About 50% of patients with cirrhosis develop ascites within 10 years of diagnosis and 50% of these will die within 2 years. The process by which ascites forms in cirrhosis is not fully understood but appears to involve the accumulation of vasodilator substances, activation of the renin-angiotensin-aldosterone system (causing renal retention of sodium and water), and the production of antidiuretic hormone (causing hyponatraemia due to dilution, not deficiency, of plasma sodium).
The aim is to induce natriuresis with consequent loss of water. Fluid restriction is unnecessary unless the plasma sodium falls below 120mmol/l. The initial management must include a diagnostic tap of the ascitic fluid as spontaneous bacterial peritonitis complicates up to 25% of patients on presentation.
A combination of bed-rest (which lowers plasma renin activity) and dietary sodium restriction are effective in about 10% of patients but diuretic therapy is usual. The most useful drug is spironolactone but its maximum effect can take up to 2 weeks to develop as it is metabolised to products with long duration of action, e.g. canrenone t1/ 10-35 h. A loop diuretic, e.g. frusemide (furosemide), is therefore given in combination, which also helps to counteract hyperkalemia induced by spironolactone. A dose ratio of spironolactone 100 mg and frusemide 40 mg o.d. works well, and can be increased every 3-4 days to a maximum of spironolactone 400 mg + frusemide 160 mg.
Body weight and urinary sodium excretion should be monitored. Patients who have oedema as well as ascites exhibit rapid weight loss. When ascites only is present weight loss should not exceed 0.5 kg/day, which is the maximum rate that fluid can move from the peritoneal cavity into the circulation. Creating a negative fluid balance runs the risk of hypovolaemia, electrolyte disturbance, renal impairment and eventually hepatic encephalopathy. Patients should lose weight if their urinary sodium excretion exceeds that provided by the diet; those who do not respond despite high urinary sodium outputs are almost certainly receiving additional sodium in their diet or medications, e.g. antacids. Should spironolactone cause painful gynaecomastia, amiloride is a useful substitute (10-40 mg/day) with a more rapid onset of action.
Abdominal paracentesis is useful particularly when ascites is tense; rapid drainage of 5 litres leads to prompt relief of discomfort and improves circulatory dynamics. Provided renal function is not compromised, extensive paracentesis is safe and can be used as an adjunct to diuretic therapy to shorten hospital stay. When more than 5 litres are drained it is customary to infuse colloid or albumin (6-8 g per litre of fluid removed) to prevent hypovolaemia.
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