Compartmentalization of Ascites and Edema in Patients with Hepatic Cirrhosis

Shear, Leroy; Ching, Santiago; Gabuzda, George J.

doi:10.1056/nejm197006182822502

Cited by 172 publications

(49 citation statements)

References 8 publications

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“…The failure of ascitic fluid to be mobilized promptly in the same manner as peripheral edema in the face of total body fluid reduction is reminiscent of that occurring in cirrhotic patients as a result of diuretic therapy [11]. This compartmentalization of ascites and nonascitic edema may be related to the fact that the rates of reabsorption from the peritoneal cavity of certain fluids are limited, as compared to that of reabsorption of peripheral edema.…”

Section: Discussionmentioning

confidence: 99%

Ascites in Patients Treated with Maintenance Hemodialysis

Wang¹,

Pillay²,

Ing³

et al. 1974

Nephron

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Eight patients treated with maintenance hemodialysis developed significant ascites. Fluid retention appears to be a common denominator. Increased capillary permeability from uremia may be a contributory factor. Compartmentalization of ascitic and nonascitic fluids is often observed. Therapeutic measures include fluid and sodium restriction, fluid removal by dialysis, abdominal paracentesis, intravenous infusion of ascitic fluid or albumin and renal transplantation. The latter appears to be the ideal therapy.

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Section: Discussionmentioning

confidence: 99%

Ascites in Patients Treated with Maintenance Hemodialysis

Wang¹,

Pillay²,

Ing³

et al. 1974

Nephron

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“…In contrast, in patients without edema, ascitic fluid should be mobi lized at a slow rate of approximately 750 ml/ day [16]. In the absence of edema, forced fluid loss by using loop diuretics could result in intravascular hypovolemia and increase the risk of potentially dangerous side effects, such as encephalopathy, renal failure, and electro lyte and acid base disturbances [17,18], One approach in monitoring treatment, when one or more diuretics are added to salt restriction and bed rest, is to gradually increase the amount of diuretic administered, based on the natriuretic response.…”

Section: Diureticsmentioning

confidence: 99%

Treatment of Ascites: Old and New Remedies

Inturri¹,

Graziotto²,

Rossaro³

1996

Dig Dis

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Ascites is a common complication of chronic liver disease. Treatment of the underlying liver disease with modalities such as abstinence from alcohol in Laennec’s cirrhosis, phlebotomy in hemochromatosis, copper removal in Wilson’s disease, and steroids in autoimmune liver disease, can improve survival in many patients. In addition, therapy of ascites alleviates the symptoms and improves the quality of life of the patients, and probably decreases the incidence of life-threatening conditions including spontaneous bacterial peritonitis and hepatorenal syndrome. The mean survival rate at 2 years is approximately 50%. Precipitating factors such as gastrointestinal bleeding, nonsteroidal anti-inflammatory drugs and infections, should be identified, since most of them can be corrected. Most cirrhotics with ascites can be managed with a ‘step-by-step’ approach, including dietary salt restrictions, aldosterone antagonists, and loop diuretics. When tense or refractory ascites is present, large-volume paracentesis is safe and effective. Peritoneovenous shunting (i.e. Denver, LeVeen) is less frequently used because of perioperative morbidity and mortality, and thrombotic complications with occlusion of the stent. Reinfusion of concentrated ascites is of potential benefit and has been used in Europe. Transjugular intrahepatic portosystemic shunt (TIPS) is an alternative procedure performed by interventional radiologists that allows decompression of portal hypertension. In many cases, ascites is improved after TIPS, but long-term randomized trials for tense or refractory ascites comparing TIPS with standard therapy are not conclusive. Liver transplantation is the ultimate step for the treatment of ascites, providing the cure for the underlying liver disease as well. Transplantation is indicated when quality of life of the patient is impaired due to recurrent episodes of ascites, or in the presence of spontaneous bacterial peritonitis and hepatorenal syndrome.

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“…When used at doses that induce excessive diuresis and natriuresis, they may induce an imbal ance between renal fluid loss and fluid reab sorption from the peritoneal cavity. This may range between 300 and 900 rnl/day, so that any fluid loss greater than these limits eventu ally results in diuretic-induced hypovolaemia [59], Prerenal azotemia (pseudohepatorenal syndrome) is one of the most common sideeffects of diuretics, occurring in about onethird of all patients. The sudden worsening in renal function, with an increase in serum cre atinine concentration and oliguria, is due to the decrease in plasma volume and resulting decrease in renal blood flow and glomerular filtration rate [60], Excessive water and sodi um reabsorption in the proximal tubule re sults in the excretion of concentrated urine with a very low sodium concentration.…”

Section: Problems O F Therapymentioning

confidence: 99%

Pathogenesis and Treatment of Ascites in Hepatic Cirrhosis

Geñtilini

Villa²,

Romanelli³

et al. 1994

Cardiology

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In cirrhosis of the liver structural distortion of the sinusoidal vessels is the major factor responsible for the increase in portal venous pressure and the development of abdominal ascites. The mechanisms by which advanced cirrhosis of the liver leads to widespread changes in the systemic circulation including vasodilatation, increased cardiac output and expanded plasma volume, together with activation of a range of antina-triuretic and natriuretic factors, are unclear. Several hypotheses have been proposed to explain these pathophysiological consequences, including underfilling of the systemic arterial system, overflow and peripheral vasodilatation, with a decrease in effective arterial blood volume. The evidence for and against these hypotheses is critically examined. In patients with hepatic cirrhosis complicated by ascites, increased intra-renal release of vasodilating prostaglandins may assist in sustaining renal blood flow and glomerular filtration rate by counteracting the vasoconstrictor effects of noradrenaline and angiotensin II. In advanced stages of the syndrome, cirrhotic ascites may become refractory to medical treatment. In this situation renal function becomes progressively impaired and eventually acute renal failure, so-called hepatorenal syndrome, supervenes due to intense renal vasoconstriction and opening of intrarenal arteriovenous shunts. The progressive renal vasoconstriction may also be accentuated by the reduced synthesis of renal vasodilating prostaglandins. The medical treatment of ascites is based on bed-rest, a low-sodium diet and administration of aldosterone antagonists and loop diuretics. Patients who are refractory to such therapy may be further treated by paracentesis or by the LeVeen shunt, though the long-term results of these physical therapies are unsatisfactory.

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Compartmentalization of Ascites and Edema in Patients with Hepatic Cirrhosis

Cited by 172 publications

References 8 publications

Ascites in Patients Treated with Maintenance Hemodialysis

Ascites in Patients Treated with Maintenance Hemodialysis

Treatment of Ascites: Old and New Remedies

Pathogenesis and Treatment of Ascites in Hepatic Cirrhosis

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