Consensus report



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consensus report

Austrian consensus on the definition and treatment of portal hypertension and its complications (Billroth II)   

3

1 3


Approach to the diagnosis of portal hypertension

1.   All cirrhotic patients should be screened by endosco-

py for the presence of varices at the time of the initial 

diagnosis of cirrhosis (I).

2.   Varices should be graded as absent, small (< 5 mm of 

diameter), or large (≥ 5 mm) (II-1).

3.   In compensated patients without varices, endoscopy 

should be repeated at 2–3-year intervals to evaluate 

the development of varices (I).

4.   In compensated patients with varices but not receiv-

ing beta-blocker therapy, endoscopy should be re-

peated at 1–2-year intervals to evaluate progression of 

varices. For compensated patients with varices receiv-

ing therapy with beta-blockers, there is no indication 

for endoscopic monitoring of the varices, especially if 

they are hemodynamic responders to beta-blockers as 

measured by HVPG (I).

5.   If HVPG is measured as ≥ 10 mmHg, endoscopy should 

be repeated every year to screen for the presence of 

varices, since CSPH is predictive of the formation of 

esophagogastric varices [

7



8

] (III).


6.   There is no indication for subsequent endoscopic sur-

veillance once large varices (≥ 5 mm) are detected, (I) 

unless endoscopic band ligation is carried out.

7.   HVPG is currently the only validated and reliable pa-

rameter suitable to monitor effects of pharmacologi-

cal treatment on portal pressure [

6

] (I).


Preprimary prophylaxis of variceal bleeding

Background

1.  The pathogenetic sequence “portal hypertension—

collateral vessels—varices” is commonly accepted (I).

2.   Collateral vessels can be diagnosed before varices de-

velop (I).

3.   Portal pressure is predictive for development of vari-

ces (I).

4.   “Low risk varices” are small-sized varices (diamater 



< 5 mm) without red color signs (I).

5.   The risk of bleeding within 2 years of low risk varices 

is < 10 % [

9

] (I).



6.   Spontaneous regression of varices is a rare event (I).

7.  Treatment with nonselective beta-blockers (NSBB) 

does not generally prevent the occurrence of varices 

[

7



] (I).

8.   A subgroup of cirrhotic patients without varices at en-

doscopy but with HVPG ≥ 10 mmHg may benefit from 

beta-blocker treatment to prevent the occurrence of 

varices [

7

] (II-1).



Recommendation

1.  All patients should be screened endoscopically for 

varices after diagnosis of cirrhosis (II-1).

2.   Measurement of HVPG may be performed in centers 

with adequate expertise to obtain important prognos-

tic information (decompensation, HCC development) 

and to assess the risk of variceal bleeding and other 

complications of cirrhosis and portal hypertension 

(II-2).

3.   Treatment with beta-blockers is not generally recom-



mended in cirrhotic patients without varices at en-

doscopy (I).

Primary prophylaxis

Medical prophylaxis with nonselective beta-blockers 

(NSBB) is recommended in patients with portal hyper-

tension and varices of all grades. Thereby the progression 

of the varices as well as the incidence of variceal bleeding 

can be reduced.



Indications for medical treatment and follow-up 

endoscopy

1.  All patients with large varices (≥ 5  mm) should be 

treated either with beta-blockers or with variceal 

band ligation [

10



11



] (I).

2.   Even patients with small varices (< 5 mm) should re-

ceive beta-blocker prophylaxis, since this can reduce 

the incidence of variceal bleeding [

12

] (II-3).



3.   Additional endoscopic signs such as red color signs 

are of no prognostic relevance and should not influ-

ence the indication for therapy (III).

4.   There is no need for follow-up endoscopy in patients 

on pharmacologic therapy (I).

Monitoring of beta-blockade

1.   Increasing the dose of NSBB to achieve a 25 % reduc-

tion in resting heart rate (but not < 50 bpm) or devel-

opment of symptoms can be used to adjust the dose of 

beta-blockers in cirrhotic patients (I).

2.   Some, but not all, patients treated with NSBB achiev-

ing these targets will be protected from variceal bleed-

ing (I).


3.   There is no relationship between reduction in portal 

pressure or protection from variceal bleeding and the 

degree of beta-blockade, as assessed by the reduction 

in resting heart rate (I).

4.   A reduction in HVPG below 12 mmHg—or more than 

20 % from baseline—is the only tested parameter to 

identify those patients treated with NSBB, who are 

protected from variceal bleeding. The average dose of 

propranolol to reach this target is 80 mg/day [

13

]. The 



average dose of carvedilol to achieve these reductions 

is 12.5 mg/day [

14



15



] (II-1).


4

    Austrian consensus on the definition and treatment of portal hypertension and its complications (Billroth II)



consensus report

1 3


5.   Since hemodynamic response to NSBB defines an ex-

cellent long-term prognosis, centers with adequate 

expertise in HVPG measurement should evaluate 

the hemodynamic response to NSBB therapy [

16



17



(II-2).


6.  However, since about 60 % of patients treated with 

NSBB who do not achieve these targets will not bleed 

within 2 years, in primary prophylaxis it is not manda-

tory to check the HVPG response (II-2).



Choice of primary prophylaxis for patients with 

large varices

1.   Propranolol or Carvedilol [

10



11



] should be used for 

prophylactic pharmacologic treatment of patients 

with varices [

10



18

]. Carvedilol may be more effective 

than propranolol in primary prophylaxis of variceal 

bleeding [

19



20



] (II-1).

2.   In patients who have contraindications to beta-block-

er therapy or are intolerant or not adherent to beta-

blockers or do not respond to beta-blockers, endo-

scopic band ligation should be used. In particular, if 

patients have a low bleeding tolerance (decompen-

sated cirrhosis) (II-2).

3.  If hemodynamic monitoring of HVPG is available, 

treatment with beta-blockers should be preferred and 

hemodynamic response should be evaluated (II-1).

4.   Therapy with isosorbide-5-mononitrate (ISMN) is not 

a good alternative [

21

].

5.   There is no consensus if NSBB treatment should be 



continued in patients without hemodynamic re-

sponse to NSBB treatment, although patients with a 

reduction of HVPG ≤ 20 % may also benefit from NSBB 

treatment (III).



Combination of treatments for primary prophylaxis

1.  For primary prophylaxis, the combination of NSBB 

and ISMN cannot be recommended, because this 

does not increase the effectiveness but the side effects 

of therapy (I).

2.   The combination of endoscopic treatment and phar-

macologic therapy cannot be recommended at pres-

ent because there are no data to support its use (III).

Acute variceal bleeding and rebleeding:  

definition and prognostic value



Definition of acute variceal bleeding

1.   Active bleeding at endoscopy.

2.   When active bleeding cannot be detected: signs of an 

upper GI bleeding (hematemesis, blood or coagulated 

blood, melena) in patients with varices in the absence 

of another source of bleeding.

3.   Active variceal bleeding at endoscopy is characterized 

by eminating blood from a varix (oozing or sprouting).

4.   Active bleeding at endoscopy is a poor prognostic sign 

regarding successful control of bleeding for the short-

term period after variceal bleeding [

22

].



Failure to control acute bleeding (based on  

international consensus)

1.   FCB (failure to control bleeding) is defined as death 

or need to change therapy due to one of the following 

occurrences within 120 h (5 days) of the initial bleed-

ing episode.

2.   Occurrence of fresh hematemesis within ≥ 2 h of start-

ing specific drug therapy of therapeutic endoscopy.

3.   Development of hypovolemic shock.

4.  Drop in Hb by ≥ 3  g/dL (9 % in hematocrit) within 

any 24-h period as long as no blood transfusions are 

administered.

Failure of secondary prophylaxis (every variceal 

bleeding after initiation of secondary prophylaxis)

1.   Any clinically significant rebleeding caused by portal 

hypertension from day 5 on.

2.   Clinically significant rebleeding is defined as recur-

rent melena or hematemesis resulting in: hospital 

admission, blood transfusions, drop in Hb ≥ 3  g/dL, 

death within 6 week interval.

Treatment of acute variceal bleeding (AVB)

Treatment of patients with acute variceal bleeding 

should be carried out in an institution where the thera-

peutic interventions are performed routinely and where 

the staff is experienced in taking care of such patients.



Prerequisites for therapy (III)

1.   Facilities for tight hemodynamic monitoring

2.   Continuous monitoring of O

2

 saturation



3.   A sufficient intravenous line for hemodynamic stabili-

sation and treatment

4.   Intubation for endoscopy is desirable under the fol-

lowing conditions:

–   Massive and uncontrollable variceal bleeding

–   Hepatic encephalopathy (HE grade III and IV)

–   Impossibility to maintain blood oxygenation at 90 %  

or above


–  

Evidence of aspiration (or rarely aspiration 

pneumonia)



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