Cirrhotic livers may contain various types of enhancing lesions and pseudolesions. In clinical practice with cirrhotic patients, however, we have sometimes encountered small nodular early enhancing hepatic lesions on arterial phase contrast-enhanced dynamic CT or MRI that resembled hepatocellular carcinomas but disappeared or decreased in size during the clinical follow-up examinations. These lesions are considered to be nonneoplastic hypervascular pseudolesions caused by small arterioportal or other shunts including unknown causes and are often difficult to differentiate from hypervascular hepatocellular carcinomas (HCCs). Some reports indicate that single-level dynamic CT during hepatic arteriography and less invasive contrast-enhanced dynamic MRI with higher temporal resolution from early to late arterial phase may be helpful for differentiating the early enhancing lesions from HCC.

According to some authors, arterioportal (AP) shunt is commonly associated with hepatocellular carcinoma and intrahepatic cholangiocarcinomas. However, congenital or acquired AP shunt without any associated hepatic tumor may occur and cause difficulty in diagnosis on ultrasound and computed tomography (CT). Particularly, on CT images the enhancing area of the liver may mimic a lesion. State-of-the-art MR imaging of the liver combines the information concerning the vascularity and soft tissue characteristics of the lesions and can make a more confident diagnosis.

Budd-Chiari syndrome (BCS) is a rare and potentially lethal condition related to the obstruction of the hepatic venous outflow tract. Women of about 35 years are the most affected group. Heart failure and sinusoidal obstruction syndrome (formerly known as venoocclusive disease) also impair hepatic venous outflow and share many features with BCS, but these are separate entities as causes and treatments differ. Thrombosis is the cause of primary BCS. As compared with pure hepatic vein thrombosis, IVC thrombosis is more common in the Far East; it is more indolent and is complicated more commonly by hepatocellular carcinoma. Thus, the recently proposed distinction of primary hepatic vein thrombosis (true BCS) from primary IVC thrombosis (obliterative hepatocavopathy) is well suited for clinical and therapeutic objectives. However, etiologies are similar. In most studies, primary myeloproliferative disorders are found to be the leading cause of BCS. The blood outflow obstruction of the liver may result in liver congestion, portal hypertension, ischemic necrosis caused by sudden interruption of hepatic perfusion followed by fibrosis and liver failure, and ascites. Imaging evaluation of patients with suspected BCS may be critical, since the clinical presentation of this potentially fatal disease is often nonspecific. The overall accuracy of US and CT for detecting hepatic venous thrombosis has been reported as approximately 70 and 50 %, respectively.