Hepatic venous pressure gradient (HVPG) predicts liver failure after transjugular intrahepatic portal shunt: a retrospective cohort study
Introduction
The development of cirrhosis from the asymptomatic compensatory period to the decompensation of obvious complications requires a long physiological period. Variceal hemorrhage (VH) is the most severe life-threatening complication (1). VH occurs when the variceal wall ruptures due to excessive wall tension. The mortality of variceal bleeding, especially rupture, is very high. According to the American Association for the Study of Liver Diseases (AASLD) guidelines, transjugular intrahepatic portosystemic shunt (TIPS) is only recommended as a salvage treatment option (1,2). TIPS is used in the treatment of complications of portal hypertension in decompensated cirrhotic patients, but there are potential postoperative complications with non-negligible results (3,4). Acute liver failure (ALF) that occurs after reducing portal pressure is often overlooked (5,6). The exact incidence and mortality rates are not well known, but the clinical observation is that the prognosis is very poor once it occurs. Therefore, this study investigated the incidence and predictors of liver failure after TIPS in patients with current variceal hemorrhage.
In the present study, we investigated the frequency of post-TIPS liver failure in the treatment of variceal hemorrhage as an indicator to measure mortality after surgery. We present the following article in accordance with the STROBE reporting checklist (available at https://atm.amegroups.com/article/view/10.21037/atm-22-4737/rc).
Methods
Patient selection
This study was conducted in accordance with the Declaration of Helsinki (as revised in 2013), and was approved by the Ethics Committee of The First Affiliated Hospital of Soochow University (application No. 2021-295). Informed written consent was provided by all patients before their inclusion in this study. We analyzed the data of patients admitted to the First Affiliated Hospital of Soochow University between January 2013 and December 2018 with portal hypertension with an episode of acute gastroesophageal variceal bleeding. A total of 121 patients were referred to the regional liver unit for TIPS. Hepatic venous pressure gradient (HVPG) and clinical data were collected. In addition, case notes were analyzed retrospectively. Patients with incomplete data were excluded, and 93 patients were ultimately enrolled in the study. Primary outcomes were morbidity and hospital mortality within 4 weeks of surgery.
Preoperative and TIPS procedures
Postoperative clinical data before TIPS insertion were recorded, including age, gender, primary disease, alanine aminotransferase (ALT), total bilirubin (TBIL), albumin (ALB), hemoglobin (HGB), platelets (PLT), leukocytes (WBC), venous blood ammonia level, and model for end-stage liver disease (MELD) scores. Intraoperative data included HVPG.
A team of experienced interventional radiologists performed the TIPS procedures. Because of the recognized complication of hepatic encephalopathy (HE), the procedure in our center aimed to decrease HVPG to 12 mmHg or below using stents dilated to 5–10 mm according to the reduction in pressure gradient achieved. Only 2 patients required 10-mm shunts to achieve this pressure, and the remaining patients received 5–9-mm stents.
Criteria for liver failure and recurrent portal hypertension after TIPS
Postoperative liver failure was defined as a rise in bilirubin from <85.5 to >171.0 µmol/L, aspartate aminotransferase (AST) ≥400 U/L, and prothrombin time (PT) activity <40% without improvement. These data were assessed daily starting from the day of surgery until 4 weeks after surgery. Patients with recurrent portal hypertension underwent electronic gastroscopy for definite diagnosis within 24 hours to exclude non-portal hypertensive hemorrhage.
Evaluation of routine postoperative observation and treatment
All patients needed absolute bed rest for 24 hours after the TIPS procedure and were monitored for 72 hours. Subcutaneous injection of low-molecular-weight heparin (5,000 IU, twice a day) was performed from the day after surgery and continued for 5–7 days, after which treatment was switched to an oral intake. Routine postoperative administration of aspartate ornithine and stool maintenance were used to prevent HE.
Statistical analysis
The results are shown in graphical, tabular, and numerical forms. Continuous variables are expressed as mean ± standard deviation () or median and interquartile range (IQR) and compared with the Mann-Whitney U-test. Categorical variables were compared with the χ2 test with the Yates correction or Fisher’s exact tests. Significant variables (P<0.05) in the univariate analysis were used in the multivariate analysis. Multivariate analysis was performed using stepwise logistic regression analysis. All statistical analyses in this study were performed with SPSS 21.0. Statistical significance was defined as P<0.05.
Results
Baseline characteristics of patients
Baseline characteristics of the 93 variceal hemorrhage patients enrolled in this study are shown in Table 1. The patients included 58 males (62.37%) and 35 females (37.63%), and the mean age was 58.43±11.85 years (range, 29–86 years). The main cause was hepatitis B virus (HBV), which was found in 50.54% of patients, followed by schistosomiasis in 18.28%, primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC) in 17.20%, alcoholism in 5.38%, and hepatitis C virus (HCV) in 1 patient. Comorbid illnesses were present in 48 patients (51.90%), including cardiovascular disease (n=27, 29.32%), chronic renal failure (n=5, 5.38%), and chronic respiratory disease (n=16, 17.20%). Biochemical examination showed that WBC was (7.11±3.59)×109/L, median PLT was 88×109/L, hematocrit (HCT) was 0.27±0.07 L/L, TBIL was 1.43±0.77 mg/dL, median AST was 34.10 U/L, ALB was 30.44±7.25 g/L, PT was 16.72±2.68 seconds, median serum creatinine (SCr) was 0.69 mg/dL, and median ammonia was 31.45 µmol/L. MELD score was 15.91±5.30, and HVPG was 23.15±5.15 mmHg.
Table 1
Characteristics | Values |
---|---|
Sex, n (%) | |
Male | 58 (62.37) |
Female | 35 (37.63) |
Age (years), mean ± SD [range] | 58.43±11.85 [29–86] |
Causes, n (%) | |
Hepatitis B virus-induced cirrhosis | 47 (50.54) |
Hepatitis C virus-induced cirrhosis | 1 (1.08) |
Alcoholism | 5 (5.38) |
Schistosomiasis | 17 (18.28) |
PBC + PSC | 16 (17.20) |
Multiple causes* | 3 (3.23) |
Cryptogenic cirrhosis | 2 (2.15) |
Comorbid illness, n (%) | |
Cardiovascular disease | 27 (29.32) |
Chronic renal disease | 5 (5.38) |
Chronic respiratory disease | 16 (17.20) |
Biochemical indicators | |
WBC (×109/L), mean ± SD | 7.11±3.59 |
PLT (×109/L), median [IQR] | 88 [60, 124] |
HCT (L/L), mean ± SD | 0.27±0.07 |
TBIL, mg/dL, mean ± SD | 1.43±0.77 |
AST (U/L), median [IQR] | 34.10 [26.35, 43.00] |
ALB (g/L), mean ± SD | 30.44±7.25 |
PT (sec), mean ± SD | 16.72±2.68 |
SCr (mg/dL), median [IQR] | 0.69 [0.54, 0.86] |
Ammonia (µmol/L), median [IQR] | 31.45 [20.00, 49.25] |
MELD score, mean ± SD | 15.91±5.30 |
HVPG (mmHg), mean ± SD | 23.15±5.15 |
*, some patients had 2 or more causes. PBC, primary biliary cirrhosis; PSC, primary sclerosing cholangitis; SD, standard deviation; WBC, leukocytes; PLT, platelet; IQR, interquartile range; HCT, hematocrit; TBIL, total bilirubin; AST, aspartate aminotransferase; ALB, albumin; PT, prothrombin time; SCr, serum creatinine; IQR, interquartile range; MELD, model for end-stage liver disease; HVPG, hepatic vein pressure gradient.
Postoperative morbidity and mortality
The overall success rate of the operation was 83.87% (78/93), which could achieve effective hemostasis without serious complications. Three patients bled to death before TIPs. Of the 93 patients, 8 patients (8.6%) were still rebleeding within 4 weeks of surgery and chose other treatment methods. Twelve patients (12.90%) died in the hospital after the operation. The primary causes leading to death included liver failure (n=5), rebleeding of portal hypertensive (n=3), progressive HE (n=3), and intra-abdominal hemorrhage (n=1) (Table 2). Postoperative complications of the 9 patients who died in the hospital are shown in Table 3. Complications occurred in 46.24% (43/93) of patients, with only 34.41% (32/93) developing 1 complication. The most common complications were HE (39.78%) and postoperative liver failure, which had an incidence as high as 30.11% and was often a very high mortality complication (17.86%). There was a significant difference in HVPG values between the death and non-death groups (t=−2.843, P=0.016).
Table 2
Characteristics | Morbidity (%) | Mortality (%) |
---|---|---|
HE | 37 (39.78) | 3 (8.11) |
LF | 28 (30.11) | 5 (17.86) |
Rebleeding of portal hypertensive | 8 (8.60) | 3 (37.5) |
Spontaneous peritonitis | 11 (11.83) | 0 (0) |
Respiratory infection | 5 (5.38) | 0 (0) |
Intra-abdominal hemorrhage | 1 (1.08) | 1 (100.0) |
Acute pancreatitis | 1 (1.08) | 0 (0) |
TIPS, transjugular intrahepatic portosystemic shunt; HE, hepatic encephalopathy; LF, liver failure.
Table 3
No. | Sex | Age (years) | Cause | Complication | Comorbid illness | WBC (×109/L) | PLT (×109/L) | HCT (%) | TBIL (mg/dL) | AST (U/L) | ALB (g/L) | PT (sec) | SCr (mg/dL) | Ammonia (μmol/L) | MELD score | HVPG (mmHg) |
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
1 | F | 78 | PBC | LF & rebleeding | Yes | 12.11 | 31 | 0.21 | 1.37 | 77 | 17.9 | 18.3 | 0.54 | 26 | 15 | 29 |
2 | F | 61 | PBC | HE | No | 5.46 | 163 | 0.22 | 0.96 | 32 | 31 | 14.5 | 1.07 | 40 | 9 | 27 |
3 | F | 69 | HBV | HE & AF | Yes | 7.85 | 94 | 0.28 | 1.50 | 28 | 29.3 | 12.7 | 0.95 | 79 | 13 | 27 |
4 | F | 83 | Schistosomiasis | AF | Yes | 11.16 | 33 | 0.37 | 1.43 | 59 | 36.9 | 15.9 | 0.51 | 58 | 12 | 29 |
5 | F | 66 | Schistosomiasis | Rebleeding | Yes | 3.09 | 62 | 0.27 | 1.18 | 25.6 | 32.9 | 15.5 | 0.63 | 49 | 11 | 22 |
6 | M | 48 | HBV | AF | No | 9.20 | 123 | 0.6 | 0.61 | 56 | 34 | 16.1 | 1.81 | 87 | 17 | 21 |
7 | M | 47 | HBV | HE | Yes | 14.52 | 63 | 0.26 | 2.89 | 241 | 21.7 | 18.6 | 0.75 | 16.4 | 20 | 27 |
8 | M | 50 | HBV | AF | Yes | 6.41 | 84 | 0.22 | 0.54 | 32 | 26.7 | 22.1 | 0.29 | 36 | 18 | 34 |
9 | F | 53 | HBV | Rebleeding | Yes | 2.93 | 103 | 0.24 | 0.54 | 23.7 | 31.7 | 15.3 | 1.03 | 40 | 9 | 25 |
TIPS, transjugular intrahepatic portosystemic shunt; F, female; M, male; PBC, primary biliary cirrhosis; HBV, hepatitis B virus; LF, liver failure; HE, hepatic encephalopathy; AF, acute hepatic failure; WBC, white blood count; PLT, platelet; HCT, hematocrit; TBIL, total bilirubin; AST, aspartate aminotransferase; ALB, albumin; PT, prothrombin time; SCr, serum creatinine; MELD, model for end-stage liver disease; HVPG, hepatic vein pressure gradient.
Risk factors for post-TIPS liver failure
Univariate analyses of pre-TIPS variables that potentially influenced the risk of post-TIPS morbidity are shown in Table 4. All risk factors with P<0.1 in the univariate analysis were subjected to stepwise multivariate logistic regression analysis. The results showed that only HVPG was an independent risk factor for post-TIPS morbidity in patients with portal hypertension [relative risk (RR) 1.156; 95% confidence interval (CI): 1.041 to 1.283; P=0.006].
Table 4
Index | β value | SE | χ2 value | P value | RR value |
---|---|---|---|---|---|
Sex | 0.048 | 0.461 | 0.011 | 0.917 | 1.049 |
Age | 0.005 | 0.019 | 0.058 | 0.809 | 1.005 |
Comorbid illness | −0.439 | 0.457 | 0.923 | 0.337 | 0.645 |
WBC | 0.060 | 0.060 | 0.982 | 0.322 | 1.062 |
PLT | −0.014 | 0.007 | 3.463 | 0.063 | 0.986 |
HCT | 0.474 | 3.015 | 0.025 | 0.875 | 1.606 |
TBIL | −0.053 | 0.028 | 3.481 | 0.062 | 0.948 |
AST | 0.005 | 0.008 | 0.049 | 0.484 | 1.005 |
ALB | 0.010 | 0.033 | 0.087 | 0.768 | 1.010 |
PT | 0.152 | 0.121 | 1.561 | 0.212 | 1.164 |
SCr | 0.000 | 0.002 | 0.004 | 0.950 | 1.000 |
Ammonia | 0.007 | 0.007 | 1.024 | 0.312 | 1.007 |
MELD score | 0.021 | 0.080 | 0.069 | 0.793 | 1.021 |
HVPG | 0.145 | 0.053 | 7.408 | 0.006 | 1.156 |
TIPS, transjugular intrahepatic portosystemic shunt; WBC, white blood count; PLT, platelet; HCT, hematocrit; TBIL, total bilirubin; AST, aspartate aminotransferase; ALB, albumin; PT, prothrombin time; SCr, serum creatinine; MELD, model for end-stage liver disease; HVPG, hepatic vein pressure gradient; SE, standard error; RR, relative risk.
Risk factors of hospital mortality
Univariate analysis showed the risk of hospital mortality after TIPS in portal hypertension (Table 5). All risk factors with P<0.1 in the univariate analysis were subjected to stepwise multivariate logistic regression analysis. The result showed that preoperative HVPG (RR 1.133; 95% CI: 1.021 to 0.539; P=0.016) was an independent risk factor of hospital mortality.
Table 5
Index | β value | SE | χ2 value | P value | RR value |
---|---|---|---|---|---|
Sex | −1.281 | 0.743 | 2.973 | 0.085 | 0.278 |
Age | 0.031 | 0.031 | 1.021 | 0.312 | 1.031 |
Comorbid illness | −0.462 | 0.702 | 0.429 | 0.512 | 0.630 |
WBC | 0.076 | 0.092 | 0.692 | 0.406 | 1.079 |
PLT | −0.005 | 0.008 | 0.391 | 0.532 | 0.996 |
HCT | 4.983 | 4.092 | 1.483 | 0.223 | 145.982 |
TBIL | −0.009 | 0.028 | 3.481 | 0.062 | 0.948 |
AST | 0.021 | 0.011 | 3.437 | 0.064 | 1.021 |
ALB | 39.847 | 5.486 | 0.002 | 0.966 | 0.000 |
PT | −1.001 | 0.324 | 9.519 | 0.002 | 0.367 |
SCr | 0.000 | 0.003 | 0.004 | 0.948 | 1.000 |
Ammonia | 0.008 | 0.009 | 0.804 | 0.370 | 1.007 |
MELD score | 0.287 | 0.119 | 5.814 | 0.016 | 1.332 |
HVPG | 0.125 | 0.066 | 3.617 | 0.016 | 1.133 |
TIPS, transjugular intrahepatic portosystemic shunt; WBC, white blood count; PLT, platelet; HCT, hematocrit; TBIL, total bilirubin; AST, aspartate aminotransferase; ALB, albumin; PT, prothrombin time; SCr, serum creatinine; MELD, model for end-stage liver disease; HVPG, hepatic vein pressure gradient; SE, standard error; RR, relative risk.
Discussion
Gastrointestinal hemorrhage is a common and severe complication in the natural history of cirrhosis due to portal hypertension. Liver transplantation is a good choice for patients with end-stage liver disease, especially for patients with esophageal and gastric varices rupture and bleeding. However, due to limited viscera or high surgical costs, liver transplantation cannot be carried out in a wide range in China. HVPG is an invasive measurement of portal hypertension and the most accurate predictor for variceal bleeding (7). When HVPG reaches 12 mmHg, the probability of bleeding increases greatly (1). Portal hypertensive hemorrhage is the deadliest complication of patients with cirrhosis. TIPS is used to treat portal hypertension, and it is an effective therapy for patients with bleeding esophageal varices (8,9). But due to its potential risks (10), it is only recommended as a savage treatment (11-13).
The primary function of TIPS is to create a low-resistance shunt between the intrahepatic portion of the portal vein and the hepatic vein. TIPS procedure works as a bridge therapy. Several reviews have reported a success rate of about 90% in achieving portal decompression in most series (14-16). Our study also showed that the overall surgical success rate was 83.87%. The overall treatment effect was satisfactory, but one or more complications can occur during or after surgery (3,17). However, few studies on post-TIPS liver failure report that patients typically present with marked elevation in liver function test values and severe coagulopathy. Liver failure (LF) after TIPS is rare and frequently ignored, but it is often fatal once it occurs (18). Therefore, preprocedural assessment and patient selection are crucial for minimizing this complication, and it may be beyond saving, the aim of this study was to identify possible study complications.
End-stage liver disease assessment models are diverse, and the MELD score and Child grade are frequently used clinically, in this study we introduced the MELD score as a representative in our baseline analysis. And we found the mean of MELD score was 23.15±5.15. The diagnostic criteria for liver failure differ (19-21), and we defined it as a rise in TBIL from <85.5 to >171.0 µmol/L, AST ≥400 U/L, and PTA <40% without improvement. We retrospectively studied 93 patients who received TIPS in our hospital between January 2013 and December 2018. The results showed that post-TIPS adverse complications mainly included HE (39.78%), LF (30.11%), spontaneous peritonitis (11.83%), and portal hypertensive rebleeding (8.06%). The main causes of death during postoperative hospitalization were rebleeding (33.33%), LF (17.86%), HE (8.11%), and intra-abdominal hemorrhage (100%). The overall morbidity rate in the present study was comparable to that of previous studies (11,22). Further research has shown that rebleeding and LF were the 2 highest all-cause death factors. Masson et al. reported that although HE was relatively common after TIPS insertion, with careful selection of patients, it was usually short-lived and easily managed (22). Still, liver failure after TIPS insertion is a rare but grave complication with a poor prognosis, and patients typically present with marked elevation in liver function test values and severe coagulopathy (23). Rouillard et al. reported that 19 of 354 patients developed severe hyperbilirubinemia within 1 month of TIPS creation, and 95% of these patients either died or required liver transplantation within 90 days of TIPS (24). Our study showed that liver failure occurred at a rate of 30.11%, with a death rate of 17.86% and a total cause of death of 55.56% (5/9). While this result seems to show a significant improvement, the mortality rate is still very high.
Although the pathogenesis of cirrhosis is complex, liver fibrosis is a significant promotor (25). It has been reported that there is a good correlation between HVPG and liver stiffness, and the measurement of HVPG is the most accurate and direct method of assessing portal hypertension, making it a useful surrogate marker for predicting the development of cirrhosis-related complications and mortality (26,27). As previously reported, HVPG is an independent risk factor for death (28,29). We found that HVPG was a risk factor of post-TIPS liver failure and an independent risk factor for postoperative morbidity for patients. The pathogenetic mechanisms of liver failure after TIPS are not precise. One study reported that it might be related to LF complicating segmental hepatic ischemia induced by a TIPS stent (30). Another study found that the covered portion of the TIPS stent occludes hepatic veins, particularly when there are shared origins, resulting in a Budd-Chiari-type hepatic ischemia and acute hepatic failure (31). Acute ischemia and hypoxia changes in the liver are possible originating mechanisms.
The present study showed that preoperative AST and HVPG were correlated with postoperative hospital mortality. Portal hypertension develops because of structural distortion by fibrosis and microvascular thrombosis, dysfunction of liver sinusoidal endothelial cells, and hepatic stellate cell activation (32,33). The TIPS puncture aims to reduce portal pressure by diverting portal flow away from the hepatic sinusoids, and it is possible that patients may fail to have a compensatory increase of hepatic arterial flow (34-36). The association between elevated AST and the progression of liver fibrosis may be due to the reduction of AST clearance caused by liver fibrosis progression, leading to increased serum AST levels (37). Moreover, advanced liver disease may be associated with mitochondrial injury, resulting in a marked release of AST (38).
HVPG measurement has been reported to be a helpful tool for evaluating the severity of cirrhosis and predicting the prognosis (39). Kim et al. reported higher HVPG values were an independent risk factor for survival. HVPG was found to be useful for predicting long-term mortality in patients with decompensated cirrhosis, especially in the presence of ascites (27), which may be related to acute ischemia of the liver (6). The applicability of this strategy to patients with less severe liver dysfunction is still a matter of debate (40-42). The TIPS procedure aims to decrease portal pressure gradient (PPG) to just <12 mmHg or at least 20% from baseline levels (10). We hypothesized that in patients with cirrhosis with high levels of AST, the higher the HVPG, the higher the likelihood of acute ischemia and hypoxia in hepatocytes after TIPS. There is reason to believe that both HVPG and AST can be used as risk factors for hospital death in patients with liver cirrhosis after TIPS puncture.
Conclusions
TIPS is an integral part of currently available methods used to treat the complications of portal hypertension. Our study demonstrated that TIPS puncture for portal hypertension patients could be performed in highly selective cirrhosis patients. Our data suggested that the incidence of post-TIPS liver failure could not be ignored, and the hospital mortality rate was exceptionally high. HVPG was a good predictor of post-TIPS morbidity and hospital mortality, and AST was also an indicator of postoperative hospitalization death. Clinical necessity will often dictate that this procedure is undertaken even in those patients at most significant risk. However, such patients with portal hypertensive hemorrhage should be carefully assessed so that the risk of post-TIPS liver failure does not outweigh the benefit.
Complications related to the technique or the stent complications that may appear during stent placement are: accidental puncture of the carotid artery, cardiac arrhythmia, hepatobiliary fistula, puncture of the capsule or migration of the stent. Perioperative infection can appear in the form of bacteremia or stent infection, known as endotoxemia. It is recommended to administer prophylactic antibiotics before the procedure. Another important complication is stent occlusion; although the appearance of covered stents has managed to reduce occlusion rates, this complication still appears.
There are no guidelines on how often imaging follow-up should be to ensure that the TIPS stent is patent. However, Doppler ultrasound imaging is generally accepted first at 3 months and then every 6 months to assess shunt patency. The shunt may need to be revised if complications that once prompted TIPS reappear, such as varices or ascites.
With the introduction of covered stents, shunt patency has improved compared with earlier, uncovered stents. Before considering performing TIPS, the physician needs to assess the suitability of each patient and be aware of potential TIPS stent-related and perioperative complications. Once the stent has been placed, regular monitoring of shunt patency is recommended.
Defects
However, it is important to point out that this study has some limitations. We also admit that we neglected the correlation between the amount of blood loss and the amount of blood transfusion before and after hospitalization. First, it is a single-center study with a limited number of enrolled cases. There may be some missing data. This is a preliminary Exploratory research, which limits further statistical analysis of the study, in the later period, we plan to convene more research centers to join the follow-up study in the hope of getting more comprehensive data to guide clinical work. Second, because of the very small sample sizes of liver failure and died patients, the current data are not suitable for analyzing the factors associated with liver failure after transjugular intrahepatic portal shunt and HVPG. Therefore, we analyzed the factors related to poor prognosis of TIPS, and finally found that preoperative HVPG may be used as a predictor of postoperative success by comparing surgical liver failure with other complications.
Acknowledgments
The authors appreciate the academic support from the AME Gastroenterology and Hepatology Collaborative Group.
Funding: The study was supported by Chinese Foundation for Hepatitis Prevention and Control-Tian Qing Liver Disease Research Fund Subject 20200098 (No. TQGB20200098); Beijing iGandan Foundation (No. iGandanF-1082022-RGG044).
Footnote
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://atm.amegroups.com/article/view/10.21037/atm-22-4737/rc
Data Sharing Statement: Available at https://atm.amegroups.com/article/view/10.21037/atm-22-4737/dss
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-22-4737/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki (as revised in 2013), and was approved by the Ethics Committee of The First Affiliated Hospital of Soochow University (application No. 2021-295). Informed written consent was provided by all patients before their inclusion in this study.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
References
- European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018;69:406-60. [Crossref]
- Zanetto A, Barbiero G, Battistel M, et al. Management of portal hypertension severe complications. Minerva Gastroenterol (Torino) 2021;67:26-37. [PubMed]
- Li HB, Yue ZD, Zhao HW, et al. Pathological Features of Mitochondrial Ultrastructure Predict Susceptibility to Post-TIPS Hepatic Encephalopathy. Can J Gastroenterol Hepatol 2018;2018:4671590. [Crossref] [PubMed]
- Vizzutti F, Schepis F, Arena U, et al. Transjugular intrahepatic portosystemic shunt (TIPS): current indications and strategies to improve the outcomes. Intern Emerg Med 2020;15:37-48. [Crossref] [PubMed]
- Halabi SA, Sawas T, Sadat B, et al. Early TIPS versus endoscopic therapy for secondary prophylaxis after management of acute esophageal variceal bleeding in cirrhotic patients: a meta-analysis of randomized controlled trials. J Gastroenterol Hepatol 2016;31:1519-26. [Crossref] [PubMed]
- Dias E, Azevedo F, Afonso A, et al. Upper Gastrointestinal Bleeding in a Patient with Liver Cirrhosis: Gastroesophageal Varices Are not Always to Blame. J Gastrointestin Liver Dis 2021;30:323. [Crossref] [PubMed]
- Vorobioff J, Groszmann RJ, Picabea E, et al. Prognostic value of hepatic venous pressure gradient measurements in alcoholic cirrhosis: a 10-year prospective study. Gastroenterology 1996;111:701-9. [Crossref] [PubMed]
- Garcia-Tsao G, Abraldes JG, Berzigotti A, et al. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology 2017;65:310-35. [Crossref] [PubMed]
- Sauerbruch T, Wong F. Treatment of Oesophageal Varices in Liver Cirrhosis. Digestion 2019;99:261-6. [Crossref] [PubMed]
- Marschner CA, Geyer T, Froelich MF, et al. Diagnostic Value of Contrast-Enhanced Ultrasound for Evaluation of Transjugular Intrahepatic Portosystemic Shunt Perfusion. Diagnostics (Basel) 2021;11:1593. [Crossref] [PubMed]
- Siramolpiwat S. Transjugular intrahepatic portosystemic shunts and portal hypertension-related complications. World J Gastroenterol 2014;20:16996-7010. [Crossref] [PubMed]
- Rajesh S, George T, Philips CA, et al. Transjugular intrahepatic portosystemic shunt in cirrhosis: An exhaustive critical update. World J Gastroenterol 2020;26:5561-96. [Crossref] [PubMed]
- Garcia-Pagan JC, Francoz C, Montagnese S, et al. Management of the major complications of cirrhosis: Beyond guidelines. J Hepatol 2021;75:S135-46. [Crossref] [PubMed]
- Fidelman N, Kwan SW, LaBerge JM, et al. The transjugular intrahepatic portosystemic shunt: an update. AJR Am J Roentgenol 2012;199:746-55. [Crossref] [PubMed]
- Khan F, Tripathi D. Role of early transjugular intrahepatic portosystemic stent-shunt in acute variceal bleeding: An update of the evidence and future directions. World J Gastroenterol 2021;27:7612-24. [Crossref] [PubMed]
- Wang CM, Li X, Fu J, et al. Technological modification of transjugular intrahepatic portosystemic shunt: the precise covering of parenchymal shunt with stent-graft. Beijing Da Xue Xue Bao Yi Xue Ban 2014;46:165-8. [PubMed]
- Vilstrup H, Amodio P, Bajaj J, et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology 2014;60:715-35. [Crossref] [PubMed]
- Kloster ML, Ren A, Shah KY, et al. High Incidence of Hepatic Encephalopathy After Viatorr Controlled Expansion Transjugular Intrahepatic Portosystemic Shunt Creation. Dig Dis Sci 2021;66:4058-62. [Crossref] [PubMed]
- Liver Failure and Artificial Liver Group, Chinese Society of Infectious Diseases, Chinese Medical Association. Severe Liver Disease and Artificial Liver Group, Chinese Society of Hepatology, Chinese Medical Association. Guideline for diagnosis and treatment of liver failure. Zhonghua Gan Zang Bing Za Zhi 2019;27:18-26.
- European Association for the Study of the Liver. EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure. J Hepatol 2017;66:1047-81. [Crossref] [PubMed]
- Flamm SL, Yang YX, Singh S, et al. American Gastroenterological Association Institute Guidelines for the Diagnosis and Management of Acute Liver Failure. Gastroenterology 2017;152:644-7. [Crossref] [PubMed]
- Masson S, Mardini HA, Rose JD, et al. Hepatic encephalopathy after transjugular intrahepatic portosystemic shunt insertion: a decade of experience. QJM 2008;101:493-501. [Crossref] [PubMed]
- Suhocki PV, Lungren MP, Kapoor B, et al. Transjugular intrahepatic portosystemic shunt complications: prevention and management. Semin Intervent Radiol 2015;32:123-32. [Crossref] [PubMed]
- Rouillard SS, Bass NM, Roberts JP, et al. Severe hyperbilirubinemia after creation of transjugular intrahepatic portosystemic shunts: natural history and predictors of outcome. Ann Intern Med 1998;128:374-7. [Crossref] [PubMed]
- Xu M, Wang X, Zou Y, et al. Key role of liver sinusoidal endothelial cells in liver fibrosis. Biosci Trends 2017;11:163-8. [Crossref] [PubMed]
- Lee JG, Sohn JH, Jeong JY, et al. Combined effect of hepatic venous pressure gradient and liver stiffness on long-term mortality in patients with cirrhosis. Korean J Intern Med 2020;35:88-98. [Crossref] [PubMed]
- Kim TY, Lee JG, Sohn JH, et al. Hepatic Venous Pressure Gradient Predicts Long-Term Mortality in Patients with Decompensated Cirrhosis. Yonsei Med J 2016;57:138-45. [Crossref] [PubMed]
- Kim TY, Kim TY, Kim Y, et al. Diagnostic Performance of Shear Wave Elastography for Predicting Esophageal Varices in Patients With Compensated Liver Cirrhosis. J Ultrasound Med 2016;35:1373-81. [Crossref] [PubMed]
- Pang JX, Zimmer S, Niu S, et al. Liver stiffness by transient elastography predicts liver-related complications and mortality in patients with chronic liver disease. PLoS One 2014;9:e95776. [Crossref] [PubMed]
- Vizzutti F, Arena U, Rega L, et al. Liver failure complicating segmental hepatic ischaemia induced by a PTFE-coated TIPS stent. Gut 2009;58:582-4. [Crossref] [PubMed]
- Hauenstein KH, Haag K, Ochs A, et al. The reducing stent: treatment for transjugular intrahepatic portosystemic shunt-induced refractory hepatic encephalopathy and liver failure. Radiology 1995;194:175-9. [Crossref] [PubMed]
- Kumar A, Khan NM, Anikhindi SA, et al. Correlation of transient elastography with hepatic venous pressure gradient in patients with cirrhotic portal hypertension: A study of 326 patients from India. World J Gastroenterol 2017;23:687-96. [Crossref] [PubMed]
- Gioia S, Nardelli S, Faccioli J, et al. Post TIPS hepatic encephalopathy: Look at muscle and fat! Clin Nutr 2022;41:1150. [Crossref] [PubMed]
- Wolf DC, Siddiqui S, Rayyan Y, et al. Emergent stent occlusion for TIPS-induced liver failure. Dig Dis Sci 2005;50:2356-8. [Crossref] [PubMed]
- Zhang X, Tsauo J, Tie J, et al. Emergent Transjugular Intrahepatic Portosystemic Shunt Creation for Acute Gastric Variceal Bleeding in Patients with Hepatocellular Carcinoma. J Vasc Interv Radiol 2022;33:702-6. [Crossref] [PubMed]
- Patel NH, Sasadeusz KJ, Seshadri R, et al. Increase in hepatic arterial blood flow after transjugular intrahepatic portosystemic shunt creation and its potential predictive value of postprocedural encephalopathy and mortality. J Vasc Interv Radiol 2001;12:1279-84. [Crossref] [PubMed]
- Kamimoto Y, Horiuchi S, Tanase S, et al. Plasma clearance of intravenously injected aspartate aminotransferase isozymes: evidence for preferential uptake by sinusoidal liver cells. Hepatology 1985;5:367-75. [Crossref] [PubMed]
- Okuda M, Li K, Beard MR, et al. Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein. Gastroenterology 2002;122:366-75. [Crossref] [PubMed]
- Bihari C, Rastogi A, Sen B, et al. Quantitative fibrosis estimation by image analysis predicts development of decompensation, composite events and defines event-free survival in chronic hepatitis B patients. Hum Pathol 2016;55:63-71. [Crossref] [PubMed]
- Thabut D, Rudler M, Lebrec D. Early TIPS with covered stents in high-risk patients with cirrhosis presenting with variceal bleeding: are we ready to dive into the deep end of the pool? J Hepatol 2011;55:1148-9. [Crossref] [PubMed]
- Rajesh S, George T, Philips CA, et al. Transjugular intrahepatic portosystemic shunt in cirrhosis: An exhaustive critical update. World J Gastroenterol 2020;26:5561-96. [Crossref] [PubMed]
- Gioia S, Ridola L, Cristofaro L, et al. The improvement in body composition including subcutaneous and visceral fat reduces ammonia and hepatic encephalopathy after transjugular intrahepatic portosystemic shunt. Liver Int 2021;41:2965-73. [Crossref] [PubMed]
(English Language Editor: A. Muylwyk)