiologists to be familiar with the various appearances of HPD to avoid false-positive diagnosis of pseudolesions and not to overestimate the extent of the disease.