Loss Of Portal Perfusion Research Articles

Relationship between pre-TIPS liver perfusion by the portal vein and the incidence of post-TIPS chronic hepatic encephalopathy

OBJECTIVE: In the present study we evaluated the predictive value of pretransjugular intrahepatic portosystemic shunt (TIPS) portal perfusion as assessed by Doppler ultrasonography for the onset of chronic encephalopathy after TIPS. METHODS: A total of 231 cirrhotic patients were followed-up prospectively after TIPS placement. The pattern of intrahepatic portal flow was assessed before TIPS. Patients were divided into two groups according to Doppler findings. Group 1 comprised patients with prograde portal flow (n = 200), whereas group 2 comprised those with loss of portal perfusion (hepatofugal or back-and-forth flow or portal vein thrombosis; n = 31). The presence of chronic encephalopathy during a median follow-up of 32 months was prospectively recorded. The prognostic value of the following parameters for the onset of chronic recurrent encephalopathy after TIPS was evaluated: age, presence of encephalopathy before TIPS, alcoholism, Pugh score, and loss of portal perfusion before TIPS. The independent prognostic value of each variable was tested with a multiple logistic regression analysis. RESULTS: The two groups were comparable in terms of age, incidence of prior episodes of hepatic encephalopathy, and portacaval gradient before and after the procedure; however, liver failure was more severe in patients in group 2 (Pugh score: 9.2 ± 1.9 vs 10.3 ± 1.7). The 3-yr survival was identical for both groups; 25% of the 200 patients in group 1 developed chronic encephalopathy as compared to 6% of the 31 patients in group 2 ( p = 0.03). Multiple logistic regression analysis demonstrated that loss of portal perfusion and age >65 yr were the only independent predictors of the onset of post-TIPS chronic encephalopathy (odds ratios 0.24 and 1.98, respectively). CONCLUSIONS: Cirrhotic patients with loss of portal perfusion before TIPS were protected against post-TIPS chronic hepatic encephalopathy despite a more severe liver dysfunction at baseline. The only other independent predictive factor for the onset of this complication was age.

Relationship Between Pre-Tips Liver Perfusion by The Portal Vein and The Incidence of Post-Tips Chronic Hepatic Encephalopathy

In the present study we evaluated the predictive value of pretransjugular intrahepatic portosystemic shunt (TIPS) portal perfusion as assessed by Doppler ultrasonography for the onset of chronic encephalopathy after TIPS. A total of 231 cirrhotic patients were followed-up prospectively after TIPS placement. The pattern of intrahepatic portal flow was assessed before TIPS. Patients were divided into two groups according to Doppler findings. Group 1 comprised patients with prograde portal flow (n = 200), whereas group 2 comprised those with loss of portal perfusion (hepatofugal or back-and-forth flow or portal vein thrombosis; n = 31). The presence of chronic encephalopathy during a median follow-up of 32 months was prospectively recorded. The prognostic value of the following parameters for the onset of chronic recurrent encephalopathy after TIPS was evaluated: age, presence of encephalopathy before TIPS, alcoholism, Pugh score, and loss of portal perfusion before TIPS. The independent prognostic value of each variable was tested with a multiple logistic regression analysis. The two groups were comparable in terms of age, incidence of prior episodes of hepatic encephalopathy, and portacaval gradient before and after the procedure; however, liver failure was more severe in patients in group 2 (Pugh score: 9.2 +/- 1.9 vs 10.3 +/- 1.7). The 3-yr survival was identical for both groups; 25% of the 200 patients in group 1 developed chronic encephalopathy as compared to 6% of the 31 patients in group 2 (p = 0.03). Multiple logistic regression analysis demonstrated that loss of portal perfusion and age >65 yr were the only independent predictors of the onset of post-TIPS chronic encephalopathy (odds ratios 0.24 and 1.98, respectively). Cirrhotic patients with loss of portal perfusion before TIPS were protected against post-TIPS chronic hepatic encephalopathy despite a more severe liver dysfunction at baseline. The only other independent predictive factor for the onset of this complication was age.

The effect of propranolol on portal perfusion in patients with alcoholic cirrhosis having distal splenorenal shunt

This study tested the hypothesis that reduction in the hyperdynamic systemic circulation with propranolol in patients with alcoholic cirrhosis and distal splenorenal shunt would lead to improved maintenance of portal perfusion. After standard distal splenorenal shunt, 50-75% of patients with alcoholic cirrhosis lose portal flow in 6-12 months: this is associated with an increased hyperdynamic systemic circulation. Twelve patients with alcoholic cirrhosis with distal splenorenal shunt received propranolol in a dose sufficient to provide beta blockade. Pulse was reduced by 25%, cardiac output reduced by 32% and hepatic venous pressure gradient reduced by 15% (p < 0.05). These significant hemodynamic changes with propranolol did not lead to any improvement in the maintenance of portal perfusion: overall, 66% of patients lost prograde portal flow within 1 year. We conclude that the hyperdynamic systemic circulation is not the primary mediator of loss of portal perfusion in this group of patients. Rather, it appears that differences in either intrahepatic resistance or collateral pathway (portal vein to shunt) resistance must account for the different patterns or maintenance of portal perfusion after distal splenorenal shunt.

The role of continued drinking in loss of portal perfusion after distal splenorenal shunt

Fifty percent of patients with alcoholic cirrhosis who undergo distal splenorenal shunting for variceal bleeding lose portal perfusion within 1 year. Although it was previously considered that this loss of portal flow was irrevocable, the present study shows that with resolution of alcoholic hepatitis, portal perfusion can be restored. A 34-year-old patient with alcoholic liver disease and a distal splenorenal shunt lost portal perfusion 1 year after the operation. He had continued to drink alcohol and had high sinusoidal pressure. Following forced abstinence over the next 2 years, his sinusoidal pressure fell, liver volume decreased, results of liver biopsy improved, and portal perfusion was restored. Shunt patency was documented, and the same collaterals from the portal vein to the shunt could still be visualized as had been seen when portal flow was absent. Restoration of portal perfusion was attributed to decreased intrahepatic resistance secondary to abstinence from alcohol. A return to drinking in the next 9 months led to alcoholic hepatitis and once again loss of portal perfusion. This study places emphasis on increased intrahepatic resistance rather than the development of portal-to-shunt collaterals as important in the loss of portal flow in such patients.

Early hemodynamic changes following selective distal splenorenal shunt for portal hypertension: Comparison of surgical techniques

Ninety patients with cirrhosis undergoing elective distal splenorenal shunt (DSRS) for variceal bleeding between January, 1977 and September, 1988 comprised the study group. In 63 cases, the original technique of Warren was used and, in 15, the modified Britton procedure was employed. Twelve patients had a DSRS plus splenopancreatic disconnection. Thirty-four had alcoholic cirrhosis and 56 had nonalcoholic cirrhosis. Intraoperative portal pressure remained high after the shunt (29.4 cm H2O) even if its initial value was probably decreased by the loss of the splenic flow. Splenic pressure was reduced to 21 cm H2O. The hepatic artery diameter enlarged even after selective shunt (from 6.5 to 7.1 mm). The persistence of a high portal pressure allowed for the preservation of hepatopedal portal flow in 87% of cases. Disconnection between the high-pressure mesenteric area and the low-pressure splenic area seemed to be ideal in only 17% of cases. Fifty-five percent of cases had the early development of minimal or moderate portomesenteric gastrosplenic (PM-GS) collateral pathways. In 33%, the PM-GS collaterals were generally abundant and often allowed visualization of the splenic and caval veins during the venous phase of the superior mesenteric arteriograms. In this group, portal flow was generally highly reduced and even abolished. The incidence of portal thrombosis was 11%. Early angiographic checks after DSRS did not show a different hemodynamic behavior between alcoholics and nonalcoholics. Splenopancreatic disconnection seems to prevent the development of collaterals and the loss of portal perfusion after shunt surgery.

Duplex sonography accurately assesses portacaval shunt patency.

Among 42 patients who had undergone portacaval shunt (PCS) to treat bleeding esophageal varices, shunt patency was assessed with duplex sonography 1 month to 5 years postoperatively. Patency was confirmed in all patients (100%). Correlative angiograms confirming the sonographic findings were obtained in 24 patients. Duplex scanning showed hepatofugal or stagnant flow in the distal portal vein in all 42 patients. Very low rates of liver-failure-related mortality (6%) and morbidity (6% incidence of encephaloparthy) in this series despite loss of portal perfusion of the liver in patients incriminate factors other than magnitude and direction of portal vein flow as the cause of complications occurring after PCS. Duplex sonography offers accurate and relevant clinical and physiologic data about shunt hemodynamics in patients who have undergone PCS.

Portaprival collaterals following distal splenorenal shunt: Incidence, magnitude and associated portal perfusion changes

Collateral venous pathways develop between the high pressure portal vein and low pressure splenic vein following distal splenorenal shunt. This review of angiography in 50 patients with cirrhosis prior to and 1 year after DSRS shows that 98% developed collaterals: 72% transpancreatic, 48% transgastric, and 46% colonic. Multiple pathways developed in 64% of patients. Grading of the size of these collaterals showed that in 74% these exceeded the size of the portal and/or superior mesenteric vein. The effect of these collaterals on portal perfusion showed that 32% lost perfusion at 1 year, but significantly (P less than 0.05) more alcoholics (48%) lost perfusion than nonalcoholics (16%). The size, site and number of collaterals was not different between etiologies. Late follow-up in a subset of 32 of the patients showed no change in the site, and minimal increase in size of the collaterals at 3-11 years, with no further loss of portal perfusion. We conclude that virtually all patients develop collaterals after DSRS, these are along predictable pathways and are of significant size in the majority. However, development of collaterals per se does not equate to loss of portal venous flow, and a stable pattern is set in the first year after shunt. Characterization of these pathways will permit new approaches to minimizing their development.