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Introduction In 2021, the latest Baveno VII version of the portal hypertension consensus will be released, with the theme of "personalized care of portal hypertension"
.
This article focuses on the prevention of decompensation in cirrhosis
.
Related reading: How is acute variceal bleeding managed? The latest consensus on portal hypertension was released (Baveno VII version).
This consensus grades recommendations according to the GRADE system.
The level of evidence is divided from A (high) to D (very low), and the strength of the recommendation is divided into 1 (strong) and 2 ( weak)
.
Baveno VII: Prevention of first decompensation 1.
Compensated liver cirrhosis refers to the current or previous complications of liver cirrhosis
.
The transition from compensated to decompensated cirrhosis leads to an increased risk of death
.
(A1) 2.
Compensated cirrhosis can be divided into 2 stages according to the presence or absence of clinically significant portal hypertension (CSPH)
.
Patients with CSPH are at increased risk of decompensation
.
The goal of treatment in compensated cirrhosis is to prevent complications from decompensation
.
(A1) 3.
Prevention of decompensation is particularly important in compensated patients with CSPH and/or esophageal or gastric varices, as these patients are at higher risk of developing decompensation
.
(B1) 4.
Events that define decompensation in compensated patients are overt ascites [or pleural effusion with elevated serum-ascites albumin gradient (SAAG) (>1.
1 g/dL)], overt hepatic encephalopathy (West Haven grade ≥ II) and variceal bleeding
.
(B1) 5.
Other liver-related events in compensated cirrhosis are the development of additive liver injury (see consensus 12)/acute-on-chronic liver failure (ACLF) and hepatocellular carcinoma
.
(B1) 6.
There are insufficient data on whether occult bleeding due to small amounts of ascites, mild hepatic encephalopathy, and portal hypertensive gastroenteropathy detected only on imaging can be considered decompensated
.
(D1) 7.
Limited data suggest that in a minority of patients, pure jaundice (non-cholestatic etiology) may be the first manifestation of cirrhosis; however, should its definition be considered true first decompensation, or does it reflect The superimposed liver injury/ACLF in compensated cirrhosis needs further study
.
(D1) 8.
Non-hepatic comorbidities are common in patients with compensated cirrhosis, can adversely affect prognosis, and should be addressed specifically
.
(A1) 9.
There are insufficient data to draw firm conclusions regarding the effect of sarcopenia and frailty on the natural history of compensated cirrhosis
.
(D1) 10.
Bacterial infections are common in compensated patients with CSPH and can lead to decompensation (ascites, variceal hemorrhage, hepatic encephalopathy), thereby adversely affecting the natural history
.
(B1) 11.
There are insufficient data on whether infection occurs frequently in compensated cirrhosis without CSPH and whether infection itself may affect prognosis
.
(D1) 12.
Superimposed liver injury, such as (acute) alcoholic hepatitis, acute viral hepatitis [hepatitis E virus (HEV), hepatitis A virus (HAV)], hepatitis B virus (HBV) attack, or drugs Liver injury can induce decompensation
.
(A1) 13.
Other factors (eg, hepatocellular carcinoma and major surgery) can induce decompensation of cirrhosis in patients with CSPH
.
(B1) 14.
Treatment with a nonselective beta-blocker (NSBB) (propranolol, nadolol, or carvedilol) should be considered to prevent decompensation in patients with CSPH
.
(B1) 15.
Carvedilol is the NSBB of choice for the treatment of compensated cirrhosis because it reduces the hepatic venous pressure gradient (HVPG) more effectively (A1) and is more effective in preventing decompensation and resistance than conventional NSBBs.
There is a trend toward greater benefit in receptivity, showing improved survival in compensated patients with CSPH compared with no active treatment (B1)
.
16.
When clinically indicated, NSBB therapy should be used, regardless of whether HVPG measurements are available
.
(B2) 17.
Patients with decompensated cirrhosis receiving NSBB prophylaxis for decompensated cirrhosis do not require screening endoscopy to detect varicose veins because endoscopy does not alter treatment regimens
.
(B2) 18.
There is no evidence that endoscopic therapy [eg, endoscopic band ligation (EBL) or fibrin glue] prevents ascites or hepatic encephalopathy
.
(D1) 19.
For compensated patients with high-risk varicose veins who have contraindications or intolerance to NSBB, EBL is recommended to prevent first variceal bleeding
.
(A1) 20.
There is currently no indication for the use of NSBB in patients without CSPH
.
(A1) 21.
Although one study showed that cyanoacrylate injection was more effective than propranolol in preventing first bleeding in patients with type 2 gastroesophageal varices or type 1 isolated gastric varices, both were significantly associated with survival.
There is no difference
.
NSBB is suitable for the above patients to prevent decompensation (B1)
.
In addition to NSBB, further research is needed on new approaches to treat these patients
.
(D1) 22.
There is currently no balloon-occluded retrograde transveno-occlusion (BRTO)/balloon-occluded antegrade transveno-occlusion (BATO)/BARTO/transjugular intrahepatic portosystemic shunt (TIPS) for Indications for primary prevention of gastric variceal bleeding in compensated patients
.
(D1) Reference: Franchis R, Bosch J, Garcia-Tsao G, et al.
BAVENO VII - RENEWING CONSENSUS IN PORTAL HYPERTENSION[J].
J Hepatol.
2021 Dec 29.
DOI: https://doi.
org/10.
1016 /j.
jhep.
2021.
12.
022.
.
This article focuses on the prevention of decompensation in cirrhosis
.
Related reading: How is acute variceal bleeding managed? The latest consensus on portal hypertension was released (Baveno VII version).
This consensus grades recommendations according to the GRADE system.
The level of evidence is divided from A (high) to D (very low), and the strength of the recommendation is divided into 1 (strong) and 2 ( weak)
.
Baveno VII: Prevention of first decompensation 1.
Compensated liver cirrhosis refers to the current or previous complications of liver cirrhosis
.
The transition from compensated to decompensated cirrhosis leads to an increased risk of death
.
(A1) 2.
Compensated cirrhosis can be divided into 2 stages according to the presence or absence of clinically significant portal hypertension (CSPH)
.
Patients with CSPH are at increased risk of decompensation
.
The goal of treatment in compensated cirrhosis is to prevent complications from decompensation
.
(A1) 3.
Prevention of decompensation is particularly important in compensated patients with CSPH and/or esophageal or gastric varices, as these patients are at higher risk of developing decompensation
.
(B1) 4.
Events that define decompensation in compensated patients are overt ascites [or pleural effusion with elevated serum-ascites albumin gradient (SAAG) (>1.
1 g/dL)], overt hepatic encephalopathy (West Haven grade ≥ II) and variceal bleeding
.
(B1) 5.
Other liver-related events in compensated cirrhosis are the development of additive liver injury (see consensus 12)/acute-on-chronic liver failure (ACLF) and hepatocellular carcinoma
.
(B1) 6.
There are insufficient data on whether occult bleeding due to small amounts of ascites, mild hepatic encephalopathy, and portal hypertensive gastroenteropathy detected only on imaging can be considered decompensated
.
(D1) 7.
Limited data suggest that in a minority of patients, pure jaundice (non-cholestatic etiology) may be the first manifestation of cirrhosis; however, should its definition be considered true first decompensation, or does it reflect The superimposed liver injury/ACLF in compensated cirrhosis needs further study
.
(D1) 8.
Non-hepatic comorbidities are common in patients with compensated cirrhosis, can adversely affect prognosis, and should be addressed specifically
.
(A1) 9.
There are insufficient data to draw firm conclusions regarding the effect of sarcopenia and frailty on the natural history of compensated cirrhosis
.
(D1) 10.
Bacterial infections are common in compensated patients with CSPH and can lead to decompensation (ascites, variceal hemorrhage, hepatic encephalopathy), thereby adversely affecting the natural history
.
(B1) 11.
There are insufficient data on whether infection occurs frequently in compensated cirrhosis without CSPH and whether infection itself may affect prognosis
.
(D1) 12.
Superimposed liver injury, such as (acute) alcoholic hepatitis, acute viral hepatitis [hepatitis E virus (HEV), hepatitis A virus (HAV)], hepatitis B virus (HBV) attack, or drugs Liver injury can induce decompensation
.
(A1) 13.
Other factors (eg, hepatocellular carcinoma and major surgery) can induce decompensation of cirrhosis in patients with CSPH
.
(B1) 14.
Treatment with a nonselective beta-blocker (NSBB) (propranolol, nadolol, or carvedilol) should be considered to prevent decompensation in patients with CSPH
.
(B1) 15.
Carvedilol is the NSBB of choice for the treatment of compensated cirrhosis because it reduces the hepatic venous pressure gradient (HVPG) more effectively (A1) and is more effective in preventing decompensation and resistance than conventional NSBBs.
There is a trend toward greater benefit in receptivity, showing improved survival in compensated patients with CSPH compared with no active treatment (B1)
.
16.
When clinically indicated, NSBB therapy should be used, regardless of whether HVPG measurements are available
.
(B2) 17.
Patients with decompensated cirrhosis receiving NSBB prophylaxis for decompensated cirrhosis do not require screening endoscopy to detect varicose veins because endoscopy does not alter treatment regimens
.
(B2) 18.
There is no evidence that endoscopic therapy [eg, endoscopic band ligation (EBL) or fibrin glue] prevents ascites or hepatic encephalopathy
.
(D1) 19.
For compensated patients with high-risk varicose veins who have contraindications or intolerance to NSBB, EBL is recommended to prevent first variceal bleeding
.
(A1) 20.
There is currently no indication for the use of NSBB in patients without CSPH
.
(A1) 21.
Although one study showed that cyanoacrylate injection was more effective than propranolol in preventing first bleeding in patients with type 2 gastroesophageal varices or type 1 isolated gastric varices, both were significantly associated with survival.
There is no difference
.
NSBB is suitable for the above patients to prevent decompensation (B1)
.
In addition to NSBB, further research is needed on new approaches to treat these patients
.
(D1) 22.
There is currently no balloon-occluded retrograde transveno-occlusion (BRTO)/balloon-occluded antegrade transveno-occlusion (BATO)/BARTO/transjugular intrahepatic portosystemic shunt (TIPS) for Indications for primary prevention of gastric variceal bleeding in compensated patients
.
(D1) Reference: Franchis R, Bosch J, Garcia-Tsao G, et al.
BAVENO VII - RENEWING CONSENSUS IN PORTAL HYPERTENSION[J].
J Hepatol.
2021 Dec 29.
DOI: https://doi.
org/10.
1016 /j.
jhep.
2021.
12.
022.
