10
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.