Refractory ascites

1. Refractory Ascites Demitrost Laloo

2. Definition A scites that cannot be mobilized or whose early recurrence after paracentesis cannot be satisfactorily prevented by medical therapy Can be divided into Diuretic-resistant ascites : lack of response to dietary sodium restriction and intensive diuretic treatment Diuretic-intractable ascites : development of diuretic-induced complications that preclude the use of an effective diuretic dosage

3. Causes of ascites Ascites Cirrhosis of liver (75%) Malignancies (12%) Cardiac failure (5%) Tuberculosis (1%) Pancreatitis (1%) other rarer causes

4. Pathogenesis of cirrhotic ascites 1. increased resistance to portal flow at the sinusoidal sinusoidal portal hypertension backward transmission of this increased pressure into splanchnic capillaries ↑ fluid preferentially localizes in the peritoneal cavity also associated with the development of a peripheral, mainly splanchnic , arterial vasodilation

5. Pathogenesis of ascites 2. Renal sodium retention hepatorenal baroreflex initiated by portal hypertension subtle state of hypovolaemia with minimal activation of the renin–angiotensin–aldosterone system

6. Mechanism of refractoriness Progression of systemic and portal haemodynamic abnormalities avid renal re-absorption of sodium and water renal perfusion and GFR progressively decline 1. Na re-absorption at the proximal convoluted tubule markedly increases and its delivery to distal segments of the nephron is markedly reduced retention mainly occurs proximally to the site of action of both antimineralocorticoid and loop diuretics

7. Mechanism of refractoriness 2. reduced CVS responsiveness to vasoconstrictor systems perpetuates relative underfilling of the effective arterial blood volume compounds the hypovolaemic effects of diuretics diuretic-related side effects frequently occur

8. Diagnostic criteria

9. Diagnostic criteria

10. Treatment Large-volume paracentesis Repeated large-volume paracentesis plus albumin (8 g/L of ascitic fluid removed) is the first line of treatment to prevent paracentesis -induced circulatory dysfunction Diuretics in patients with refractory ascites discontinued permanently in patients with diuretic-induced complications continued only when urinary sodium excretion under diuretic therapy is greater than 30 mmol /day

11. Treatment Transjugular intrahepatic portosystemic shunts (TIPS) reduction in portal pressure reduction in systemic vascular resistance and lead to effective arterial blood volume increase in urinary sodium excretion and glomerular filtration rate may have beneficial effects on nitrogen balance and body weight complications: shunt thrombosis and stenosis (80%) hepatic encephalopathy in 30–50% cardiac failure (2.5%), renal failure (4.3%) and liver failure (1.9%)

12. Treatment TIPS not recommended in severe liver failure (serum bilirubin >5 mg/dl, INR >2 or Child-Pugh score>11, current hepatic encephalopathy grade 2 or chronic hepatic encephalopathy), concomitant active infection, progressive renal failure, or severe cardiopulmonary diseases Liver transplantation Others vasopressin antagonists ( vaptans ): antagonize V2 receptors increase free water excretion and serum sodium concentrations acceleration of ascites mobilization

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