Ascites

Background

Ascites is not always due to primary liver disease: consider cardiac cause (if the JVP is elevated and there are no other obvious signs of cardiac disease, constrictive pericarditis is a possibility); kidney disease, especially nephrotic syndrome (check the urine for protein); vascular diseases (portal or hepatic vein thrombosis – Doppler ultrasound as first investigation) and infective causes (e.g. tuberculous peritonitis – do protein and ADA on the fluid.)

Acute presentation

This may not be a prominent part of the presentation of acute liver failure, except when it is associated with Budd-Chiari syndrome, when the ascites can be of dramatic onset and considerable size.

Consider primary bacterial peritonitis – polymorphs in the ascitic fluid.

After that, do relatively little – in the setting of acute liver failure, any reasonably vigorous attempt to get rid of fluid will worsen renal failure.

Budd-Chiari syndrome.

This is a rare condition characterised by ascites (90%), abdominal pain (50%) and hepatomegaly (90%) due to obstruction of hepatic venous drainage from the liver by either thrombosis or tumour. Tuberculosis is listed as a cause, but the condition itself may be confused with abdominal tuberculosis as it presents with abdominal discomfort and either transudative or exudative ascites. Diagnosis can be strongly suspected on Doppler ultrasound, but a contrast CT scan showing adequate caudate lobe venous drainage but obstruction of the rest of the liver is highly characteristic. Therapy is problematic and the mortality is high (up to 30% in some series). Various interventions go in and out of fashion but all revolve around one or other form of venous decompression.

Ascites – chronic presentation

• Stop non-steroidal analgesics and other salt-retaining medications.
• Encourage moderate sodium restriction: < 5 g/d of salt, (1 g sodium = 44 mmol; I g salt, i.e. sodium chloride, contains 390 mg sodium or 16 mmol, therefore diet should contain no more than 80 to 100 mmol sodium per day.) There are concerns that in ‘salt sensitive’ individuals, excessive salt restriction may contribute to intravascular volume contraction so previous recommendations of <2g/d have fallen out of favour.¹,² although the evidence either way is still weak and confounded by associated differences in energy intake.³
• The evidence for fluid restriction is equally weak; it makes sense in patients who are hyponatraemic ([Na] < 125 mmol/L) and clearly fluid overloaded; in patients with intravascular volume depletion, commonly from over-diuresis, it may cause harm.
• Spironolactone, conventionally starting with 100 mg daily, increasing in weekly increments of 100 mg/d to max 400 mg/d. Add 40 mg furosemide for every 100 mg of spironolactone. This recommendation is also being challenged with some cohort evidence finding less hyponatraemia with a lower starting dose (e.g. 25 to 50 mg/d)⁴
• Large volume paracentesis – if remove 5 litres of fluid or more, give 40 g of albumin IV at the end of the process. ⁵The people most at risk of cardiovascular collapse appear to be those already on highish doses of diuretics, and those in whom very large volumes are removed. It is probably safe to remove one or two litres daily without albumin replacement.
• Watch the urea and potassium in patients having a major diuresis, and be aware of how easy it is to dehydrate such patients (which may precipitate encephalopathy). A target weight loss of no more than 1 kg per day is reasonable.

Refractory ascites

This is about ascites due to cirrhosis, and these points don’t apply to other causes, except, in some cases, end-stage nephrotic syndrome patients.

• Review the diagnosis (JVP definitely not elevated? No other features to suggest constrictive pericarditis?)
• Put a conscious effort into enforcing salt restriction – low salt diet, no added salt source. Water restriction is difficult to enforce and probably not that effective, but try to persuade the patient to not overdo it.
• Optimise diuretic regimen – step up in increments to about 400 mg per day of spironolactone (200 mg 2x/d) and 80 mg per day of furosemide (40 mg 2x/d).
• The addition of hydrochlorothiazide 12.5 mg/d may help occasionally.

Large volume paracentesis is reasonably safe, but occasionally leads to hypotension 4-8 hours after the procedure. Do paracentesis in the morning, not in the late afternoon, so that if complications occur there is still someone around.

• Ensure that you have adequate venous access.
• Using a giving set and cannula, remove 3-4 litres of fluid on the first occasion. (Don’t expect the nursing staff to judge when sufficient fluid has been removed – this is your responsibility!)
• Infuse about 8g/litre of fluid removed of salt-poor albumin – e.g. 40g, or whichever synthetic colloid is available.
• Ensure that the patient is observed after the procedure, and check BP and pulse yourself before you go home that day.

Perspectives – draining ascites

• Daily large volume (4-6L) paracentesis with IV albumin (40g) is more effective than in-hospital diuretic therapy in the short-term elimination of tense ascites.
• Daily paracentesis with albumin replacement (8g/litre of fluid removed) may also be associated with fewer complications, shorter length of stay and lower short-term mortality then diuretic therapy.
• Large volume paracentesis with albumin replacement does not induce significant changes in renal function, plasma volume or electrolytes.

In one review ascites was eliminated in 97% of patients undergoing paracentesis versus 73% of those given diuretics (ARR 24%, NNT 4) and the mortality rate was lower 9% versus 22%) and hospital stay was shorter (12 days versus 31 days.) Albumin replacement is favoured based in part on a trial⁶ which found renal impairment or hyponatraemia in 11 of 53 patients not given albumin versus 1 of 52 who received it (ARR 18.9%, NNT 6.) The patient relevance of this outcome is less clear.

Another trial⁷ which compared hydroxyethylstarch showed no difference compared to albumin, but was probably underpowered to draw that conclusion. (They used albumin 8g for each litre of fluid tapped, or hydroxyethylstarch 200 ml per litre of fluid tapped.)

The bottom line at present is that plasma expanders seem equally effective when compared one with another, but that there was insufficient evidence when compared to placebo/saline to determine if they do anything clinically useful at all. A systematic review⁸ found only three useable trials, and for the endpoints of hyponatraemia, renal impairment, encephalopathy and death, the summary odds ratios in each case favoured albumin, but in no case reached statistical significance.

Post-paracentesis circulatory dysfunction (PPCD)

After removal of large volumes of ascitic fluid, circulatory volume may be reduced, and this reduction is associated with hypotension, renal dysfunction, recurrence of ascites, hyponatraemia, and increased mortality. A more recent systematic review⁹ found that using albumin reduced hyponatraemia and PPCD incidence, but without advantages in readmission rates, ascites recurrence, or mortality

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2. Aithal GP, Palaniyappan N, China L, et al.  Guidelines on the management of ascites in cirrhosis. Gut 2021;70:9–29. doi:10.1136/gutjnl-2020-321790 ↩

3. Kumar R, Marrapu S. Dietary salt in liver cirrhosis: With a pinch of salt! World J Hepatol. 2023 Oct 27;15(10):1084-1090. doi: 10.4254/wjh.v15.i10.1084. PMID: 37970619; PMCID: PMC10642432. ↩

4. Vogel AS, Li M, Zucker SD. Aldosterone Antagonist Dosing and the Risk of Hyponatremia in Patients With Cirrhosis and Ascites. Gastro Hep Adv. 2022 Jul 16;2(1):2-4. doi: 10.1016/j.gastha.2022.06.014. PMID: 39130144; PMCID: PMC11307619. ↩

5. Lindsay AJ, Burton J, Ray CE Jr. Paracentesis-induced circulatory dysfunction: a primer for the interventional radiologist. Semin Intervent Radiol. 2014 Sep;31(3):276-8. doi: 10.1055/s-0034-1382799. PMID: 25177092; PMCID: PMC4140947. ↩

6. Gines P, Tito L, Arroyo V, et al. Randomized comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. Gastroenterology. 1988;94:1493-502 ↩

7. Altman C, Bernard B, Roulot D, et al. Randomized comparative multicenter study of hydroxyethyl starch versus albumin as a plasma expander in cirrhotic patients with tense ascites treated with paracentesis. Eur J Gastroenterol Hepatol.1998;10:5-10 ↩

8. Wong CL, Holroyd-Leduc J, Thorpe KE, et al. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA. 2008;299:1166-78 ↩

9. Dhan Bahadur Shrestha, Pravash Budhathoki, Yub Raj Sedhai, Ramkaji Baniya, Shila Awal, Jashpal Yadav, Lila Awal, Brian Davis, Markos G. Kashiouris, Casey A. Cable,Safety and efficacy of human serum albumin treatment in patients with cirrhotic ascites undergoing paracentesis: A systematic review and meta-analysis,Annals of Hepatology,Volume 26,2021,100547,ISSN 1665-2681,https://doi.org/10.1016/j.aohep.2021.100547.(https://www.sciencedirect.com/science/article/pii/S166526812100246 ↩

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