Ascites in Cirrhosis: Why Fluid Collects in the Abdomen, and What Can Be Done About It

Ascites — fluid collecting in the abdomen — is the commonest complication of cirrhosis and a turning point in the disease. Once moderate or large ascites appears, the European liver society’s 2018 guideline puts one-year mortality at about 40%. That is why I treat its first appearance as the moment to begin discussing liver transplant evaluation, not merely to prescribe a water tablet.
— Dr Chetan Kalal, DM Hepatology, Gleneagles Hospital Mumbai

Fluid in the abdomen is often the first thing that brings a person with cirrhosis to my clinic at Gleneagles Hospital. Sometimes the liver disease has been known for years and quietly ignored. More often the patient had no idea the liver was damaged; the belly swelled over a few weeks, the ankles puffed up, and a sonography reported “gross ascites with a cirrhotic liver”. That report changes everything.

Ascites is not just an inconvenience to be drained. It marks the point at which cirrhosis has become decompensated, and from here the arithmetic of survival changes. This article explains why cirrhosis produces fluid, how we grade and test it, what treatment involves (and what it does not), when a procedure called TIPS enters the picture, what the fluid means for your life expectancy, and the handful of things you must avoid. It is written for patients and families in India, and for the physicians who look after them between visits to a hepatologist.

Why does cirrhosis cause fluid in the abdomen?

Two things go wrong at once. The scarred liver resists blood flowing through it, so pressure builds in the portal vein carrying blood from the gut to the liver. That is portal hypertension, the engine behind ascites, varices and most other complications of cirrhosis. At the same time the vessels of the abdominal organs widen, the body misreads this as a shortage of circulating blood, and the hormones that tell the kidneys to hold on to sodium and water switch on and stay on.

The result is a kidney that retains salt relentlessly while high portal pressure pushes fluid out of congested vessels into the abdominal cavity. In effect, ascites is salt water the body refused to excrete — which is why treatment revolves around sodium rather than water, and why diuretics, medicines that make the kidneys excrete sodium, are the backbone of management.

Cirrhosis from any cause can do this. In Mumbai, alcohol-related liver disease and fatty liver account for most of the ascites I see. Whatever the cause, my first question is whether the injury can still be removed — stopping alcohol, treating hepatitis B — because that is the one intervention that can make ascites recede on its own.

How is ascites graded, and does the grade change the treatment?

Yes, and the grading is simple enough for patients to follow. The European Association for the Study of the Liver (EASL) 2018 guideline on decompensated cirrhosis uses three grades: grade 1 is detectable only on ultrasound, grade 2 produces visible symmetrical swelling, and grade 3 causes marked distension that is uncomfortable to live with. The table sets out what each grade means and how it is managed.

Two points deserve emphasis. Prolonged bed rest, still advised by some, has no evidence behind it and the EASL guideline does not recommend it. And grade 3 ascites is not treated by pushing diuretics harder; it is drained, because drainage with albumin is both more effective and safer than high-dose diuretics in that situation.

What does a diagnostic paracentesis tell us?

Every patient with new grade 2 or 3 ascites, and every patient admitted with a complication of cirrhosis, should have a small sample of fluid drawn with a needle and tested — a level 1 recommendation in the EASL guideline. It takes a few minutes at the bedside and answers three questions.

First, is this ascites really due to portal hypertension? The serum-ascites albumin gradient (SAAG) — the difference between albumin in blood and in the fluid — tells us. A gradient of 1.1 g/dL or more means portal hypertension is the cause. Runyon’s classic study of 901 paired samples found the SAAG classified the cause of ascites correctly 96.7% of the time, against 55.6% for the older “exudate–transudate” method. A low gradient sends us looking elsewhere: tuberculosis, cancer, pancreatic disease.

Second, is the fluid infected? A neutrophil count above 250 cells per cubic millimetre diagnoses spontaneous bacterial peritonitis (SBP), a silent infection that can tip a stable patient into kidney failure within days. Third, a total protein below 1.5 g/dL marks higher SBP risk and shapes the decision about preventive antibiotics. None of this comes from a blood test or scan, which is why I do not accept “ascites — start diuretics” without a tap.

How is ascites in cirrhosis treated?

The principles are salt, diuretics and drainage — in that order of invasiveness, and all three together where needed.

Salt restriction is moderate, not extreme. The EASL 2018 guideline recommends restricting sodium to 80–120 mmol a day, corresponding to 4.6–6.9 g of salt — in practice a “no added salt” diet that avoids pickles, papad, packaged snacks and restaurant food. Very low-sodium diets (under 40 mmol a day) are specifically warned against: they make diuretic complications more likely and, in a population already prone to muscle loss, they starve the patient. Salt restriction alone clears ascites in roughly 10% of patients, usually those with a first episode. The rest need medicine.

Diuretics are built up slowly and monitored closely. Treatment starts with a tablet that blocks the salt-retaining hormone aldosterone; a second diuretic is added if the response is inadequate. Doses are stepped up over days, not hours, with frequent blood tests for sodium, potassium and creatinine in the first weeks. The aim is a weight loss of no more than half a kilogram a day without leg swelling, or one kilogram a day with it; faster loss drains the circulation and injures the kidneys. Your hepatologist sets and adjusts these doses. Do not change them yourself, and tell your doctor at once if you develop cramps, confusion or a sharp fall in urine output.

Large-volume paracentesis handles grade 3 ascites. A cannula is placed in the lower abdomen under sterile conditions and the fluid — often five to ten litres — is drained in one session. Bleeding is rare even when clotting tests are abnormal. What follows matters more: removing that much fluid can collapse the circulation, leading to kidney failure and low sodium. To prevent it, when more than 5 litres are removed, albumin is infused at 8 g for every litre drained. A meta-analysis of 17 randomised trials with 1,225 patients found albumin reduced circulatory dysfunction (odds ratio 0.39) and lowered mortality (odds ratio 0.64) compared with cheaper alternatives. Do not let anyone drain a large volume without it.

Diuretics and paracentesis relieve ascites; they do not cure it, because they act downstream of the real problem, and the EASL guideline is candid that neither improves survival on its own. Nutrition is not optional either — ascites, salt restriction and diuretics together erode muscle, and I have written separately on protein, sarcopenia and diet in cirrhosis.

What is refractory ascites, and when is TIPS considered?

Ascites becomes refractory when it cannot be cleared, or returns within four weeks of drainage, despite salt restriction and maximum tolerated diuretic doses — or when the diuretics themselves cause complications (kidney impairment, low sodium, encephalopathy, disabling cramps) that make an effective dose impossible. About one patient in ten reaches this stage within five years of first ascites, in a Spanish series of 263 patients. Its significance is hard to overstate: the EASL guideline quotes a median survival of about six months, and in that series one-year survival after refractory ascites was 31.6%.

Management has three strands. Repeated paracentesis with albumin remains first-line. Diuretics are usually stopped, since they no longer work. And the patient is assessed for a transjugular intrahepatic portosystemic shunt (TIPS) — a stent placed through the neck vein to connect the portal vein directly to a hepatic vein, lowering portal pressure and, within four to six weeks, restoring the kidneys’ ability to excrete sodium.

The evidence for TIPS is good but needs careful reading. An individual-patient meta-analysis of four randomised trials (305 patients) found tense ascites recurred in 42% of those given TIPS versus 89% managed with paracentesis, with better transplant-free survival after TIPS. In a later French trial with modern covered stents, 93% of patients with recurrent ascites were alive without a transplant at one year against 52% treated by repeated paracentesis — and the TIPS group needed 32 drainage procedures over the year against 320. The price is hepatic encephalopathy, which TIPS makes more frequent, and the procedure can harm patients with the most advanced cirrhosis. Selection is a hepatologist-and-radiologist judgement, never a routine step.

How long can you live with ascites — and why it is the moment to discuss transplant

The honest answer is that it depends heavily on what is done next, and the figures vary with how patients were selected. In the Spanish series of 263 patients hospitalised with their first significant ascites, survival was 85% at one year and 56.5% at five years, with age, Child-Pugh score and later low sodium as the main predictors. The EASL 2018 guideline, summarising the wider literature, quotes one- and two-year mortality of about 40% and 50% once ascites develops. Both sets of numbers say the same thing: ascites roughly halves the expected lifespan of a person with cirrhosis unless the course of the disease is changed.

The only treatment that changes the course is liver transplantation. The EASL guideline recommends that transplant be considered from the moment grade 2 or 3 ascites appears, and that patients with refractory ascites be referred to a transplant centre immediately. There is a reason for the urgency: the MELD score used to prioritise waiting lists includes creatinine and bilirubin but not ascites itself, and the guideline warns that it can underestimate the risk of death in these patients. Waiting for the score to “look bad enough” is a mistake I see too often.

Evaluation is not the same as transplant; it is a structured assessment of liver, heart, kidneys, fitness and — in India — a living donor in the family, and starting it early buys time to optimise nutrition and arrange that donor. I lead the process as a liver transplant physician, and the most useful thing a referring doctor can do is send the patient at the first episode of ascites, not the third admission.

What should a person with ascites avoid?

Four things, and the first is the one most often missed. NSAID painkillers — ibuprofen, diclofenac, naproxen, aceclofenac and their combinations, many sold over the counter in India — block the kidney’s protective prostaglandins, which in a patient with ascites are all that stand between the kidney and the vasoconstricting hormones already switched on. The EASL guideline states plainly that NSAIDs should not be used in cirrhosis with ascites: they cause acute kidney failure, low sodium and diuretic resistance. Ask your doctor what you may take for pain or fever before buying anything.

Alcohol, in any amount. Self-adjusted diuretics: doubling the tablets because the belly looks bigger is how patients arrive in emergency with a creatinine of 4. And very low-salt or very low-protein diets adopted on well-meaning advice, which weaken the patient without controlling the fluid.

Finally, know the warning signs of spontaneous bacterial peritonitis, the complication that most often turns ascites fatal. Go to the emergency department immediately if you have ascites and develop fever, abdominal pain or tenderness, vomiting, new confusion or drowsiness, a marked drop in urine, or black stools or vomited blood. SBP does not always announce itself with pain; sometimes confusion or a rising creatinine is the only clue. A tap of the fluid settles it within an hour.

Ascites is treatable, and in the right hands it is also a signal that arrives in time. Use it. The full picture of cirrhosis and what can be done at each stage is on my liver cirrhosis page.

References

1. European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406–460. PMID 29653741. doi:10.1016/j.jhep.2018.03.024
2. Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014–1048. PMID 33942342. doi:10.1002/hep.31884
3. Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117(3):215–220. PMID 1616215. doi:10.7326/0003-4819-117-3-215
4. Bernardi M, Caraceni P, Navickis RJ, Wilkes MM. Albumin infusion in patients undergoing large-volume paracentesis: a meta-analysis of randomized trials. Hepatology. 2012;55(4):1172–1181. PMID 22095893. doi:10.1002/hep.24786
5. Salerno F, Cammà C, Enea M, Rössle M, Wong F. Transjugular intrahepatic portosystemic shunt for refractory ascites: a meta-analysis of individual patient data. Gastroenterology. 2007;133(3):825–834. PMID 17678653. doi:10.1053/j.gastro.2007.06.020
6. Bureau C, Thabut D, Oberti F, et al. Transjugular intrahepatic portosystemic shunts with covered stents increase transplant-free survival of patients with cirrhosis and recurrent ascites. Gastroenterology. 2017;152(1):157–163. PMID 27663604. doi:10.1053/j.gastro.2016.09.016
7. Planas R, Montoliu S, Ballesté B, et al. Natural history of patients hospitalized for management of cirrhotic ascites. Clin Gastroenterol Hepatol. 2006;4(11):1385–1394. PMID 17081806. doi:10.1016/j.cgh.2006.08.007