Ascites

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Ascites, also called hydroperitoneum or dropsy of the peritoneum, is the accumulation of serous fluids in the space between the tissues and organs of the abdominal (peritoneal) cavity. It can be a sign of serious health problems. It is often associated with cirrhosis or hepatitis, but may occur due to constrictive pericarditis, congestive heart failure, liver and ovarian cancer, pancreatitis, nephrotic syndrome, protein-losing enteropathy or portal vein thrombosis. The fluids can build up enough to cause pain and shortness of breath due to pressure on the diaphram.[1]

Classification

The Serum-ascities albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for classifying ascites.[2]A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive etiology.

Causes of high SAAG ("transudate") are:[3]

Causes of low SAAG ("exudate") are:

Mixed causes

Among patients with cirrhosis, 5%[2] will have an additional etiology present. The most common second etiologies are tuberculous peritonitis and malignancy.[2] Among patients who have

Diagnosis

Physical examination

Physical examination findings have been systematically reviewed by the Rational Clinical Examination.[4][5]

Physical findings for ascites[4][5]
  Likelihood ratio+ Likelihood ratio-
Bulging flanks 1.8 0.48
Fluid wave 6.0 0.4
Peripheral edema 3.8 0.17

Ascitic fluid analysis

Ascitic fluid analysis has been systematically reviewed by the Rational Clinical Examination[6]

The serum-ascites albumin gradient (SAAG) is usually above 1.1 g/dl; however, even lower values usually are due to portal hypertension.[7]

Treatment

In patients with mild ascites, therapy is usually as an outpatient. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone.[8] In those with severe ascites causing a tense abdomen, hospitalization is generally necessary for paracentesis.[9][10]

Salt restriction

Salt restriction is the initial treatment, which allows diuresis (production of urine) since the patient now has more fluid than salt concentration. Salt restriction is effective in about 15% of patients.[11]

Diuretics

Since salt restriction is the basic concept in treatment, and aldosterone is one of the hormones that acts to increase salt retention, a medication that counteracts aldosterone should be sought. Spironolactone (or other distal-tubule diuretics such as triamterene or amiloride) is the drug of choice since they block the aldosterone receptor in the collecting tubule. This choice has been confirmed in a randomized controlled trial.[12] Diuretics for ascites should be dosed once per day.[13] Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). 40% of patients will respond to spironolactone.[11] For nonresponders, a loop diuretic may also be added and generally, furosemide is added at a dose of 40 mg/day (max 160 mg/day), or alternatively (bumetanide or torasemide). The ratio of 100:40 reduces risks of potassium imbalance.[13] Serum potassium level and renal function should be monitored closely while on these medications.[14]

Monitoring diuresis

Diuresis can be monitored by weighing the patient daily. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and peripheral edema and no more than 0.5 kg/day for patients with ascites alone.[8] If daily weights cannot be obtained, diuretics can also be guided by the urinary sodium concentration. Dosage is increased until a negative sodium balance occurs.[13] A random urine sodium-to-potassium ratio of > 1 is 90% sensitive in predicting negative balance (> 78-mmol/day sodium excretion).[15]

Diuretic resistance

Diuretic resistance can be predicted by giving 80 mg intravenous furosemide after 3 days without diuretics and on an 80 mEq sodium/day diet. The urinary sodium excretion over 8 hours < 50 mEq/8 hours predicts resistance.[16]

Water restriction

Water restriction is needed if hyponatremia < 130 mmol per liter develops.[14]

Paracentesis

In those with severe (tense) ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above.[9][10] As this may deplete serum albumin levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed.

Liver transplantation

Ascites that is refractory to medical therapy is considered an indication for liver transplantation. In the United States, the MELD Score (online calculator)[17] is used to prioritize patients for transplantation.

Shunting

In a minority of the patient with advanced cirrhosis that have recurrent ascites, shunts may be used. Typical shunts used are portacaval shunt, peritoneovenous shunt, and the transjugular intrahepatic portosystemic shunt (TIPS). However, none of these shunts has been shown to extend life expectancy, and are considered to be bridges to liver transplantation. A meta-analysis of randomized controlled trials by the international Cochrane Collaboration concluded that "TIPS was more effective at removing ascites as compared with paracentesis...however, TIPS patients develop hepatic encephalopathy significantly more often"[18]

Complications

Spontaneous bacterial peritonitis

For more information, see: Spontaneous bacterial peritonitis.


References

  1. ↑ The National Institutes of Health [1]
  2. ↑ 2.0 2.1 2.2 Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG (1992). "The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites.". Ann Intern Med 117 (3): 215-20. PMID 1616215.
  3. ↑ Warrell, D. A. (2003). Oxford textbook of medicine. Oxford: Oxford University Press. ISBN 0-19-262922-0. 
  4. ↑ 4.0 4.1 Williams JW, Simel DL (May 1992). "The rational clinical examination. Does this patient have ascites? How to divine fluid in the abdomen". JAMA 267 (19): 2645–8. PMID 1573754. [e]
  5. ↑ 5.0 5.1 Drummond Rennie; David Simel; Keitz, Sheri A. (2008). The rational clinical examination: evidence-based clinical diagnosis. New York: McGraw-Hill. ISBN 0-07-159030-7. 
  6. ↑ Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE (2008). "Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results?". JAMA 299 (10): 1166-78. DOI:10.1001/jama.299.10.1166. PMID 18334692. Research Blogging.
  7. ↑ Khandwalla HE, Fasakin Y, El-Serag HB (June 2009). "The utility of evaluating low serum albumin gradient ascites in patients with cirrhosis". Am. J. Gastroenterol. 104 (6): 1401–5. DOI:10.1038/ajg.2009.117. PMID 19491852. Research Blogging.
  8. ↑ 8.0 8.1 Shear L, Ching S, Gabuzda GJ (1970). "Compartmentalization of ascites and edema in patients with hepatic cirrhosis". N. Engl. J. Med. 282 (25): 1391-6. PMID 4910836. [e]
  9. ↑ 9.0 9.1 Ginés P, Arroyo V, Quintero E, et al (1987). "Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study". Gastroenterology 93 (2): 234-41. PMID 3297907. [e]
  10. ↑ 10.0 10.1 Salerno F, Badalamenti S, Incerti P, et al (1987). "Repeated paracentesis and i.v. albumin infusion to treat 'tense' ascites in cirrhotic patients. A safe alternative therapy". J. Hepatol. 5 (1): 102-8. PMID 3655306. [e]
  11. ↑ 11.0 11.1 Gatta A, Angeli P, Caregaro L, Menon F, Sacerdoti D, Merkel C (1991). "A pathophysiological interpretation of unresponsiveness to spironolactone in a stepped-care approach to the diuretic treatment of ascites in nonazotemic cirrhotic patients". Hepatology 14 (2): 231-6. PMID 1860680. [e]
  12. ↑ Fogel MR, Sawhney VK, Neal EA, Miller RG, Knauer CM, Gregory PB (1981). "Diuresis in the ascitic patient: a randomized controlled trial of three regimens". J. Clin. Gastroenterol. 3 Suppl 1: 73-80. PMID 7035545. [e]
  13. ↑ 13.0 13.1 13.2 Runyon BA (1994). "Care of patients with ascites". N. Engl. J. Med. 330 (5): 337-42. PMID 8277955. [e]
  14. ↑ 14.0 14.1 Ginès P, Cárdenas A, Arroyo V, Rodés J (2004). "Management of cirrhosis and ascites". N. Engl. J. Med. 350 (16): 1646-54. DOI:10.1056/NEJMra035021. PMID 15084697. Research Blogging.
  15. ↑ Runyon BA, Heck M. Utility of 24-hour urine sodium collection and urine Na/K ratios in the management of patients with cirrhosis and ascites [abstract]. Hepatology. 1996;24:571A.
  16. ↑ Spahr L, Villeneuve JP, Tran HK, Pomier-Layrargues G (2001). "Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites". Hepatology 33 (1): 28-31. DOI:10.1053/jhep.2001.20646. PMID 11124817. Research Blogging.
  17. ↑ Cosby RL, Yee B, Schrier RW (1989). "New classification with prognostic value in cirrhotic patients". Mineral and electrolyte metabolism 15 (5): 261-6. PMID 2682175. [e]
  18. ↑ Saab S, Nieto JM, Lewis SK, Runyon BA (2006). "TIPS versus paracentesis for cirrhotic patients with refractory ascites". Cochrane database of systematic reviews (Online) (4): CD004889. DOI:10.1002/14651858.CD004889.pub2. PMID 17054221. Research Blogging.

External links

National Institutes of Health [2]

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