Consensus report



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



consensus report

1 3


TIPS for variceal bleeding

TIPS in acute variceal bleeding

1.   TIPS is the standard first line treatment for high-risk pa-

tients with acute bleeding from esophageal varices after 

initial combined medical/endoscopic control of bleed-

ing (see “Early TIPS-implantation”, Chap. 7.10) (I).

2.   TIPS is a therapeutic option in acute esophageal or 

gastric variceal bleeding refractory to medical and en-

doscopic therapy [

44

] (II-2).



3.   TIPS might be a good first-line treatment option also 

for high-risk patients with gastric variceal bleeding 

(GOV2, IGV1 + 2; “early TIPS”) but has not been stud-

ied specifically in this patient population (III).

TIPS for prophylaxis of variceal bleeding

1.   TIPS is not indicated for primary prophylaxis (III).

2.   TIPS can be the therapy of choice in secondary pro-

phylaxis in patients who rebled at least twice despite 

adequate secondary prophylaxis with a combination 

of NSBB and endoscopic therapy (see 8.3 and 8.5); 

documentation of nonresponse to drug therapy by 

HVPG-measurement can help in the decision making 

process (I). 

TIPS for refractory ascites (III)

1.   In patients with refractory ascites, SBP has to be ex-

cluded by investigation of ascitic fluid. The ascitic 

fluid neutrophil count has to be < 250/µL, and bacte-

rial cultures of ascitic fluid must be negative.

2.   After total paracentesis with albumin substitution (8 g 

albumin/L ascitic fluid), recurrence of ascites using a 

maximal dose of 400 mg spironolactone and 160 mg 

furosemide cannot be prevented despite dietary so-

dium restriction to 5.2 g/day.

3.   After total paracentesis with albumin substitution (8 g 

albumin/L ascitic fluid), recurrence of ascites cannot 

be prevented because the maximal dose of 400  mg 

spironolactone and 160  mg fursoemide cannot be 

administered due to side effects of diuretic treatment 

(hyponatremia, impairment of renal function, etc.).

4.   If total paracentesis is required more often than once 

within 4 weeks, TIPS placement should be considered.

5.  In patients with previous episodes of spontaneous 

encephalopathy (in the absence of triggers like bleed-

ing, infection, electrolyte disturbances, or overdose of 

diuretics), TIPS implantation should be restricted to 

very selected cases only. 

TIPS for other indications

1.   TIPS should be considered in patients with liver cirrho-

sis and nonmalignant portal vein thrombosis [

54

] (II-2).



2.   TIPS is a very good therapeutic option in patients with 

Budd-Chiari-Syndrome, who do not improve from an-

ticoagulation alone [

44



55

56



]. (see Chap. 15) (II-2).

3.   TIPS is a therapeutic option in hepatic hydrothorax 

[

44

] (II-2).



4.   TIPS is also a therapeutic option for hepatorenal syn-

drome (II-2).

Hepatorenal syndrome (HRS)

Diagnosis of HRS

1.   HRS describes the emergence of renal dysfunction in 

decompensated cirrhosis with portal hypertension 

and circulatory dysfunction [

57

]. HRS may also com-



plicate other liver diseases including alcoholic hepa-

titis, acute liver failure, or Budd-Chiari-syndrome in 

combination with portal hypertension [

58

].



2.   HRS is usually triggered by events leading to circula-

tory compromise including SBP, diuretics overdose, 

large-volume paracentesis without albumin replace-

ment, variceal bleeding, infection, and sepsis.

3.  The pathophysiological basis of HRS is a progres-

sive systemic vasodilatation and renal vasoconstric-

tion that emerges in response to splanchnic hyper-

emia, circulatory dysfunction, and neurohormonal 

activation.

4.   It has been demonstrated that low cardiac output pre-

dicts development of hepatorenal syndrome and sur-

vival in patients with cirrhosis and ascites [

59

].

5.   If HRS persists for a longer period, acute renal failure 



with acute tubular necrosis may develop. ATN may be 

difficult to differentiate from HRS clinically, but frac-

tional excretion of urea (FeU) may be helpful in the 

differential diagnosis. An FeU of < 35 % is indicative of 

HRS.

6.   The diagnosis of HRS mandates [



58

]

−   presence of ascites.



−   no improvement in creatinine to < 1.5 mg/dL after 

at least 2 days without diuretics and volume expan-

sion with albumin (at 1  g/kg body weight, maxi-

mum 100 g/day).

−   absence of shock.

−   no recurrent or recent administration of nephro-

toxic drugs.

−   absence of parenchymal kidney disease (protein-

uria  < 500  mg/day, no hematuria, normal renal 

ultrasound). HRS can be subdivided into type I and 

type II HRS.

a.   Type I HRS: progressive renal failure with serum 

creatinine  > 2.5  mg/dL or a doubling of serum 

creatinine within 2 weeks and

b.   Type II HRS: refractory ascites with serum cre-

atinine concentration between 1.5  mg/dL and 

2.5 mg/dL. In type II HRS, the risk of progression 

to type I HRS has substantially increased.




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