Ascites- Diagnosis and Management

What are the causes of ascites?

Cirrhosis (75%), malignancy (10%), heart failure (3%), tuberculosis (2%), pancreatitis (1%), and other rare causes.

Discuss the diagnostic algorithm for ascites?

  • History and physical examination frequently reveal the underlying cause of ascites.
  • Diagnostic paracentesis- essential tests include cell count and type, ascitic fluid albumin or protein, ascitic fluid culture (in blood culture bottles) and ascitic fluid amylase. Ascitic fluid cytology should be requested when there is a clinical suspicion of underlying malignancy. Gram’s stain of ascitic fluid is not indicated, as it is rarely helpful.
  • An ascitic neutrophil count of > =250 cells/mm3 is diagnostic of SBP in the absence of a known perforated viscus or inflammation of intrabdominal organs.
  • High ascitic amylase is diagnostic of pancreatic ascites
  • USS scan to evaluate for portal hypertension. CT scan may be needed if malignancy is suspected

Discuss serum albumin ascitic gradient (SAAG)?

SA-AG = serum albumin concentration minus ascitic fluid albumin concentration. Conventionally ascites is classified as exudate (ascitic fluid protein >25g/l) or transudate (<25g/l). The purpose of this subdivision is to help identify the cause of ascites. Thus ‘‘malignancy classically causes an exudative ascites and cirrhosis causes a transudate’’. However, there are many misconceptions in clinical practice. For example, it is often presumed that cardiac ascites is a transudate when this is rarely the case, ascitic protein is >25 g/l in up to 30% of patients with cirrhosis, and patients with cirrhosis and tuberculous ascites may have a low ascitic protein. The serum ascites-albumin gradient (SA-AG) is far
superior in categorising ascites with 97% accuracy. Thus
High SAAG (>=11g/l) is caused by cirrhosis, cardiac failure, nephrotic syndrome
Low SAAG (<11g/l) is caused by malignancy, pancreatitis, tuberculosis

Discuss the various grades of ascites?
Grade 1 (mild). Ascites is only detectable by ultrasound examination.
Grade 2 (moderate). Ascites causing moderate symmetrical distension of the abdomen.
Grade 3 (large). Ascites causing marked abdominal distension.
Initial investigations

Discuss the management of ascites in cirrhosis?
The development of ascites is an important landmark in the natural history of cirrhosis as it is associated with a 50% mortality over two years and signifies the need to consider liver transplantation as a therapeutic option.

  • Bed rest is not recommended for the treatment of ascites.
  • Dietary salt should be restricted to a no-added salt diet of 90 mmol salt/day (5.2 g salt/day).
  • There is no role for water restriction in patients with uncomplicated ascites.
  • Spironolactone is the drug of choice in the initial treatment of ascites due to cirrhosis. It is started at a daily dose 100 mg may and progressively increased up to 400 mg to achieve adequate natriuresis. It is a better diuretic than furosemide. The dose is increased every 3-5 days. Side effects- decreased libido, impotence, and gynaecomastia in men and menstrual irregularity in women and hyperkalaemia
  • Furosemide is added if 400 mg/day of spironolactone fails to resolve ascites. The initial dose of furosemide is 40 mg/day and it is generally increased every 2–3 days up to a dose not exceeding 160 mg/day.
  • Therapeutic paracentesis is the first line treatment for patients with large or uncomfortable ascites

Discuss the management of hyponatremia in cirrhotic ascites?

  • Serum sodium 126–135 mmol/l and normal serum creatinine- Continue diuretic therapy but observe serum electrolytes. Do not water restrict.
  • Serum sodium 121–125 mmol/l and normal serum creatinine- British society of Gastroenterology (BSG) recommends stopping diuretic therapy or adopting a more cautious approach.
  • Serum sodium 121–125 mmol/l and serum creatinine elevated (>150 mmol/l or >120 mmol/l and rising) – Stop diuretics and give volume expansion.
  • Serum sodium (<=120 mmol/l, stop diuretics. Management of these patients is difficult and controversial. We (BSG) believe that most patients should undergo volume expansion with colloid (haemacel, gelofusine, or voluven) or saline. However, avoid increasing serum sodium by >12 mmol/l per 24 hours.

Discuss hyponatremia and water restriction?
Water restriction for patients with ascites and hyponatraemia is the standard clinical practice. However, the best management of these patients is not known. However, hyponatremia is caused by non-osmotic secretion of ADH due to effective central hypovolemia in cirrhotic ascites. Thus water restriction may worsen the problem by exacerbating the hypovolemia (and further increases in ADH). Therefore, some hepatologists, advocate further plasma
expansion to normalise and inhibit stimulation of ADH release. Gelofusine, haemacel, and
4.5% albumin solutions contain sodium concentrations equivalent to normal saline (154 mmol/l). This will worsen their salt retention but it is better to have ascites with normal renal function than to develop potentially irreversible renal failure.
Water restriction should be reserved for those who are clinically euvolaemic with severe hyponatraemia in which free water clearance is decreased, and who are not currently taking diuretics, and in whom serum creatinine is normal.

What is the target weight loss in cirrhotic ascites?

In patients with severe oedema there is no need to slow down the rate of daily weight loss. Once the oedema has resolved but ascites persists, then the rate of weight loss should not exceed about 0.5 kg/day.

How do you assess compliance with salt restriction?

By measurement of urinary sodium excretion. If 24 hr urinary sodium exceeds the recommended sodium intake (90 mmol/day) – then the patient is non compliant

Discuss refractory ascites (RA)?

  • Ascites that cannot be mobilised or early recurrence of which (that is, after therapeutic paracentesis) cannot be satisfactorily prevented by medical therapy. This includes two different subgroups.
    Diuretic resistant ascites—ascites that is refractory to dietary sodium restriction and intensive diuretic treatment (spironolactone 400 mg/day and furosemide 160 mg/day for at least one week, and a salt restricted diet of less than 90 mmol/day (5.2 g of salt)/day).
    Diuretic intractable ascites—ascites that is refractory to therapy due to the development of diuretic induced complications that preclude the use of an effective diuretic dosage.
  • 50% of patients with refractory ascites die within six months.
  • Therapeutic paracentesis is the first line treatment for patients with RA.
  • TIPS can be used for the treatment of RA requiring frequent therapeutic paracentesis (> 3 a month) with appropriate assessment of risk benefit ratio.
  • Liver transplantation, if appropriate, is the definitive treatment option.


  1. EASL Clinical Practice Guidelines (2010): The management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis
  2. AASLD Practice Guidelines (2009): Management of Adult Patients with Ascites Due to Cirrhosis: An Update
  3. Moore KP and Aithal GP. Guidelines on the management of ascites in cirrhosis. Gut 2006; 55; 1-12 (archived copy at Webcite)

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