Consensus report



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consensus report

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

11

1 3


7.   Due to muscular atrophy and tubular creatinine secre-

tion in cirrhosis, serum creatinine and creatinine clear-

ance significantly overestimate renal function in HRS.

Management, general measures

HRS type 1 occurs in patients with severe liver dysfunc-

tion and is associated with a high short term mortality 

rate. Patients with HRS 1 should receive intensive care 

treatment and be immediately listed for liver transplan-

tation if they are appropriate candidates. The ideal treat-

ment for HRS should aim to improve renal function, 

prolong survival, and increase the likelihood of receiv-

ing a liver transplant in suitable candidates. In order to 

prevent further impairment of renal function (I), therapy 

should be initiated as soon as the diagnosis is made.

−   The first therapeutic goal is targeted at the precipitating 

event and includes adequate hydration to ensure eu-

volemia, discontinuation of diuretics and nephrotoxic 

medication, and withholding vasodilative agents (I).

−   Bacterial infection should be diagnosed early and 

treated aggressively with antibiotics (I).

−   Gastrointestinal bleeding should be managed appro-

priately (I).

Specific treatment for HRS

The role of vasoconstrictors

The most extensively investigated and thus widely used 

vasoconstrictors are vasopressin analogues, in particular 

terlipressin [

60



62

]. Terlipressin is able to improve cir-

culatory dysfunction via vasoconstriction of the dilated 

splanchnic vascular bed by increasing arterial pressure 

in type I HRS [

50

] (I). Treatment should be initiated at 



a dose of 1 mg/4–6 h (i.v. bolus) and may be increased 

to a maximum of 2  mg/4–6  h, if an appropriate thera-

peutic response cannot be achieved within 3 days [

63

]. 



Response to treatment is defined as:

−   reversal of HRS or complete response, when serum 

creatinine decreases below 1.5 mg/dL;

−   partial response, indicated by a decrease of serum cre-

atinine of > 50 %, but not below 1.5 mg/dL;

−   no response, when serum creatinine levels do not de-

crease more than 50 % of pretreatment values.

Response to therapy with vasoconstrictors can be 

achieved in approximately 50 % of patients within several 

days up to 2 weeks [

64



66



]. There is no evidence that in 

case of nonresponse, the treatment with vasocontrictors 

beyond 2 weeks is beneficial.

Recurrence of HRS after withdrawal of therapy is rare 

and retreatment with vasoconstrictors is generally effec-

tive. In selected patients with recurrent HRS type 1, treat-

ment may be extended for more than 2 weeks and used 

as a bridging therapy to liver transplantation [

67

] (II-3). 



Predictive factors of response are pretreatment serum 

creatinine levels, bilirubin levels, increase in mean arte-

rial pressure through therapy, and age [

68



69

].

Although not investigated prospectively in random-



ized controlled trials, continuous infusion of terlipressin 

may achieve response rates comparable with those of i.v. 

bolus administration, but possibly with less severe com-

plications [

70

] (II-2).



Terlipressin is associated with a significant risk of sys-

temic ischemic complications.

Noradrenaline (0.5–3 mg/h starting dose) is an equally 

effective and much cheaper alternative to terlipressin. It 

is administered as a continuous infusion to achieve a rise 

in arterial pressure. It is less well studied than terlipres-

sin, but this regime may be even preferred over terlipres-

sin for less side effects [

71

] (I).


Another vasoconstrictor reported in the literature but 

not in general use in Austria is the alpha adrenergic ago-

nist midodrine. Midodrine is given orally at doses start-

ing from 2.5 to 75 mg/8 h in combination with octreotide 

subcutaneously at doses from 100 µg to 200 µg/8 h, but 

even higher doses may be necessary to achieve a thera-

peutic response [

72



73

] (II-2).

It is generally accepted that terlipressin and norepi-

nephrine are given in combination with albumin (1  g/

kg on day 1 followed by 40 g/day) in order to improve the 

effect of treatment on hemodynamics [

74

] and should 



preferably be administered via a central venous line (II-1).

TIPS in HRS

Basically, insertion of a transjugular intrahepatic por-

tosystemic shunt (TIPS) should be considered in all 

patients with HRS. TIPS has been shown to improve renal 

function in type 1 and 2 HRS [

72



75



76

]. Although TIPS 



may be effective in reversing HRS in some patients, its 

use is often limited due to advanced liver disease with 

serum bilirubin exceeding 5 mg/dL or hepatic enceph-

alopathy [

76



77



]. TIPS is indicated in selected patients, 

mostly with HRS type II and often serves as a bridge to 

liver transplantation (III).

Role of renal replacement therapy and artificial 

liver support systems

Currently, there are no larger randomized controlled trials 

showing a survival benefit for any extracorporeal treatment 

modality (neither renal replacement therapy nor liver 

support system) for patients with hepatorenal syndrome 

[

78



79

]. Extracorporeal treatments (both renal replace-



ment therapy and additive liver support systems) can only 

provide a bridge to liver transplant, but evidence from 

randomized controlled trials is lacking as well. No ran-

domized controlled trials comparing renal replacement 

therapy vs. extracorporeal liver support systems looking 

at survival benefit have been performed so far. Both treat-




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