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Clinical decompensation of cirrhosis is associated with poor prognosis. Clinically significant portal hypertension (CSPH), defined by a hepatic venous pressure gradient (HVPG) ≥10 mm Hg, is the strongest predictor of decompensation. This study aimed at assessing whether lowering HVPG with β blockers could decrease the risk of decompensation or death in compensated cirrhosis with CSPH. This study on β blockers to prevent decompensation of cirrhosis with portal hypertension (PREDESCI) was an investigator-initiated, double-blind, randomised controlled trial done in eight hospitals in Spain. We enrolled patients with compensated cirrhosis and CSPH without high-risk varices. All participants had HVPG measurements with assessment of acute HVPG-response to intravenous propranolol. Responders (HVPG-decrease ≥10%) were randomly assigned to propranolol (up to 160 mg twice a day) versus placebo and non-responders to carvedilol (≤25 mg/day) versus placebo. Doses were individually determined during an open-label titration period after which randomisation was done with 1:1 allocation by a centralised web-based system. The primary endpoint was incidence of cirrhosis decompensation (defined as development of ascites, bleeding, or overt encephalopathy) or death. Since death in compensated cirrhosis is usually unrelated to the liver, an intention-to-treat analysis considering deaths unrelated to the liver as competing events was done. This study is registered with ClinicalTrials.gov, number NCT01059396. The trial is now completed. Between Jan 18, 2010, and July 31, 2013, 631 patients were evaluated and 201 were randomly assigned. 101 patients received placebo and 100 received active treatment (67 propranolol and 33 carvedilol). The primary endpoint occurred in 16 (16%) of 100 patients in the β blockers group versus 27 (27%) of 101 in the placebo group (hazard ratio [HR] 0·51, 95% CI 0·26–0·97, p=0·041). The difference was due to a reduced incidence of ascites (HR 0·42, 95% CI 0·19–0·92, p=0·03). The overall incidence of adverse events was similar in both groups. Six patients (four in the β blockers group) had severe adverse events. Long-term treatment with β blockers could increase decompensation-free survival in patients with compensated cirrhosis and CSPH, mainly by reducing the incidence of ascites. Spanish Ministries of Health and Economy.

Background Transjugular intrahepatic portosystemic shunt (TIPS) has recently been reported to be effective in the treatment of cirrhotic patients with refractory ascites. However, the clinical utility of TIPS in the subset of refractory ascitic patients with good hepatic and renal function is uncertain. The aim of this study was to compare the efficacy of TIPS to that of large-volume paracentesis in cirrhotic patients with refractory ascites who have good hepatic and renal function. Methods Sixty cirrhotic patients with refractory ascites who presented with a Child-Pugh score of <11, serum bilirubin of <3 mg/dl and creatinine of <1.9 mg/dl were assigned randomly to TIPS (n = 30) or large-volume paracentesis plus albumin (n = 30). The primary endpoint was survival. The secondary endpoints were response to treatment and development of hepatic encephalopathy. Results The baseline characteristics were similar in the two groups. Seventeen patients treated with TIPS and 21 treated with paracentesis died during the study period. The cumulative probabilities of survival at 1 and 2 years were 80 and 64% in the TIPS group and 49 and 35% in the paracentesis group (p < 0.005). TIPS was significantly superior to paracentesis in the control of ascites (p < 0.005). Treatment failure was more frequent in the paracentesis group, whereas the frequency of hepatic encephalopathy was greater in the TIPS group. Conclusions In cirrhotic patients with refractory ascites who have good hepatic and renal function, TIPS improves survival and provides better control of ascites than large-volume paracentesis.

ObjectiveSatavaptan, a vasopressin V2 receptor antagonist, has been shown to improve the control of ascites in cirrhosis in short-term phase II studies. The aim of this study was to evaluate the efficacy and safety of satavaptan in three different populations of patients with cirrhosis and ascites.Methods1200 patients were included in three randomised double-blind studies comparing satavaptan with placebo in uncomplicated ascites (study 1: n=463 patients) and difficult-to-treat ascites, with and without concomitant diuretic treatment (studies 2 and 3: n=497 and n=240 patients, respectively).ResultsSatavaptan was not more effective than placebo in the control of ascites in any of the populations studied as estimated by the primary efficacy endpoints: worsening of ascites (study 1) and the cumulative number of large-volume paracenteses during 12 weeks (studies 2 and 3). Nevertheless, some of the secondary efficacy endpoints related to the treatment of ascites were met in the three studies, suggesting a slight advantage of satavaptan over placebo in delaying ascites formation. Moreover, satavaptan was more effective than placebo in improving the serum sodium concentration in patients with hyponatraemia. The incidence of major complications of cirrhosis during follow-up did not differ significantly between the satavaptan and placebo groups in the three studies. Overall, the rate of any treatment-related adverse events, serious treatment-related events and treatment-related events leading to permanent discontinuation of treatment did not differ significantly between the treatment groups. However, in study 2 mortality was higher in patients treated with satavaptan compared with placebo (HR 1.47; 95% CI 1.01 to 2.15); no significant differences in mortality between the two groups were observed in the other two studies. No specific cause for the increased mortality was identified. Most deaths were associated with known complications of liver cirrhosis.ConclusionSatavaptan, alone or in combination with diuretics, is not clinically beneficial in the long-term management of ascites in cirrhosis.

Background Massive postoperative ascites remains a major threat that can lead to liver failure and other fatal complications, especially in patients with poor liver function. Branched-chain amino acid (BCAA) administration increases biosynthesis and secretion of albumin by hepatocytes and increases oncotic pressure by elevating blood albumin concentration, thereby decreasing peripheral edema, ascites, and pleural effusion. Method We randomly allocated consecutive patients undergoing major liver resection for hepatocellular carcinoma to either a group where oral BCAA administration was initiated 3 weeks before liver resection, or a non-BCAA group. The primary study endpoint was development of postoperative ascites. Results Overall, 39 patients were allocated to the BCAA group, while 38 were assigned to the non-BCAA group. No significant difference in the rate of refractory ascites, considered alone, was evident between the BCAA (5.1 %) and non-BCAA groups (13.2 %; p  = 0.263). However, the occurrence of refractory ascites and/or pleural effusion was significantly less frequent in the BCAA group (5.1 %) than in the non-BCAA group (21.1 %; p  = 0.047). Furthermore, the postoperative serum concentration of reduced-state albumin was greater immediately after liver resection in the BCAA group than in the non-BCAA group. Conclusion Preoperative administration of BCAA did not significantly improve prevention of refractory ascites, but significant effectiveness in preventing ascites, pleural effusion, or both, as well as improving metabolism of albumin, was demonstrated [University Hospital Medical Information Network (UMIN) reference number 000004244].

Two main stages are differentiated in patients with advanced chronic liver disease (ACLD), one compensated (cACLD) with an excellent prognosis, and the other decompensated (dACLD), defined by the appearance of complications (ascites, variceal bleeding and hepatic encephalopathy) and associated with high mortality. Preventing the progression to dACLD might dramatically improve prognosis and reduce the burden of care associated with ACLD. Portal hypertension is a major driver of the transition from cACLD to dACLD, and a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH) as the threshold from which decompensating events may occur. In recent years, innovative studies have provided evidence supporting new strategies to prevent decompensation in cACLD. These studies have yielded major advances, including the development of noninvasive tests (NITs) to identify patients with CSPH with reasonable confidence, the demonstration that aetiological therapies can prevent disease progression and even achieve regression of cirrhosis, and the finding that non-selective β-blockers can effectively prevent decompensation in patients with cACLD and CSPH, mainly by reducing the risk of ascites, the most frequent decompensating event. Here, we review the evidence supporting new strategies to manage cACLD to prevent decompensation and the caveats for their implementation, from patient selection using NITs to ancillary therapies. This Review describes the progression of advanced chronic liver disease (ACLD) from its early stages (compensated ACLD) to more advanced disease (decompensated ACLD). Evidence supporting strategies to manage ACLD and prevent decompensation, as well as the tests used to stratify risk, are discussed. Key points Advanced chronic liver disease (ACLD) describes the liver disease in patients who may already have cirrhosis and is widely used in the era of noninvasive tests (NITs). Two main successive stages are differentiated in ACLD: compensated (cACLD) and, later, decompensated (dACLD), characterized by the presence of complications of portal hypertension and with poor prognosis. In cACLD, a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH), a substage at which varices and decompensation may occur, resulting in significantly higher mortality. Among patients with CSPH, those with varices have higher decompensation risk. Currently, NITs, such as liver stiffness measurements by transient elastography in combination with platelet count, can identify patients with CSPH and predict decompensation risk. Aetiological therapies, ideally commenced in early cACLD, can prevent disease progression and even achieve cirrhosis regression. Non-selective β-blockers (NSBBs) can effectively prevent decompensation and improve survival in patients with cACLD and CSPH. Carvedilol is the preferred NSBB in cACLD because it is more effective than classic NSBBs in decreasing portal pressure, is better tolerated and has been shown to prevent decompensation and improve survival.

We present a case of intraoperative detection of an iatrogenic chyle duct injury during laparoscopic sleeve gastrectomy. The chyle duct injury was identified and managed by ligature, preventing postoperative chylous ascites.

Purpose Recurrent esophageal variceal bleeding and/or refractory ascites in patients with cavernous transformation of the portal vein (CTPV) is associated with a high fatality rate. Transjugular intrahepatic portosystemic shunt (TIPS) provides a treatment option for preventing esophageal variceal rebleeding and/or refractory ascites. This retrospective study evaluated the safety and efficacy of TIPS for the patients involved. Methods The records of 41 consecutive patients with CTPV who underwent TIPS at our institution from January 2015 to May 2019 were reviewed. Among the 41 patients, 36 patients had variceal rebleeding only, and 5 patients exhibited both variceal rebleeding and refractory ascites. Ten of these patients underwent TIPS via a transjugular pathway alone; a combined transjugular/transhepatic pathway and a combined transjugular/transsplenic pathway were adopted for 21 and 3 patients, respectively; and the remaining 7 patients failed TIPS. Results TIPS succeeded in 34 of 41 (82.9%) patients. Four of 34 patients with CTPV were successfully cured with a thick collateral caval stent shunt operation. After TIPS, the mean portosystemic pressure gradient declined from 24.60 ± 6.15 mmHg to 15.89 ± 4.08 mmHg ( P  < 0.01). The occurrence rate of variceal rebleeding in the TIPS success group was lower than that in the TIPS failure group (11.8% vs 42.9%, P  < 0.05). The occurrence rate of recurrent ascites in the TIPS failure group was greater than that in the TIPS success group (75% vs 15.8%, P  < 0.05). TIPS patency was 76.5% (26 of 34 patients). During the follow-up time (median 12.64 months), the rate of hepatic encephalopathy was 5.9%, and the survival rate was 85.3%. Conclusions TIPS is an effective and safe alternative therapy for preventing esophageal variceal rebleeding and/or refractory ascites in patients who exhibit CTPV, and these findings may be beneficial to clinical research.

Background Endomyocardial fibrosis (EMF), the commonest restrictive cardiomyopathy worldwide, is characterized by inflammation and fibrosis of the endocardium. Inflammation in other parts of the body such as the peritoneum has been described and may explain the accumulation of ascites, a painful and disabling feature of this disease. We determined the efficacy and safety of prednisolone to prevent re-accumulation of ascites among EMF patients attending Mulago hospital cardiology service. Methods This was a pilot randomised placebo controlled trial with a 1:1 parallel design. Over a period of 10 months, participants were recruited and randomized to receive 1 mg/kg per day of prednisolone or placebo and were followed for a maximum of 8 weeks. The primary outcome was re-accumulation of ascites from baseline (grade 2) to grade 3. Safety was assessed by self-reported side effects, physical exam, and laboratory assessment. Results Sixteen study participants were randomised to prednisolone, while nineteen were randomised to placebo. Six were lost to follow up (1-prednisolone arm, 5-placebo). Baseline characteristics were similar between groups. Prednisolone was safely administered in this setting. There was no statistically significant difference in the overall risk of developing grade 3 ascites over 8 weeks. RR (95 % confidence interval) 0.70 (0.43–1.11), P value 0.12. The rate of the primary outcome per 1000 person days of follow-up was also similar in both arms P value 0.63. Conclusion Short term prednisolone use was generally safe and did not prevent reaccumulation of ascites in this study population. Trial registration number: ISRCTN63999319, 28/03/2013

Despite thorough selection during the last decade, the incidence of ascites is still high in modern broiler strains. Although ascites occurs mostly at the end of the rearing period, there are indications that the etiology of this problem may have started during embryonic development. Recent studies have shown that the post-hatch performance of the broiler chick might be influenced by changing the environmental conditions in the incubator during embryonic development. This study investigated the effect of increasing incubator CO₂ concentration up to 0.7%, by nonventilation during the first 10 d of incubation, on the embryonic development of 2 commercial broiler strains (Cobb and SAS) differing in their susceptibility for ascites syndrome. The Cobb strain is suspected to be less susceptible than the SAS strain. Overall, the chick embryos of the Cobb strain had a faster development than those of the SAS strain as expressed by their higher BW from embryonic day (ED)10 until ED18. Nonventilation stimulated embryonic development resulting in higher embryonic BW, early hatch, and narrower spread of hatch in both strains. In the SAS strain, nonventilation improved hatchability by more than 10%. Gas composition of the air cell in the egg of the nonventilation groups (both Cobb and SAS) had higher partial pressure of CO₂ and lower partial pressure of O₂ from ED11 until ED14 compared with the ventilation groups. During the entire incubation period, partial pressure of CO₂ was higher in eggs of the Cobb strain compared with the SAS strain. Plasma triiodothyronine, thyroxine, and corticosterone levels were different at the end of the incubation period and during hatching due to nonventilation at the beginning of incubation. It is concluded that nonventilation during the first 10 d of incubation had a stimulatory effect on embryonic development of the 2 broiler strains with no effect of heart weights but with effects on hormone levels, air cell pressures, and hatching parameters.

Background Statin has been more and more widely used in chronic liver disease, however, existed studies have attained contradictory results. According to the present study, we aimed to test the efficacy and safety of statin via a meta-analysis. Methods Different databases were searched for full-text publication based on inclusion and exclusion criteria. For data-pooling, fixed-effect model was applied if heterogeneity wasn’t detected. Otherwise, random-effect model was adopted. Heterogeneity was detected by I squire ( I 2 ) test. All results of analysis were illustrated as forest plots. Publication bias was assessed using the Begg’s adjusted rank correlation test. Standard mean difference (SMD) was calculated in continuous variables. Pooled hazard ratio or odds ratio was calculated in catergorical variables. Results Seventeen clinical studies were finally included. Hepatic portal hemodynamic parameters were improved in statin users for a short-term response. For a long-term follow-up, statin treatment surprisingly decreased mortality rate (HR = 0.782, 95% CI: 0.718–0.846, I 2  > 50%) and lower the occurrence of hepatocellular carcinoma (HR = 0.75, 95% CI: 0.64–0.86, I 2  > 50%) in liver cirrhosis. Statin seemed not to decrease the risk of esophageal variceal bleeding and spontaneous bacterial peritonitis. However, statin was proved to decrease the risk of hepatic encephalopathy and ascites. Incidence of drug related adverse events didn’t increase in statin users. Dose-dependent effects of statin on hepatocellular carcinoma development, decompensated cirrhosis events occurrence, and liver cirrhosis progression. Conclusion Statin influenced parameters of hepatic portal vessel pressure in short-term treatment. Prognosis of liver cirrhosis benefited from statin treatment in long term follow-up. The efficacy and safety of statin in liver cirrhosis treatment is confirmed. To date, similar study is hardly seen before.