Examine this patient's abdomen.



· History of abdominal distension, dyspnoea.

· History of pain in the abdomen (spontaneous bacterial peritonitis, malignancy).

· History of heart failure, renal failure or liver disease.

· History of TB (peritoneal tuberculosis).

· History of malignancy (mesothelioma, metastatic spread from primary tumours).


· Full flanks and umbilicus.

· Presence of shifting dullness (always percuss with your finger parallel to the level of fluid).

· If the ascites is gross, use the 'dipping' method of palpation to feel the liver and spleen.

· Look for stigmata of underlying disease (e.g. signs of cirrhosis, cardiac failure, renal failure or malignancy).

Proceed as follows:

Check for sacral oedema and swollen ankles.


This patient has marked ascites and leg oedema with splenomegaly (lesions) due to portal hypertension, the cause of which needs to be investigated



What are the causes of a distended abdomen?

Fat, fluid, faeces, flatus and fetus.

What do you understand by the term 'ascites'?

It is the pathological accumulation of fluid in the peritoneal cavity.

What are the common causes of ascitic fluid?

· Portal hypertension with cirrhosis.

· Abdominal malignancy.

· Congestive cardiac failure.

What investigations would you perform to determine the underlying ca use ?

Diagnostic paracentesis for proteins and malignant cells, ultrasonography of the abdomen, peritoneal biopsy or laparoscopy if the

cause remains unclear.

What is the difference between an exudate and a transudate?

An exudate has a protein content of over 25 g/l.


What are the mechanisms of ascites formation in cirrhosis?

· It is caused by a combination of liver failure and portal hypertension. Liver failure decreases renal blood flow, resulting in

retention of salt and water.

· Secondary hyperaldosteronism due to increased renin release and decreased metabolism of aldosterone by the liven

· Decreased metabolism of aldosterone by the liver.

· Decreased metabolism of antidiuretic hormone.

· Hypoalbuminaemia which decreases colloid oncotic pressure.

· Lymphatic obstruction, resulting in a 'weeping' liven

· More recently, overproduction of nitric oxide has been proposed to be important in the pathogenesis of ascites, sodium and

water retention and haemodynamic abnormalities in cirrhosis (N Engl J Med 1998; 339:53341 ). Inhibition of nitric oxide

synthesis improves sodium and water excretion in cirrhotic rats with ascites.

What is the relationship between ascites and chronic liver disease?

· Ascites indicates decompensation of previously asymptomatic chronic liver disease.

· Ascites occurs in about half of the patients within 10 years of a diagnosis of compensated cirrhosis.

· The development of fluid retention in patients with chronic liver disease is a poor prognostic sign - only half of these patients

survive beyond 2 years.

What do you know about the serum-ascites albumin gradient?

It is calculated by subtracting the ascitic fluid albumin concentration from the serum albumin concentration from samples obtained at

the same time. This gradient correlates directly with portal pressure; those whose gradient exceeds 1.1 g/dl have portal hypertension

and those with gradients of less than 1.1 g/dl do not. The accuracy of such determinations is 97%.

How would you manage a patient with cirrhosis and ascites?

The most important treatments are sodium restriction and diuretics (N Engl J Med 1994; 330: 33742):

· Sodium restriction to 88 mmol per day; only 15% of these patients lose weight or have a reduction in ascitic fluid with this

therapy alone.

· Fluid restriction is usually not necessary unless the serum sodium concentration drops below 120 mmol/1.

· When the patient has tense ascites, 5 litres or more of ascitic fluid should be removed to relieve shortness of breath, to

diminish early satiety and to prevent pressure-related leakage of fluid from the site of a previous paracentesis.

· Diuretic therapy should be initiated immediately, before which the serum sodium concentration of a random urine sample

should be measured. Serial monitoring of urinary sodium concentration helps to determine the optimal dose of diuretic; doses

are increased until a negative sodium balance is achieved. The most effective diuretic regimen is a combination of

spironolactone and furosemide (frusemide). More than 90% of patients respond to this therapy.

· Diuretic-resistant ascites:

-Therapeutic paracentesis with infusion of salt-free albumin (reported to

decrease hospital stay).

-Peritoneovenous shunting, e.g. LeVeen shunt, limited by the high rate of

infection and disseminated intravascular coagulation.

-Transjugular intrahepatic portosystemic stent shunt (TIPS) is a non-surgical side-to-side shunt consisting of a stented channel

between a main branch of the portal vein and the hepatic vein. The stent shunt is associated with an operative mortality rate of

1% compared with 5-39% lor surgical shunts (N Engl J Med 1995; 332:1192-7). -Extracorporeal ultrafiltration of ascitic fluid

with reinfusion. - Liver transplantation.

In patients with cirrhosis and refractory or recurrent ascites would you prefer paracentesis or TIPS?

A recent study suggests that, in comparison with large volume paracentesis, the creation of a TIPS can improve the chance of

survival without liver transplantation in these patients (N Engl J Med 2000; 342:1701-7). These investigators defined the ascites as

refractory when the patients did not respond to diuretic therapy (a dose of at least 300 mg of spironolactone per day or 120 mg

furosemide (frusemide) per day). Patients were excluded from the study if they had hepatic encephalopathy of grade 2 or higher, a

serum bilirubin concentration of more than 86 umol/l, portal vein thrombosis or a serum creatinine concentration of more than 3

mg/dl (265 gmol/1). TIPS is ineffective in those patients with associated intrinsic renal disease.

What are the complications of ascites?

· Respiratory embarrassment may complicate large amounts of ascites.

· Spontaneous bacterial peritonitis is seen in cirrhotics (suspect when there is an ascitic fluid leukocyte count of 500 cells per gl,

or more than 250 poly-morphonuclear cells per gl; empirical therapy with a non-nephrotoxic broad-spectrum antibiotic should

be initiated immediately).

Mention some uncommon causes for asdtic fluid.

· Nephrotic syndrome.

· Constrictive pericarditis.

· Tuberculous peritonitis.

· Chylous ascites.

· Budd-Chiari syndrome.

· Meigs' syndrome.

What do you know about the pathogenesis of ascites in cirrhotics? Two theories have been proposed (N Engl J Med 1982; 307: 1577):

· Underfilling theory: this suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to

portal hyper-tension. This results in a decrease in intravascular volume and the kidney responds by retaining salt and water.

· Overflow theory: this suggests that the primary abnormality is inappropriate retention of salt and water by the kidney in the absence of volume


G. Budd (1808-1882), Professor of Medicine at King's College, London.

H. Chiari (1851-1916), Professor of Pathology at the German University in Prague.

J.V. Meigs (1892-1963), Professor of Gynaecology at Harvard, Massachusetts General Hospital.

H.H. LeVeen, gastroenterologist at the Veterans Administration Hospital in New York.

Sometime during the rule of Tiberius (25-50 AD), the physician Celsus wrote about oedema. 'A chronic malady may develop in patients who collect

water under their skin. The Greeks call this hydrops. There are three types: a) Sometimes the water is all drawn within and is called ascites, b)

sometimes the body is rendered uneven by swellings arising here and there and all over. The Greeks call this hyposrka and c) sometimes the belly is

tense. The Greeks call this tympanites (adapted from BMJ1999; 318: 1610-3).'