Computational fluid dynamics simulation of time-resolved blood flow in Budd-Chiari syndrome with inferior vena cava stenosis and its implication for postoperative efficacy assessment.

BACKGROUND: This study aimed to adopt computational fluid dynamics to simulate the blood flow dynamics in inferior vena cava stenosis based on time-dependent patient-specific models of Budd-Chiari syndrome as well as a normal model. It could offer valuable references for a retrospective insight into the underlying mechanisms of Budd-Chiari syndrome pathogenesis as well as more accurate evaluation of postoperative efficacy. METHODS: Three-dimensional inferior vena cava models of Budd-Chiari syndrome patient-specific (preoperative and postoperative) and normal morphology model were reconstructed as per magnetic resonance images using Simpleware. Moreover, computational fluid dynamics of time-resolved inferior vena cava blood flow were simulated using actual patient-specific measurements to reflect time-dependent flow rates. FINDINGS: The assessment of the preoperative model revealed the dramatic variations of hemodynamic parameters of the stenotic inferior vena cava. Moreover, the comparison of the preoperative and postoperative models with the normal model as benchmark showed that postoperative hemodynamic parameters were markedly ameliorated via stenting, with the attenuation of overall velocity and wall shear stress, and the increase of pressure. However, the comparative analysis of the patient-specific simulations revealed that some postoperative hemodynamic profiles still bore some resemblance to the preoperative ones, indicating potential risks of restenosis. INTERPRETATION: Computational fluid dynamics simulation of time-resolved blood flow could reveal the tight correlation between the hemodynamic characteristics and the pathological mechanisms of inferior vena cava stenosis. Furthermore, such time-resolved hemodynamic profiles could provide a quantitative approach to diagnosis, operative regimen and postoperative evaluation of Budd-Chiari syndrome with inferior vena cava stenosis.

Liver and Spleen Stiffness Measurements for Assessment of Portal Hypertension Severity in Patients with Budd Chiari Syndrome.

Aims: Budd-Chiari Syndrome (BCS) is a rare vascular disease of the liver caused by the obstruction of the hepatic venous outflow located from the small hepatic venules up to the entrance of the inferior vena cava (IVC) into the right atrium. Current prognostic indexes are suboptimal for an individual prognostic assessment and subsequent management of patients with BCS. Liver (LSM) and spleen (SSM) stiffness measurements are widely validated prognostic tools in hepatology, but the evidence in patients with BCS is limited. This paper describes LSM and SSM in patients with BCS and their correlation with clinical, biochemical, and ultrasound findings from the same patients. Methods: We investigated a case series of seven patients with BCS diagnosis and available LSM and SSM evaluated by transient elastography (TE). Biochemical, imaging, and endoscopic findings nearest to the TE evaluation were recorded. Clinical outcomes and BCS evolution were described for each patient. When available, repeated TE assessments were also recorded. Results: Patients with acute nonfulminant manifestation of BCS presented near-the-upper-limit values (75 kPa) of LSM and SSM, which often persist until the placement of a transjugular intrahepatic portosystemic shunt (TIPS). On the other hand, TE values were markedly lower in patients with compensated BCS. In some patients with repeated TE measurement years after TIPS placement, LSM had decreased to values of <10 kPa years. SSM changes in these patients were, however, less evident. Conclusions: Extremely elevated values of LSM and SSM are suggestive of BCS. The evaluation of both LSM and SSM by TE could help clinicians in the initial evaluation, risk stratification, and therapy response monitoring of patients with BCS.

Real-time shear wave elastography (SWE) assessment of short- and long-term treatment outcome in Budd-Chiari syndrome: A pilot study.

PURPOSE: The first aim of this study was to analyze the relationships between liver stiffness measurement, hepatic venous pressure and liver fibrosis. The second aim was to demonstrate the utility of real-time shear wave elastography for evaluation of Budd-Chiari syndrome patients before and after balloon hepatic venous angioplasty. MATERIALS AND METHODS: A total of 32 patients with Budd-Chiari syndrome slated for successful balloon angioplasty met the inclusion and exclusion criteria. Shear wave elastography was used to generate dynamic liver stiffness measurement 2 days before angioplasty and 2 days, 3 months, and 6 months after angioplasty. Hepatic venous pressures were measured during balloon angioplasty. Correlations among liver stiffness, hepatic venous pressure, and fibrosis were assessed. RESULT: Mean liver stiffness was 35.17 ± 10.60 kPa, 20.15 ± 5.47 kPa, 15.36 ± 4.34 kPa and 15.68 ± 5.58 kPa at baseline and 2 days, 3 months, and 6 months after angioplasty, respectively. Liver stiffness measured at 2 days and 3 months after angioplasty was significantly decreased (P < 0.001); liver stiffness measured at 6 months after angioplasty was not significantly different from that measured at 3 months after angioplasty (P = 0.636). Analysis of liver stiffness measurement and hepatic venous pressure before balloon angioplasty yielded a coefficient of correlation r = 0.701 (P < 0.001). Before and 2d after angioplasty, liver stiffness measurement did not correlated with fibrosis (r = - 0.170, P = 0.22), (r = 0.223, P = 0.220), respectively, while the LSM difference before and 2 days after angioplasty negatively correlated with stiffness severity (r = - 0.502, P = 0.003). Liver stiffness measured at 2 days and 3 months after angioplasty was significantly decreased (P < 0.001), remaining stable at 3 months, though still in the cirrhotic range. CONCLUSIONS: The liver stiffness of Budd-Chiari syndrome patients, measured by shear wave elastography, decreased considerably after hepatic venous recanalization, and significantly correlated with hepatic venous pressure though not with degree of fibrosis. Shear wave elastography may be effective in monitoring short- and long-term treatment outcomes in Budd-Chiari syndrome.

Early sonographic assessment of Budd-Chiari syndrome after orthotopic liver transplantation.

Budd-Chiari syndrome is a rare vascular complication of liver transplantation that may result in loss of the graft and a high mortality risk. Therefore, early diagnosis is extremely important to allow preservation of the graft and improve the prognosis. We describe the sonographic findings in a patient in whom Budd-Chiari syndrome occurred 2 days after orthotopic liver transplantation.

[Assessment of hemodynamics in patients with Budd-Chiari syndrome after interventional treatment].

OBJECTIVE: To study the changes in morphology of liver and spleen and hemodynamics of the patients with Budd-Chiari syndrome (BCS) after interventional treatment. METHODS: The dimensions of liver and spleen were detected by routine ultrasonography in 30 normal control subjects and 256 BCS patients before and after inventional therapy. Color duplex sonography was employed to measure the hemodynamic changes. RESULTS: Compared with the control group, BCS patients before interventional therapy showed obvious liver and spleen enlargements (P<0.005), specially the caudate lobe of the liver (P<0.001), which were significantly reduced 7 days after interventional treatment (P<0.005), but the spleen was still larger than that of the control group (P<0.005) even till 6 months after the therapy. Color Doppler flow imaging (CDFI) revealed local high-speed blood flow in patients with stenosis of the inferior vena cave (IVC), but color flow was not detected in patients with IVC obstruction, who had hepatic vein dilation (P<0.005) with slowed blood flow and collateral formation of in the liver, as well as decreased velocity of blood flow in the portal vein. After interventional treatment, the diameter of the involved IVC increased with blood flow restoration and the size and shape of the stent were detected clearly. The velocity of blood flow was increased in both the hepatic and portal veins (P<0.005). CONCLUSION: Interventional therapy can relieve obstruction of blood flow in the liver and improve the hemodynamics of patients with BCS.

Direct transhepatic assessment of hepatic vein pressure and direction of flow using a thin needle in patients with cirrhosis and Budd-Chiari syndrome. An effective alternative to hepatic vein catheterization.

Portal pressure can be accurately measured transhepatically with a Chiba needle. Since 1980, we have used transhepatic hepatic vein pressures as our zero reference for transhepatic portal pressure measurements. To validate the latter technique, we performed hepatic vein catheterization and transhepatic hepatic vein puncture in 11 patients undergoing portal pressure measurement. Transhepatic hepatic vein puncture was simple, providing pressures as reproducible as those obtained by hepatic vein and inferior vena cava catheterization. These pressures were minimally higher than simultaneous free hepatic vein and inferior vena caval pressures, possibly reflecting the more proximal location of the small hepatic vein radicles often entered by this technique. Transhepatic hepatic vein puncture is an accurate way to determine hepatic vein pressure and, combined with transhepatic portal vein pressure measurement, completely obviates the need for venous catheterization for portal pressure determination. Transhepatic hepatic vein pressure was also measured in 3 patients with Budd-Chiari syndrome. In these patients, transhepatic hepatic vein pressure was elevated and equaled or exceeded portal vein pressure. Abnormal venous collaterals were identified in all patients. Transhepatic portal pressure studies are also an appropriate way to evaluate patients suspected of having hepatic outflow obstruction.