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Cirrhosis and ascites 

Cirrhosis and ascites

Cirrhosis and ascites

Kevin Moore


A relevant case history from Oxford Case Histories in Gastroenterology and Hepatology has been added to this chapter.

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date: 30 March 2017

Ascites is the accumulation of fluid in the peritoneal cavity: 75% of cases are associated with cirrhosis, but there are many other causes, of which the commonest are malignancy and cardiac failure. The occurrence of ascites in patients with cirrhosis is associated with a poor prognosis, with survival around 50% at 1 to 2 years.

In cirrhosis, the presence of portal hypertension (>8 mmHg) is necessary but not sufficient for the development of ascites: other factors involved include hyperaldosteronism, activation of the sympathetic nervous system, and reduction in renal blood flow, perhaps stimulated by reduction in actual or perceived central blood volume (‘vasodilatation hypothesis’).

Clinical presentation is with abdominal distension and/or abdominal pain, and many patients complain of back ache. Three grades of severity are recognized: grade 1 is only detectable by ultrasound examination; grade 2 is moderate, detected by a shifting dullness; grade 3 is gross, with tense abdominal distension and fluid thrill on palpation.


Essential tests are (1) serum electrolytes and renal function tests; patients with ascites due to cirrhosis are prone to hyponatraemia and/or renal impairment; (2) ascitic tap, with fluid sent for (a) microscopy and culture to exclude bacterial peritonitis, (b) protein/albumin concentration to determine whether the fluid is an exudate (protein >25 g/litre; serum-ascites albumin gradient <11 g/litre) or transudate (protein <25 g/litre; serum–ascites albumin gradient >11 g/litre)—exudates are most likely to be due to malignancy and transudates to cirrhosis, but the distinction is unreliable and not of great clinical utility, (c) cytology for malignant cells, (d) amylase for pancreatic cause; (3) ultrasonography of liver for evidence of cirrhosis, congestion or metastases, and of portal vein to exclude thrombosis.


First-line manoeuvres include (1) dietary salt restriction (<90 mmol/day); (2) diuretics—initially spironolactone, with addition of furosemide if required; (3) therapeutic paracentesis—all ascitic fluid should be drained in a single session as rapidly as possible, with the cannula removed immediately afterwards to reduce the risks of infection and colloid replacement given to prevent circulatory disturbance. Water restriction and (in a few centres) an oral vasopressin receptor antagonist is recommended if there is significant hyponatraemia. Refractory ascites is managed by repeated paracentesis or insertion of a transjugular intrahepatic portosystemic shunt (TIPS).


The most important complication is spontaneous bacterial peritonitis (SBP), which within 3 years will affect 15% of patients presenting with ascites. Typical symptoms are abdominal pain and fever, but there may be none. The gut and urine are the most frequent source of organisms, but treatment with appropriate antibiotics (e.g. cefotaxime; ciprofloxacin with amoxicillin; piperacillin with tazlocillin) should be started as soon as a presumptive diagnosis is made following microscopy of ascitic fluid (neutrophil count >250/mm3). Prophylactic ciprofloxacin can reduce the risk of recurrent attacks. Mortality is around 30% for the acute episode and 75% at 1 year, hence (unless contraindicated) all patients with SBP should be considered for orthotopic liver transplantation. Other complications of ascites include (1) pleural effusion; (2) paraumbilical hernia; (3) hepatorenal syndrome (see Chapter 21.5); and (4) respiratory compromise from diaphragmatic splinting.

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