Q J Med 2001; 94: 293-300
© 2001 Association of Physicians
Review |
Current management and novel therapeutic strategies for refractory ascites and hepatorenal syndrome
From the Department of Gastroenterology, Glasgow Royal Infirmary, Glasgow, UK
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Summary |
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 Top Summary IntroductionRefractory ascitesHepatorenal syndromeConclusionReferences |
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The circulatory disturbances seen in advanced cirrhosis lead to the development of ascites, which can become refractory to diet and medical therapy. These abnormalities may progress and cause a functional renal failure known as the hepatorenal syndrome. Management of refractory ascites and hepatorenal syndrome is a therapeutic challenge, and if appropriate, liver transplantation remains the best treatment. New therapeutic options have recently appeared, including the transjugular intrahepatic portosystemic shunt and selective splanchnic vasoconstrictor agents, which may improve renal function and act as a bridge to transplantation.
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Introduction |
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TopSummaryIntroductionRefractory ascitesHepatorenal syndromeConclusionReferences |
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Advanced cirrhosis is associated with a hyperdynamic circulation characterized by reduced systemic vascular resistance secondary to splanchnic vasodilation, which leads to effective hypovolaemia. Intense activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, and non-osmotic release of vasopressin occur, with consequent renal hypoperfusion. This becomes more accentuated as patients progress from decompensated cirrhosis to the hepatorenal syndrome (HRS).1
Approximately 10–20% of patients with ascites have adequate natriuresis and clinical response to dietary sodium restriction alone, and the majority of the remaining patients respond to diuretic therapy. However, 
10% of patients do not respond to the above measures, or develop complications to diuretic therapy, and these patients are classified as having refractory ascites. Prognosis for this subgroup of patients is poor, with a 50% 1-year mortality.2 The International Ascites Club recently redefined refractory ascites3 (Table 1
).
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Hepatorenal syndrome is a functional renal impairment secondary to advanced liver failure, and represents the extreme of the renal circulatory dysfunction in cirrhosis.1 Approximately 18% of patients with cirrhosis and ascites develop HRS within 1 year, with median survival 1.7 weeks.4 The functional nature of the disorder is proven by the fact that liver transplantation reverses the renal dysfunction,5 and a kidney transplanted from a patient with HRS regains function when transplanted into a recipient with renal failure.6
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Refractory ascites |
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TopSummaryIntroductionRefractory ascitesHepatorenal syndromeConclusionReferences |
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For patients with true refractory ascites, the following therapeutic options are available.
Large-volume paracentesis
Paracentesis is the oldest form of treatment for ascites, although in the past complications were frequent. With the advent of powerful diuretics in the 1960s, paracentesis fell out of favour. In a seminal paper by Ginès and colleagues in 1987, repeated large-volume paracentesis (LVP) with intravenous albumin (until disappearance of ascites) was more effective than diuretics for tense cirrhotic ascites, and was associated with fewer complications and shorter hospital stay.7 Consequently LVP was re-established for the treatment of tense ascites. Subsequent studies by the same group confirmed the safety and efficacy of repeated LVP or total paracentesis (ascites removed in a single session) with albumin replacement in patients with cirrhotic ascites.8,9
Studies on paracentesis in cirrhotic ascites demonstrated a short-term improvement in cardiac output attributable to increased cardiac compliance immediately after complete removal of ascites.10–13 However, without subsequent volume replacement, cardiac output, wedge pressure and atrial natriuretic peptide (ANP) levels declined, and RAAS activity increased, indicating hypovolaemia.10,11,13 This was prevented by albumin infusion.12,13
Paracentesis without albumin infusion in cirrhotics has been associated with reduced survival in those who developed hyponatraemia, with or without renal impairment, which could not be predicted by baseline variables. It was also noted that hyponatraemia or renal impairment developed in those who developed an increased plasma renin (PRA) level.8 Such an increase in RAAS activity indicates effective hypovolaemia, and has been confirmed to have prognostic significance.9,14,15
However, the use of albumin has only improved these indirect markers of survival, with no effect on overall mortality, leading some authors to question the routine use of albumin during paracentesis.16
The expense of albumin led to studies investigating cheaper alternative plasma expanders such as dextran 4017 and dextran 70.18 Both were less effective in preventing post-paracentesis hypovolaemia after total paracentesis. However, dextran 70 had a similar efficacy to albumin after repeated LVP in one further study.19 Haemaccel was also shown to be as effective as albumin in preventing hypovolaemia.20
The largest randomized study of almost 300 patients compared albumin, dextran 70 and polygeline after total paracentesis.21 Albumin was superior to the other volume expanders in preventing post-paracentesis hypovolaemia (defined by increased PRA), and was associated with less rapid accumulation of ascites. However, overall survival between the albumin and non-albumin groups was similar, and when the volume of ascites removed was <5 l, no difference in post-paracentesis hypovolaemia was detected between groups. Other volume expanders investigated include normal saline22 and hydroxyethyl starch,23 both of which showed no increase in short-term complications compared to albumin, although no long-term data are available.
These studies indicate that volume replacement after paracentesis is necessary to prevent further hypovolaemia when >5 l is removed. Although albumin appears to induce less hypovolaemia than other plasma expanders, no direct survival benefit has been shown.
Transjugular intrahepatic portosystemic shunt (TIPS)
Although the main indication for TIPS remains variceal bleeding refractory to endoscopic therapy,24 the procedure reduces the activity of the RAAS and increases natriuresis25–27 and GFR.27–29 Several uncontrolled series with at least 50 patients have demonstrated the effectiveness of this procedure for refractory ascites (Table 2).28,30–33 Shunt dysfunction and development of encephalopathy remain the major concerns in this patient group.
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There are two published randomized trials comparing TIPS with paracentesis for refractory or recurrent ascites.26,34 In a small study by Lebrec, TIPS relieved ascites in Child's B patients without affecting survival, whereas the procedure was ineffective in those with Child's C disease, and an increased mortality was detected in this subgroup.26 However, there were only four patients with Child C disease in each treatment group. A larger randomized trial of TIPS vs. paracentesis was recently reported by Rössle et al.34 TIPS was more effective than paracentesis in treating ascites, and on multivariate analysis, the probability of survival without liver transplantation was higher in the TIPS group. However, survival without transplantation was not significant on univariate analysis, and not all patients had true refractory ascites, with only 30% of patients having Child C disease. Therefore it is unclear whether TIPS confers survival advantage in patients with refractory ascites.
In two recent studies, variables identified as predictors of poor survival following TIPS included serum bilirubin, creatinine, prothrombin time, alanine aminotransferase, aetiology of liver disease and pre-TIPS encephalopathy unrelated to bleeding.35,36 Whether the TIPS was undertaken for variceal bleeding or refractory ascites did not affect outcome. These data may aid selection of suitable candidates for TIPS.
Surgical portosystemic shunting
Portocaval shunt operation involves the anastomosis of the portal vein and the inferior vena cava, consequently reducing the portal pressure. The shunt also produces a marked diuresis and natriuresis.37 However, despite reported efficacy, surgical portosystemic shunts are rarely used in the treatment of advanced cirrhotic ascites, because of the high incidence of post-shunt encephalopathy.38 In addition, surgical shunts may cause technical difficulties during subsequent orthotopic liver transplantation.39
Peritoneovenous shunts
LeVeen developed the peritoneovenous shunt for diuretic-resistant ascites in 1974.40 The shunt is a conduit implanted subcutaneously connecting the peritoneal cavity and the superior vena cava via the right internal jugular vein. The ascitic fluid is returned to the circulation via a pressure-sensitive unidirectional valve. The LeVeen shunt has a beneficial effect on renal sodium handling and creatinine clearance in patients with refractory ascites.41 Despite its efficacy in the treatment of ascites, no benefit in survival or total hospital stay has been reported when compared with diuretics42 or paracentesis.43,44
Another problem with the LeVeen shunt was thrombotic occlusion, which occurred in 24–45% within 1 year.43–45 The Denver shunt was developed to reduce this complication, but has an inferior patency rate.46 The high rate of complications43,46,47 and the absence of a survival advantage over therapeutic paracentesis, has led to the infrequent use of peritoneovenous shunts as therapy for refractory ascites. However, one randomized trial comparing TIPS and peritoneovenous shunt published in abstract form suggested that both treatments were equally effective in relieving ascites, and survival was similar.48
Ascites filtration and reinfusion
Paracentesis and reinfusion of ascites was used during the 1960s and 1970s.49,50 Recent trials reported the efficacy and safety of ascites filtration and intravenous reinfusion in the treatment of tense or refractory ascites, although no survival advantage was demonstrated compared with paracentesis and albumin infusion.51,52 Ultrafiltered ascitic fluid reinfusion into the peritoneal cavity has also been used to treat refractory ascites.53 However neither technique is in widespread use, due to their relative complexity.
Novel treatments
Atrial natriuretic peptide
Atrial natriuretic peptide (ANP) normally increases glomerular filtration rate (GFR) and natriuresis. Patients with advanced cirrhosis and ascites have a reduced natriuretic response to ANP despite elevated levels.54,55 Exogenous ANP administration, together with the splanchnic vasoconstrictor terlipressin to counter the hypotensive effect of ANP, increases renal blood flow, GFR and natriuresis in patients with refractory ascites.56
Dopamine
Studies with dopamine in cirrhotics, including those with refractory ascites, have failed to show an increase in GFR, diuresis or natriuresis.57,58 However, use of docarpamine (an orally active dopamine prodrug) improved ascitic control in patients with refractory ascites.59 The prolonged duration of treatment and the route of administration may account for the beneficial effect of docarpamine.
Other agents
Although not tested specifically for refractory ascites, a number of agents have been tried in humans which may increase diuresis in cirrhotic patients with ascites. These include the V2 receptor antagonist, OPC-3126,60 Niravoline, a k-opioid antagonist,61 and the adenosine-1-receptor antagonist FK352.62 Future studies using these novel agents may provide further information regarding their efficacy in refractory ascites.
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Hepatorenal syndrome |
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TopSummaryIntroductionRefractory ascitesHepatorenal syndromeConclusionReferences |
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The diagnosis of hepatorenal syndrome (HRS) requires the exclusion of other potential causes of renal impairment in patients with liver disease, and is classified into type 1 or type 2 HRS (Tables 3 and 4
).3 Its treatment has been disappointing, and neither haemodialysis nor peritoneal dialysis affects outcome.63 Current management centres on correcting hypovolaemia, treating sepsis and avoiding diuretics, nephrotoxic drugs and other causes of renal dysfunction. The only proven long-term treatment remains liver transplantation. However, attempts to reverse some of the pathophysiological processes have been met with varying degrees of success, as outlined below.
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Prostaglandin analogues
Patients with cirrhotic ascites without renal failure have increased production of vasoconstrictive factors accompanied by an increased renal synthesis of vasodilatory prostaglandins (PG), whereas those with HRS have reduced PG synthesis.64 Prostaglandin analogues have generally been ineffective in treating HRS65,66 although a small study on four patients demonstrated improved renal function with misoprostol and volume expansion.67
Dopamine
Although used by many clinicians, there is no evidence that dopamine monotherapy is effective in the treatment of HRS. Low-dose dopamine infusion increases renal blood flow and GFR in normal subjects, but despite improved renal blood flow in cirrhotic patients with renal impairment, there is no effect on GFR or outcome.58,68,69 Combined dopamine and noradrenaline led to recovery from HRS in a single case.70
Vasopressors
Splanchnic vasoconstrictor therapy, aimed at reversing the hyperdynamic circulation and increasing the central blood volume, appears promising. Vasopressin-1 receptor agonists such as ornipressin and terlipressin act as preferential splanchnic vasoconstrictors, and redistribute blood to the central circulation. These agents reverse the overactivity of the sympathetic nervous system and RAAS, and stimulate ANP release. Short-term studies have shown that they increase renal perfusion, GFR and natriuresis in cirrhotic patients with functional renal impairment.71,72
Longer administration of ornipressin or terlipressin in combination with albumin for 5–15 days reversed HRS in two small studies,73,74 and terlipressin was used successfully as a bridge to liver transplantation for 2 months in a patient with HRS.75 However, ischaemic complications necessitated discontinuation in a third of the patients in the ornipressin study, and the patient treated prior to transplantation developed limited cutaneous necrosis.73,75 Addition of ornipressin also reversed type1 HRS in patients in whom volume expansion and dopamine infusion had failed to prevent a deterioration in renal function.76
A recent small study reported reversal of HRS following therapy with midodrine (an 
-adrenergic agonist) and the selective splanchnic vasoconstrictor octreotide, whereas progressive deterioration was seen in patients treated with low-dose dopamine.77 Interestingly, patients treated with midodrine and octreotide had an improved survival compared to published data, with an 80% 30-day survival. In a small series of patients with HRS, octreotide monotherapy improved renal function which deteriorated after cessation of the drug.78 Although studies with vasoconstrictor therapy are small and lack randomization, these agents appear promising in the management of HRS, and may have a role as a bridge to transplantation in selected patients.
Transjugular intrahepatic portosystemic shunt
A number of small studies investigating TIPS procedure in the management of HRS have reported improvements in GFR and natriuresis.79–82 The largest study to date investigating TIPS as therapy for HRS recently reported improved renal function in the TIPS group, compared with a deterioration in non-shunted patients.83 Patients treated with TIPS also had improved survival. However, the study was not randomized, and the non-shunted group consisted of patients in whom TIPS had been excluded due to more severe liver disease. In addition this group had worse baseline renal function. However, when all the type 1 HRS group was analysed, survivals at 3, 6 and 12 months were 48%, 38% and 16%, respectively, which is better than previously published data.4 Most of the TIPS patients died of liver failure, which suggests that the main role of TIPS, similar to vasoconstrictor therapy, is as a bridge to liver transplantation.
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Conclusion |
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TopSummaryIntroductionRefractory ascitesHepatorenal syndromeConclusionReferences |
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Advanced cirrhosis may be complicated by the development of refractory ascites, and in some patients the development of HRS. Over the last two decades, increased understanding of the pathophysiological processes involved in these conditions have allowed development of several novel therapeutic strategies. Whilst these provide relatively short-term benefit only, they can act as a bridge to liver transplantation which remains the optimum therapy.
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Notes |
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Address correspondence to Dr A.J. Stanley, Consultant Gastroenterologist, c/o Ward 9, Glasgow Royal Infirmary, 84 Castle Street, Glasgow G4 OSF. e-mail: adrian.stanley{at}northglasgow.scot.nhs.uk
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References |
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