The development of refractory ascites in approximately 10% of patients with decompensated cirrhosis heralds the progression to a more advanced stage of cirrhosis. Its pathogenesis is related to significant hemodynamic changes, initiated by portal hypertension, but ultimately leading to renal hypoperfusion and avid sodium retention. Inflammation can also contribute to the pathogenesis of refractory ascites by causing portal microthrombi, perpetuating the portal hypertension. Many complications accompany the development of refractory ascites, but renal dysfunction is most common. Management starts with continuation of sodium restriction, which needs frequent reviews for adherence; and regular large volume paracentesis of 5 L or more with albumin infusions to prevent the development of paracentesisinduced circulatory dysfunction. Albumin infusions independent of paracentesis may have a role in the management of these patients. The insertion of a covered, smaller diameter, transjugular intrahepatic porto-systemic stent shunt (TIPS) in the appropriate patients with reasonable liver reserve can bring about improvement in quality of life and improved survival after ascites clearance. Devices such as an automated low-flow ascites pump may be available in the future for ascites treatment. Patients with refractory ascites should be referred for liver transplant, as their prognosis is poor. In patients with refractory ascites and concomitant chronic kidney disease of more than stage 3b, assessment should be referred for dual liver-kidney transplants. In patients with very advanced cirrhosis not suitable for any definitive treatment for ascites control, palliative care should be involved to improve the quality of life of these patients.
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Background/Aims In recent years, greater assessment accuracy after transjugular intrahepatic portosystemic shunt (TIPS) to ascertain prognosis has become important in decompensated cirrhosis due to portal hypertension. The aim of this study was to assess the ratio of the portal pressure gradient (PPG) pre-TIPS (pre-PPG) to albumin (PPA), which influence ascites formation in cirrhotic patients in the 6-months after TIPS placement, and is a metric introduced in our study.
Methods This was a retrospective cohort study of 58 patients with decompensated cirrhosis admitted to an academic hospital for the purpose of TIPS placement. We collected the following data: demographics, laboratory measures, and PPG during the TIPS procedure. Then we analyzed the association between the above data and ascites formation postTIPS in cirrhosis patients.
Results Twenty-two patients with ascites and 28 without ascites were evaluated. Univariate and binary logistic regression analysis were adjusted for the following variables: to determine prognosis; Child-Pugh scores, lymphocyte count, platelet count, hemoglobin level, albumin level and pre-PPG or PPA. The outcome showed that PPA was better than pre-PPG and albumin for predicting ascites according to area under receiver operating characteristic curves and a statistical model that also showed PPA’s influence 6-months post-TIPS.
Conclusions The combined measurement of pre-PPG and albumin, defined as PPA, may provide a better way to predict post-TIPS ascites in decompensated cirrhosis, which underlines the need for a large clinical trial in the future.
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