Ascites is the presence of fluid within the peritoneal cavity and is a common complication of cirrhosis of the liver. The pathogenesis of the development of ascites is controversial but is probably secondary to renal sodium and water retention. Several factors are involved:

SODIUM AND WATER RETENTION occur as a result of peripheral arterial vasodilatation and consequent reduction in the effective blood volume. Nitric oxide has been postulated as the putative vasodilator although other substances, e.g. atrial natriuretic peptide and prostaglandins, may be involved. The reduction in arterial blood volume activates various neurohumoral pressor systems such as the sympathetic nervous system and the renin-angiotensin system, thus promoting salt and water retention.
PORTAL HYPERTENSION exerts a local hydrostatic pressure and leads to increased hepatic and splanchnic production of lymph and transudation of fluid into the peritoneal cavity.

Low SERUM ALBUMIN (a consequence of poor synthetic liver function) may further contribute by a reduction in plasma oncotic pressure. In patients with ascites, urine sodium excretion rarely exceeds 5 mmol in 24 hours. Loss of sodium from extrarenal sites _accounts for approximately 30 mmol in 24 hours. The normal daily dietary sodium intake may vary between 120 and 200 mmol resulting in a positive sodium balance of approximately 90-170 mmol in 24 hours (equivalent to 600-1300 ml of fluid retained.


The abdominal swelling associated with ascites may accumulate over many weeks or as rapidly as a few days. The presence of fluid is confirmed by the demonstration of shifting dullness. Mild generalized abdominal pain and discomfort are common but, if more severe, should raise the suspicion of spontaneous bacterial peritonitis. Respiratory distress may accompany tense ascites. Many patients will also have peripheral oedema. A pleural effusion (usually on the right side) may infrequently be found and is believed to arise from the passage of ascites through congenital defects in the diaphragm.


A diagnostic aspiration of 10-20 ml of fluid should be obtained and the following performed: CELL COUNT: a neutrophil count >250 cells/nun” is indicative of an underlying (usually spontaneous) bacterial peritonitis.
GRAM STAIN AND CULTURE for bacteria and acid-fast bacilli.
PROTEIN: the ascitic protein level enables a division into transudative and exudative ascites. For this division the serum albumin must be used as a reference point. An ascitic protein of 11 g litre-lor more below the serum albumin level suggests a transudate. The level of ascitic protein provides an indirect estimate of opsonization capacity and thereby the risk of developing spontaneous bacterial peritonitis. Patients at most risk are those with ascitic protein levels <10 g litre-I. CYTOLOGY for malignant cells. AMYLASE: to exclude pancreatic ascites. The differential diagnosis of ascites is listed.


The aim is to both reduce sodium intake and increase renal excretion and by doing so produce a net reabsorption of fluid from the ascites back into the circulating volume. The maximum rate at which ascites can be mobilized is 500-700 ml in 24 hours.
The management is as follows:
CHECK SERUM ELECTROLYTES AND CREATININE at start and every other day, weigh daily, measure urinary output.
BED REST-this alone will lead to a diuresis in a smallproportion of people by improving renal perfusion but in practice is not helpful.
DIETARY SODIUM RESTRICTION. It is possible to reduce sodium intake to 22 mmol in 24 hours and still maintain an adequate protein and calorie intake. Many patients find this difficult and a 40 mmol diet is frequently an adequate compromise.
FLUID RESTRICTION is probably not necessary unless the serum sodium is less than 120 mmol Iitre “. DIU RETICs. The diuretics of first choice are those acting on the distal nephron, namely spironolactone 200 mg daily, triamterene or amiloride 10 mg daily. These agents have only mild diuretic potency and are therefore without major risks of overdiuresis and renal impairment. The potassium-sparing action of these agents may give rise to hyperkalaemia. The aim of diuretic therapy should be to produce a net loss of fluid approaching 700 rnl in 24 hours (0.700 kg weight loss or 1.5 kg if peripheral oedema is present). With this regimen diuresis is often poor. Spironolactone should be increased to 400 mg daily and a loop diuretic, such as frusemide 80 mg or bumetamide 1 mg daily, added. These diuretics have several potential disadvantages with hypokalaemia and volume depletion. Diuretics should be temporarily discontinued if a rise in creatinine level (to approximately 160 iJ.mol litre-I) occurs, representing overdiuresis and hypovolaemia. Hyponatraemia occurring during therapy almost always represents haemodilution secondary to a failure to clear free water (usually a marker of reduced renal perfusion) and should be treated by stopping the diuretics if the sodium level falls below approximately 128 mmollitre-I as well as continued water restriction. Diuretics should also be stopped if there is hypokalaemia or precoma.

Causes of ascites divided according to the type of ascitic fluid.
Causes of ascites divided according to the type of ascitic fluid.

PARACENTESIS. This is used to relieve symptomatic tense ascites. It has also been reintroduced in some countries as a means of rapid therapy in patients with ascites and peripheral oedema, thus avoiding prolonged hospital stay. The main danger of this approach is the production of hypovolaemia as the ascites reaccumulates at the expense of the circulating volume. In patients with normal renal function and in the absence of hyponatraemia, this has largely been overcome by the administration of albumin (6 g per litre ascitic fluid removed) or a plasma expander, e.g. dextran-70 (8 g per litre ascitic fluid removed) or gelatin infusion (125 ml of a 3.5-4% solution per litre removed), to maintain the plasma volume. In practice, up to 20litres can be removed over 4-{i hours. This should always be followed by the plasma expander given over half an hour, 3 hours after the paracentesis. This procedure should not be performed in endstage cirrhosis or if the patient has renal failure.
PERITONEO-VENOUS SHU T. The introduction of a catheter from the peritoneal cavity (subcutaneously) to the internal jugular vein, incorporating a one-way valve, allows passage of the ascites directly into the circulation. This is rarely used for patients with resistant ascites as it often blocks.
TRANS-JUGULAR INTRAHEPATIC PORTOCAVAL SHU T (MPS) is useful for resistant ascites.


This condition represents one of the more serious complications of ascites and occurs in approximately 8% of cirrhotics with ascites. The infecting organisms are believed to gain access to the peritoneum by haematogenous spread. The most frequently incriminated bacteria are Escherichia coli, Klebsiella and enterococci. The condition should be suspected in any patient with ascites with evidence of clinical deterioration. Features such as pain and pyrexia are frequently absent. Diagnostic aspiration should always be performed (see above). The raised neutrophil count in the ascites is alone sufficient evidence to start treatment immediately. A third-generation cephalosporin, such as cefotaxime or ceftazidime, is used and may be modified on the basis of culture results. The prognosis is grave and depends on the severity of the liver disease.
It has a 50% mortality and recurs in 70% of patients with in a year.

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