Medscape article - management of cirrhotic ascites

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I've got the full article, if anyone's interested - it's really long

Arne51 - UC 1977 - PSC 2000Alive and (mostly) well in Minnesota

The Management of Cirrhotic Ascites

from Medscape General Medicine [TM]Posted 10/22/2002

Elaine Yeung, MD; Florence S. Wong, MD, FRCP©

Background

Ascites occurs in 50% of patients within 10 years of diagnosis of compensated cirrhosis.[1] It is a poor prognostic indicator, with a 50% 2-year survival,[2] worsening significantly to 20% to 50% at 1 year when the ascites becomes refractory to medical therapy.[3,4] Ascites also predisposes patients to life-threatening complications such as spontaneous bacterial peritonitis and hepatorenal syndrome, and therefore is a major indication for liver transplantation. Effective management of ascites requires a thorough understanding of the pathophysiology of ascites formation and the rationale for various treatment modalities.

Pathogenesis

The pathophysiology leading to ascites formation is complex. Subtle sodium and water retention develops early in cirrhosis, and this becomes more avid as the cirrhotic process progresses. The presence of cirrhosis is associated with hemodynamic changes. Systemic and splanchnic vasodilatation occurs due to an imbalance of vasoactive substances, favoring vasodilators. The latter results in a decrease in effective circulating blood volume. The perceived hypovolemia in turn activates various vasoconstrictor systems, including the sympathetic nervous system, the renin-angiotensin-aldosterone system, and arginine vasopressin, producing renal vasoconstriction with a decrease in glomerular filtration rate (GFR), as well as an increase in renal sodium and water reabsorption.[5] Independent of the hemodynamic changes, hepatic dysfunction also enhances renal sodium retention through some yet undefined mechanism, as sodium excretion has been shown to be related to a threshold of hepatic function.[6,7] The presence of portal hypertension then preferentially localizes the excess fluid to the peritoneal cavity.

Treating Reversible Causes of Cirrhosis

In 1997, alcoholic liver disease accounted for 40% of deaths from cirrhosis in the United States.[8] One prospective study[9] has shown reduction of portal pressures in some patients following a period of abstinence from alcohol, with possible resolution of ascites or greater responsiveness to medical therapy. Irrespective of the etiology of cirrhosis, all patients should be advised to abstain from alcohol completely, including avoidance of alcohol-containing medications and so-called "nonalcoholic" beers.[10]

Bedrest

Sodium Restriction

Fluid Restriction

Diuretics

Monitoring Response to Sodium Restriction and Diuretics

Refractory Ascites

Large-Volume Paracentesis

Peritoneovenous Shunts

Transjugular Intrahepatic Portal Systemic Shunt

Liver Transplantation

Spontaneous Bacterial Peritonitis

Pathogenesis

Types of SBP

Clinical Signs and Symptoms

Treatment of SBP

Prevention of SBP

Prognosis

Summary and Conclusions

Effective treatment of ascites remains one of the most important aspects in the management of patients with decompensated cirrhosis, especially in those who are not candidates for liver transplantation. Currently existing therapies, aside from liver transplantation, have not been shown to have a significant impact on survival. Living-related organ donation may be an attractive option for many patients, but can only be performed in specialized centers. As our understanding of the pathophysiology of ascites improves, new therapies may become available to enhance survival while awaiting liver transplantation.

[Guest guest]

I've got the full article, if anyone's interested - it's really long

Yes please Arne,

I've managed to get some articles from Medscape but not this one.

Thanks,

Barbara (UK)

[Guest guest]

Arne.........would you please send me that article.

Best Wishes,Suzanne RECYCLE YOURSELF, BE AN ORGAN DONOR!!!!!

Medscape article - management of cirrhotic ascites

I've got the full article, if anyone's interested - it's really long

Arne51 - UC 1977 - PSC 2000Alive and (mostly) well in Minnesota

The Management of Cirrhotic Ascites

from Medscape General Medicine [TM]Posted 10/22/2002

Elaine Yeung, MD; Florence S. Wong, MD, FRCP©

Background

Ascites occurs in 50% of patients within 10 years of diagnosis of compensated cirrhosis.[1] It is a poor prognostic indicator, with a 50% 2-year survival,[2] worsening significantly to 20% to 50% at 1 year when the ascites becomes refractory to medical therapy.[3,4] Ascites also predisposes patients to life-threatening complications such as spontaneous bacterial peritonitis and hepatorenal syndrome, and therefore is a major indication for liver transplantation. Effective management of ascites requires a thorough understanding of the pathophysiology of ascites formation and the rationale for various treatment modalities.

Pathogenesis

The pathophysiology leading to ascites formation is complex. Subtle sodium and water retention develops early in cirrhosis, and this becomes more avid as the cirrhotic process progresses. The presence of cirrhosis is associated with hemodynamic changes. Systemic and splanchnic vasodilatation occurs due to an imbalance of vasoactive substances, favoring vasodilators. The latter results in a decrease in effective circulating blood volume. The perceived hypovolemia in turn activates various vasoconstrictor systems, including the sympathetic nervous system, the renin-angiotensin-aldosterone system, and arginine vasopressin, producing renal vasoconstriction with a decrease in glomerular filtration rate (GFR), as well as an increase in renal sodium and water reabsorption.[5] Independent of the hemodynamic changes, hepatic dysfunction also enhances renal sodium retention through some yet undefined mechanism, as sodium excretion has been shown to be related to a threshold of hepatic function.[6,7] The presence of portal hypertension then preferentially localizes the excess fluid to the peritoneal cavity.

Treating Reversible Causes of Cirrhosis

In 1997, alcoholic liver disease accounted for 40% of deaths from cirrhosis in the United States.[8] One prospective study[9] has shown reduction of portal pressures in some patients following a period of abstinence from alcohol, with possible resolution of ascites or greater responsiveness to medical therapy. Irrespective of the etiology of cirrhosis, all patients should be advised to abstain from alcohol completely, including avoidance of alcohol-containing medications and so-called "nonalcoholic" beers.[10]

Bedrest

Sodium Restriction

Fluid Restriction

Diuretics

Monitoring Response to Sodium Restriction and Diuretics

Refractory Ascites

Large-Volume Paracentesis

Peritoneovenous Shunts

Transjugular Intrahepatic Portal Systemic Shunt

Liver Transplantation

Spontaneous Bacterial Peritonitis

Pathogenesis

Types of SBP

Clinical Signs and Symptoms

Treatment of SBP

Prevention of SBP

Prognosis

Summary and Conclusions

Effective treatment of ascites remains one of the most important aspects in the management of patients with decompensated cirrhosis, especially in those who are not candidates for liver transplantation. Currently existing therapies, aside from liver transplantation, have not been shown to have a significant impact on survival. Living-related organ donation may be an attractive option for many patients, but can only be performed in specialized centers. As our understanding of the pathophysiology of ascites improves, new therapies may become available to enhance survival while awaiting liver transplantation.