Although patients with HVOO generally present with abdominal pain due to hepatomegaly, and jaundice and ascites due to portal hypertension chronic BCS patients may first present with cirrhosis and its complications. The variations in the ‘acuteness’ of venous obstruction leads to subtle differences in the clinical presentations of VOD, BCS, and CH. It should be noted that VOD develops within three weeks of an acute insult to the sinusoidal endothelial cells while BCS and CH may develop within a few days or may take several years of venous thrombosis and heart failure, respectively. The etiology of VOD, BCS, and CH are entirely different (Table (Table1). Site of venous obstruction in veno-occlusive disease, Budd-Chiari syndrome, and congestive hepatopathy. Although the etiology and treatment are completely different in VOD, BCS, and CH the similarities in clinical manifestations and liver histology may suggest a common mechanism of hepatic injury and adaptation in response to increased sinusoidal pressure. However, the clinical presentation depends mostly on the extent and rapidity of the outflow obstruction. Tender hepatomegaly with jaundice and ascites is common to all three conditions. The histological findings in VOD, BCS, and CH are almost identical: sinusoidal congestion and cell necrosis mostly in perivenular areas of hepatic acini which eventually leads to bridging fibrosis between adjacent central veins. This is the first article in which all three syndromes have been reviewed, enabling the reader to compare the characteristics of these disorders. Our goal is to provide a detailed review of veno-occlusive disease (VOD), Budd-Chiari syndrome (BCS), and congestive hepatopathy (CH), all of which results in hepatic venous outflow obstruction.
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