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Home | Articles | Liver Disease | Ascites in Cirrhosis

Ascites in Cirrhosis

Last updated 10th January 2024


  • Uncomplicated Ascites
    • Grade 1 (mild) – only detectable by ultrasound
    • Grade 2 (moderate) – clinically detectable but not tense
    • Grade 3 (severe) – tense ascites
  • Refractory Ascites
    • Diuretic resistant ascites – refractory to salt restriction <100mmol/day and intensive diuretic therapy with Spironolactone up to 400mg/day and Frusemide up to 160mg/day
    • Diuretic intractable ascites – refractory due to diuretic induced complications that preclude use of effective diuretic dose


  1. Important to determine cause – do not assume that the alcoholic patient with ascites necessarily has alcoholic liver disease
  2. All new and unwell patients should have urgent diagnostic tap requesting fluid albumin and protein (for serum ascites albumin gradient), WCC and culture
  3. Other tests should include routine bloods including LFTs and clotting screen, and abdominal ultrasound as per BSG/BASL Liver Bundle.

Ascitic Fluid Analysis

  1. Aspiration of ascitic fluid and its laboratory analysis is an essential step in the management of patients with newly diagnosed ascites.
  2. Request ascitic amylase if clinical suspicion of pancreatic disease.
    Cardiac FailurePancreatitis
    Nephrotic SyndromeTuberculosis
  3. Request ascitic amylase if clinical suspicion of pancreatic disease.
  4. The ascitic fluid samples required from the diagnostic paracentesis summarised in figure below (amylase sometimes, BNP or adenosine deaminase rarely done) – always call BMS first, ext 33562 or via switchboard if out of hours.
    The ascitic fluid samples required from diagnostic paracentesis. *These investigations should be considered based on pretest probability of specific diagnosis. BNP, brain natriuretic peptide.

    Plain tube for biochemistry tests (albumin, amylase*, BNP*, adenosine deaminase)

    Plain tube for cytology*

    Plain tube for ascitic fluid microscopy and culture

    NOTE: separate bottles to be sent to each of the laboratories (biochemistry, cytology and microbiology)

    EDTA tube for Automated Cell Count (additional plain tube if microbiology cell count required)

    Standard blood culture bottles with ascitic fluid for culture and sensitivity.

Treatment of Uncomplicated Ascites

  1. Sodium restriction, no added salt diet – will decrease sodium intake to around 100mmol/day
  2. First line drug treatment of ascites should be Spironolactone 100 mg/day with Frusemide added in if the patient has leg oedema at 40mg/day, aiming for weight loss not greater than 0.5kg/day
  3. Increase doses of spironolactone or both drugs every 3-5 days to a maximum of Spiro 400mg and Frusemide 160mg if necessary and if tolerated both clinically and biochemically.
  4. Large volume paracentesis (LVP) is the standard of care for managing large volume ascites if the patient’s respiration is compromised, but has the risk of introducing infection which is life threatening because patients with decompensated liver disease are immunocompromised. Strict sodium restriction and additional fluid restriction is preferable in most cases. Paracentesis relieves symptoms of a tense abdomen and can also be used in the management of refractory ascites, when diuretics become ineffective or the side effects preclude their continued use, but TIPSS should be considered.
  5. Transjugular Intrahepatic Portosystemic Stent Shunt (TIPSS) – consider for refractory ascites in patients with preserved liver function (bilirubin <60micromol/L) and no encephalopathy, who require frequent therapeutic paracentesis (blood bypassing the liver means that less toxins get cleared through the liver).
  6. Consider liver transplant in all suitable patients once cirrhotic ascites develops as therapeutic paracentesis and TIPS do not improve long term survival


What to do if Develops Hyponatraemia

  1. Sodium 126–135 mmol/l, normal creatinine. Continue diuretic therapy but observe serum electrolytes. Do not water restrict.
  2. Sodium 121–125 mmol/l, normal creatinine. BSG advises to stop diuretic therapy or adopt a more cautious approach.
  3. Sodium 121–125 mmol/l, creatinine >150 mmol/l or >120 mmol/l and rising. Stop diuretics and volume expand (in hepatorenal syndrome use albumin).
  4. Sodium <=120 mmol/l, stop diuretics. Risk of seizures. Always needs discussion with consultant. Be aware of development of central pontine myelinolysis if corrected too quickly. If encephalopathic then patient might require hypertonic saline and ICU admission.

Therapeutic Paracentesis

  1. Indicated for tense or refractory ascites if the patient has compromised respiration.
  2. Be aware of the high risk of introducing infection which is life threatening in these immunocompromised patients. Use very strict (theatre type) sterile technique.
  3. The “Bonano” suprapubic catheter is ideal for this purpose.
  4. Check clotting and platelets before the procedure. Bleeding is uncommon but discuss if INR>2 or platelets <50,000.
  5. Best site for drainage is usually right ileac fossa (on the left there can be a very lage spleen) 2 finger breath above and medial to anterior superior iliac spine – avoids liver, spleen, bladder, and the inferior epigastric arteries which run 5cm either side of the midline.
  6. Insert aseptically and drain completely over up to 6 hours – use 100ml bottle of albumin 20% infused over 30 minutes for every 2 litres ascites drained.
  7. Remove drain asap and certainly at 6 hours or earlier to limit risk of infection & fluid leak –patient can move and be turned onto the drain side towards end of procedure to maximise drainage. After removing, nurse patient on opposite side for 30-60 mins to minimise leak with occlusive dressing.
  8. If leaks at drainage site, use stitches as soon as possible to minimise risk of infection (iatrogenic bacterial peritonitis) which is life threatening.
  9. Give more albumin (100 ml 20 %) if patient becomes hypotensive.
  10. Refer to the Edinburgh Royal Infirmary Liver Unit if may be candidate for TIPSS


  1. The development of ascites is associated with a mortality of 50% within 1 years of diagnosis and all patients with ascites should be considered for liver transplant.
  2. Once ascites becomes refractory to medical therapy, 50% die within six months, therefore, at its onset, suitability of liver transplantation should be considered and assessed as a priority.
  3. Particular risks for death include spontaneous (or iatrogenic) bacterial peritonitis and hepatorenal syndrome.

Spontaneous Bacterial Peritonitis (SBP)

  1. Ascitic fluid infection that occurs in patients with advanced cirrhosis spontaneously (without prior tap, drain nor surgery) and patients have a high risk of developing hepatorenal syndrome (HRS).
  2. May be asymptomatic but can also present with local (abdominal pain or rebound tenderness) or systemic (signs of sepsis) symptoms or signs.
  3. Diagnostic paracentesis indicated in all new onset ascites and in cirrhotic patients with ascites who become ill. However, if there is suspicion of SBP (e.g. rebound tenderness in a cirrhotic patient with known ascites or shifting dullness) treat before the diagnosis is confirmed because of the high mortality if not treated in time. Every hour delay in treatment begin increases the mortality!
  4. Send ascitic fluid to lab in white topped universal bottles and into blood culture bottles. This increases chances of detecting bacteria (many infections go undetected – see work on bacterascites done in Glasgow)
  5. Diagnosis confirmed if polymorph nuclear (PMN) cell count > 250 mm3. Culture may be negative in up to 60% of cases. If high percentage of lymphocytes (rather than PMN cells) then tuberculosis has to be considered. Please discuss with the labs and your consultant further tests (ZN stain, Quantiferon Gold).
  6. Treat empirically while awaiting culture results with Cefotaxime 2 g eight hourly for 5 days. Could also use Co-amoxiclav 1.2g tds IV or Ciprofloxacin 400mg bd IV. If sepsis confirmed in these immunocompromised patients consider escalation (tazocin, meropenem, antifungals) Any delay increases mortality.
  7. Long term secondary prophylaxis with co-trimoxazole oral 960mg once daily (first line) or ciprofloxacin oral 500mg once daily (second line).
  8. In 2016 the National Institute for Health and Care Excellence (NICE) recommended offering prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites and no history of SBP with an ascitic protein of ≤15 g/L (1.5 g/dL), until the ascites has resolved.

Hepatorenal Syndrome (HRS)

Note that urea as well as creatinine is often low in these patients who have muscle wasting and are malnourished. Even an increase in creatinine within the normal range is a sign of renal failure in these patients. Early diagnosis and referral to to the liver team / transfer to ward C5 is vital because of the poor prognosis.

  1. Renal failure that occurs in patients with cirrhosis and ascites in the absence of shock or nephrotoxic drugs. Bacterial infection used to exclude HRS but is now considered a precipitating cause.
  2. Type 1 HRS characterised by doubling SC to >260µmol/l in < 2 weeks, often developing in association with SBP. Median survival 2 weeks.
  3. Type 2 HRS typically associated with use of diuretics for refractory ascites. Median survival 6 months.
  4. As a general rule the kidneys do not recover until the liver recovers, which it often does not (therefore, renal replacement therapy is futile and not recommended).
  5. For type 1 HRS (not Type 2) Rx 20% albumin (20 g per 100 ml, do not use 5 % unless severely intravascularly dry) 1 g/kg/day up to 100 g on first day then 20-40 g/day together with terlipressin 5-2 (typical starting dose is 1 mg qds) mg every 4 hours initially, reviewing the renal function and increasing as clinically indicated in discussion with the liver team. Terlipressin is contraindicated in ischaemic heart disease / peripheral vascular disease and arrhythmias. Note the risk of peripheral necrosis.

Differential Diagnosis of Ascites

  1. Cirrhosis with portal hypertension and hypoalbuminaemia – in Scotland often related to alcohol related liver disease, as above.
  2. Malignancy – see below.
  3. Venous thrombosis: portal vein (most common), splenic or hepatic vein (Budd Chiari syndrome, less common, consider thrombophilia disorders)
  4. Cardiac causes eg severe right heart failure or constricted pericarditis – uncommon (if chronic can cause cardiac cirrhosis).
  5. Others eg cancer (relatively common: gastric, gynaecological), TB, pancreatitis, malnutrition, nephrotic syndrome, myxoedema – less common.

Malignant Ascites

  1. Commonly seen with ovarian, breast, gastric, colonic and hepatocellular carcinoma.
  2. Calculate serum albumin ascites gradient (SAAG) by subtracting fluid protein concentration from serum albumin (see SAAG Calculator (MDCalc)).
  3. SAAG <11g/litre (exudate) when cause is diffuse peritoneal cancer – paracentesis is treatment of choice (send as much ascites off for cytology as possible), repeat as necessary. No evidence that albumin infusion improves outcome.
  4. Less commonly SAAG >11g/litre (transudate) when cause is portal hypertension – these patients may respond to spironolactone (see above).
  5. Prognosis generally poor – median survival is 3 months unless ovarian cancer responsive to chemotherapy.


Content by Dr Mathis Heydtmann & Dr Moawad Mahgoub