Abstract. Portal vein hypertension generally occurs in liver diseases like hepatic cirrhosis. It causes hemodynamic changes that are closely related to liver disease. At advanced stages of hepatic cirrhosis, portal vein hypertension leads to the atrophy of the right lobe of the liver and the hypertrophy of the left lobe through a process that has not yet been fully explained. Based on the hemodynamic changes that are known to occur, we hypothesize that liver volume is related to the distribution of blood flowing from the splenic vein (SV) that carries hepatotrophic factors from the spleen and pancreas. We studied blood flow in the portal vein system to validate this hypothesis through in vitro experimentation and a computational fluid dynamics (CFD) analysis involving both simplified and patient-specific models based on four healthy subjects and two patients with liver cirrhosis. The results confirmed the hypothesis that right-lobe atrophy is significantly influenced by the distribution of blood from the SV. Moreover, the patients with liver cirrhosis had a significantly larger mass fraction of spleen-derived blood in the left portal vein branch (LPV) than healthy subjects, a result consistent with right-lobe atrophy and left-lobe hypertrophy.

Portal vein thrombosis (PVT) is an important complication that is associated with cirrhotic portal hypertension. The etiology is as yet unclear but could be closely related to the hemodynamics of the portal vein system. This paper investigated the hemodynamics in the portal vein model, both with and without thrombosis, as well as the effect of obstructions on the hemodynamics of the portal vein system using the computational fluid dynamics (CFD) method. PVT can probably develop in the inlets of the portal vein as well as the left/right branches of the portal vein because the distribution of wall shear stress satisfies the conditions for PVT formation based upon the simulation of the hemodynamics in the normal portal vein model. According to the above results, geometric models for a portal vein with a thrombus were constructed and the influence of different degrees (26%, 39%, 53% and 64%) of obstructions was studied. In the model with the maximum obstruction (64% blocked), the maximum velocity of portal vein (PV) increased up to twice than in the model without thrombosis, and the maximum wall shear stress of PV in the model with thrombosis (64% blocked) increased up to 9.4 Pa, whereas it was only 1.9 Pa in the model without thrombosis (nearly one fifth of the maximum wall shear stress). Excessive wall shear stress may cause mechanical damage to the blood vessels and induce physiological changes.

MRI was clinically significant in preoperative staging and resectability assessment of pancreatic carcinoma.