Transjugular Intrahepatic Portosystemic Shunts With Covered Stents Increase Transplant-Free Survival of Patients With Cirrhosis and Recurrent Ascites

Bureau, Christophe; Thabut, Dominique; Oberti, Frédéric; Dharancy, Sébastien; Carbonell, Nicolas; Bouvier, Antoine; Mathurin, Philippe; Otal, Philippe; Cabarrou, P; Péron, Jean Marie; Vinel, Jean Pierre

doi:10.1053/j.gastro.2016.09.016

Cited by 361 publications

(367 citation statements)

References 25 publications

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“…In addition, increased mortality is often caused by infection, including SBP, pneumonia, urine infection or bloodstream infection, and any insult can quickly lead to acute renal dysfunction. There is growing evidence to consider TIPS to help treat select patients with ascites, regardless of transplant candidacy, as TIPS has been shown to be beneficial to decrease ascites volume, thus reducing the need for LVPs, decreasing the risk of SBP, and there is evidence for improved nutritional status and possible survival benefit [16,17,26]. In addition, patients who present with medically refractory hepatic hydrothorax should be considered for TIPS candidacy.…”

Section: Ascitesmentioning

confidence: 99%

“…Researchers felt the lack of survival benefit may have been related to the use of uncovered stents. Therefore, a more recent cohort of patients using only polytetrafluoroethylene-covered stents revealed that TIPS was a significantly more effective treatment option in appropriately selected patients, including improved transplant-free survival as well as ascites control without major detriment from hepatic encephalopathy [26]. In addition, the discontinuation of beta blockers for this patient population remains controversial and we would recommend that decisions to be performed on a case-by-case basis at this time [16].…”

Section: Refractory Ascitesmentioning

confidence: 99%

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Ascites, refractory ascites and hyponatremia in cirrhosis

Fortune

Cárdenas

2017

Gastroenterology Report

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Ascites is the most common complication related to cirrhosis and is associated with increased morbidity and mortality. Ascites is a consequence of the loss of compensatory mechanisms to maintain the overall effective arterial blood volume due to worsening splanchnic arterial vasodilation as a result of clinically significant portal hypertension. In order to maintain effective arterial blood volume, vasoconstrictor and antinatriuretic pathways are activated, which increase overall sodium and fluid retention. As a result of progressive splanchnic arterial vasodilation, intestinal capillary pressure increases and results in the formation of protein-poor fluid within the abdominal cavity due to increased capillary permeability from the hepatic sinusoidal hypertension. In some patients, the fluid can translocate across diaphragmatic fenestrations into the pleural space, leading to hepatic hydrothorax. In addition, infectious complications such as spontaneous bacterial peritonitis can occur. Eventually, as the liver disease progresses related to higher portal pressures, loss of a compensatory cardiac output and further splanchnic vasodilation, kidney function becomes compromised from worsening renal vasoconstriction as well as the development of impaired solute-free water excretion and severe sodium retention. These mechanisms then translate into significant clinical complications, such as refractory ascites, hepatorenal syndrome and hyponatremia, and all are linked to increased short-term mortality. Currently, liver transplantation is the only curative option for this spectrum of clinical manifestations but ongoing research has led to further insight on alternative approaches. This review will further explore the current understanding on the pathophysiology and management of ascites as well as expand on two advanced clinical consequences of advanced liver disease, refractory ascites and hyponatremia.

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Section: Ascitesmentioning

confidence: 99%

Section: Refractory Ascitesmentioning

confidence: 99%

Ascites, refractory ascites and hyponatremia in cirrhosis

Fortune

Cárdenas

2017

Gastroenterology Report

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“…In selected patients, TIPS decompresses the portal venous system, successfully treats ascites and variceal bleeding, and improves survival 14, 15, 16, 17. However, AD of liver cirrhosis can progress and develop into acute‐on‐chronic liver failure (ACLF) with poor survival 18.…”

Section: Introductionmentioning

confidence: 99%

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Praktiknjo

Lehmann

Nielsen

et al. 2018

Hepatology Communications

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Patients with end‐stage liver disease develop acute decompensation (AD) episodes, which become more frequent and might develop into acute‐on‐chronic liver failure (ACLF). However, it remains unknown how AD induces acceleration of liver disease. We hypothesized that remodeling of collagen type III plays a role in the acceleration of liver cirrhosis after AD and analyzed its formation (Pro‐C3) and degradation (matrix metalloproteinase‐degraded type III collagen [C3M]) markers in animal models and human disease. Bile duct ligation induced different stages of liver fibrosis in rats. Fibrosis development (hydroxyprolin content, sirius red staining, α‐smooth muscle actin immunohistochemistry, messenger RNA of profibrotic cytokines), necroinflammation (aminotransferases levels), fibrolysis (matrix metalloproteinase 2 expression and activity, C1M, C4M), and Pro‐C3 and C3M were analyzed 2, 3, 4, 5, and 6 weeks after bile duct ligation (n = 5 each group). In 110 patients with decompensated liver cirrhosis who underwent a transjugular intrahepatic portosystemic shunt procedure for AD, clinical and laboratory parameters as well as Pro‐C3 and C3M were measured in blood samples from portal and hepatic veins and were collected just before the transjugular intrahepatic portosystemic shunt placement and 1‐3 weeks later. Animal studies showed increased markers of collagen type III deposition with fibrosis, necroinflammation, and decompensation of liver cirrhosis, defined as ascites development. Higher Pro‐C3 levels were associated with injury, disease severity scores (Model for End‐Stage Liver Disease, Child‐Pugh, chronic liver failure‐C AD), ACLF development, and mortality. C3M decreased with AD and the chronic liver failure‐C AD score. Collagen type III deposition ratio increased with the risk of ACLF development and mortality. Conclusion: We show for the first time that AD boosts collagen type III deposition in experimental and human cirrhosis, possibly contributing to the worsened outcome in patients with decompensated cirrhosis. (Hepatology Communications 2018;2:211–222)

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“…The creation of a transjugular intrahepatic portosystemic shunt (TIPS) has been recommended now as a standard for the treatment of portal hypertension (PHT)‐related complications in selected patients . Progress in materials, combined with a suitable selection of patients, has significantly improved the prognosis of patients treated with TIPS . However, despite a careful selection of patients, two main complications limit its use as a first‐line procedure: encephalopathy and cardiac decompensation.…”

mentioning

confidence: 99%

A Prospective Study Identifying Predictive Factors of Cardiac Decompensation After Transjugular Intrahepatic Portosystemic Shunt: The Toulouse Algorithm

et al. 2019

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Background and Aims Transjugular intrahepatic portosystemic shunt (TIPS) is now a standard for the treatment of portal hypertension–related complications. After the TIPS procedure, incidence and risk factors of cardiac decompensation are poorly known. The main objectives were to measure the incidence of the onset of cardiac decompensation after TIPS and identify the predictive factors. Approach and Results All patients with cirrhosis treated with TIPS between May 2011 and June 2016 were considered for inclusion. They received a cardiac assessment by standard biological parameters, transthoracic echocardiography, and right heart catheterization. Patients were followed for 1 year after TIPS insertion. The main endpoint was the incidence of cardiac decompensation requiring hospitalization. One hundred seventy‐four patients were treated by TIPS during the period. One hundred patients who underwent a complete cardiac evaluation were included. A cardiac decompensation occurred in 20% of the patients. The parameters associated with the occurrence of severe cardiac decompensation were a prolonged QT interval corrected (462 vs. 443 ms; P = 0.05), an elevated pre‐TIPS brain natriuretic peptide (BNP) or N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) level, an elevated E/A ratio (1.5 vs. 1.0; P = 0.001) and E/e′ ratio (11 vs. 7; P < 0.001), and a left atrial dilatation (40 vs. 29 mL/m2; P = 0.011). The presence of aortic stenosis was also associated with cardiac decompensation. A level of BNP <40 pg/mL and NT‐proBNP <125 pg/mL allowed identifying patients without risk of cardiac decompensation. Additionally, absence of diastolic dysfunction criteria at echocardiography ruled out the risk of further cardiac decompensation. Conclusions Hospitalization for cardiac decompensation is observed in 20% of patients in the year after TIPS insertion. Combining BNP or NT‐proBNP levels and echocardiographic parameters should help improve patient selection.

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Transjugular Intrahepatic Portosystemic Shunts With Covered Stents Increase Transplant-Free Survival of Patients With Cirrhosis and Recurrent Ascites

Cited by 361 publications

References 25 publications

Ascites, refractory ascites and hyponatremia in cirrhosis

Ascites, refractory ascites and hyponatremia in cirrhosis

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

A Prospective Study Identifying Predictive Factors of Cardiac Decompensation After Transjugular Intrahepatic Portosystemic Shunt: The Toulouse Algorithm

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