Ascites

Soung Won Jeong

doi:10.4166/kjg.2018.72.2.49

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Jeong: Ascites

Review Article

Korean J Gastroenterol 2018;72(2):49-55.

Published online: 4 October 2018

DOI: https://doi.org/10.4166/kjg.2018.72.2.49

Ascites

Soung Won Jeong

Department of Internal Medicine, Soonchunhyang University Hospital Seoul, Soonchunhyang University College of Medicine, Seoul, Korea

Correspondence to: Soung Won Jeong, Department of Internal Medicine, Soonchunhyang University Hospital Seoul, Soonchunhyang University College of Medicine, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Korea. Tel: +82-2-710-3076, Fax: +82-2-709-9696, E-mail: jeongsw@schmc.ac.kr

Received 18 July 2018 Revised 7 August 2018 Accepted 8 August 2018

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ascites is the most common cause of decompensation in cirrhosis, and 5% to 10% of patients with compensated cirrhosis develop ascites each year. The main factor of ascites formation is renal sodium retention due to activation of the renin-angiotensin-aldosterone system and sympathetic nervous system by the reduced effective volume secondary to splanchnic arterial vasodilation. Diagnostic paracentesis is indicated in all patients with a new onset of grade 2 or 3 ascites and in those admitted to hospital for any complication of cirrhosis. A serum-ascites albumin gradient of ≥1.1 g/dL indicates portal hypertension with an accuracy of approximately 97%. Sodium restriction, diuretics, and large volume paracentesis are the mainstay of treatment in grade 1 to 3 ascites. The refractoriness of ascites is associated with a poor prognosis with a median survival of approximately six months. Repeated large volume paracentesis plus albumin is the first line treatment, and liver transplantation is recommended in patients with refractory ascites. A careful selection of patients is also important to obtain the beneficial effects of transjugular intrahepatic portosystemic shunts in refractory ascites. This review details the recent diagnosis and treatment of cirrhotic ascites.

Keywords: Ascites, Liver cirrhosis, Hypertension portal

References

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Table 1.

Ascitic Fluid Analysis⁸

	Analysis	Diagnosis
Routine	Cell count and differential	Ascites differential diagnosis, spontaneous bacterial
	Albumin	peritonitis
	Total protein
Optional	Gram stain	Bacterial infection
	Culture in blood culture bottle
	Cytology	Malignant ascites
	Acid-fast bacilli smear and culture	Tuberculous peritonitis
	Adenosine deaminase
	Lactate dehydrogenase	Secondary bacterial peritonitis
	Glucose
	Carcinoembryonic antigen
	Alkaline phosphatase
	Amylase	Pancreatic ascites
	Triglyceride	Chylous ascites
	Bilirubin	Biliary tract perforation
	Urea, creatinine	Urinary ascites

Table 2.

Grading of Ascites and Suggested Treatment⁸

	Grade 1 ^a	Grade 2 ^b	Grade 3 ^c
Sodium intake restriction	●	●	●
Diuretics		●	●
Paracentesis			●
First-line treatment	Treating underlying disease
	Nutritional treatment and education Discontinue NSAIDs, ACE inhibitors, or angiotensin receptor blockers

NSAID, nonsteroidal anti-inflammatory drug; ACE, angiotensin converting enzyme.

^a Mild ascites only detectable by ultrasound

^b Moderate ascites evident by moderate symmetrical distension of the abdomen

^c Large or gross ascites with marked abdominal distension.

Table 3.

Definition and Diagnostic Criteria for Refractory Ascites in Cirrhosis²⁹

Diuretic-resistant ascites	Ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of a lack of response to sodium restriction and diuretic treatment
Diuretic-intractable ascites	Ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of the development of diuretic-induced complications that preclude the use of an effective diuretic dosage
Requisites
Treatment duration	Intensive diuretic therapy (spironolactone 400 mg/day and furosemide 160 mg/day) for at least 1 week and on a salt-restricted diet of less than 5 g/day
Response of therapy	Mean weight loss of <800 g over 4 days and urinary sodium output less than the sodium intake
Early ascites recurrence	Recurrence of grade 2–3 ascites within 4 weeks of initial mobilization
Diuretic-induced complications	Hepatic encephalopathy: development of encephalopathy in the absence of any other precipitating factor
	Renal impairment: >0.3 mg/dL increase of sCr within 48 hours of baseline or 1.5-fold increase within 1 week Hyponatremia: decrease of serum sodium by >10 mEq/L to serum sodium of <125 mEq/L
	Hypo- or hyperkalemia: change in serum potassium to <3 mmol/L or >6 mmol/L

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