eMedicine Specialties > Gastroenterology > Systemic Disease

Ascites: Treatment & Medication

Author: Rahil Shah, MD, Consulting Staff, Department of Gastroenterology, University Medical Center
Coauthor(s): Janice M Fields, MD, Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, William Beaumont Hospital, St. John Macomb-Oakland Hospital
Contributor Information and Disclosures

Updated: May 8, 2009

Treatment

Medical Care

Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard medical management for ascites and are effective in approximately 95% of patients.

  • Water restriction is used only if persistent hyponatremia is present (see Diet, below).
  • Recent research has focused on the treatment of refractory ascites with aquaretics—vasopressin V2-receptor antagonists that promote excretion of electrolyte-free water and thus might be beneficial in patients with ascites and hyponatremia.4 Although study results have been promising,5 aquaretics still await approval by the Food and Drug Administration (FDA).
  • Therapeutic paracentesis may be performed in patients who require rapid symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid are removed, saline alone is an effective plasma expander.6 The removal of 5 L of fluid or more is considered large-volume paracentesis. Total paracentesis, that is, removal of all ascites (even >20 L), can usually be performed safely. Supplementing 5 g of albumin per each liter over 5 L of ascitic fluid removed decreases complications of paracentesis, such as electrolyte imbalances and increases in serum creatinine levels secondary to large shifts of intravascular volume. Note: The AASLD indicates that postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L; however, for large-volume paracenteses, the AASLD suggests considering an albumin infusion of 8-10 g per liter of fluid removed (Grade II-2).3
  • To avoid exposing patients to blood products, the use of terlipressin (eg, 1 mg every 4 hours for 48 hours) rather than albumin has been proposed for prevention of circulatory dysfunction after large-volume paracentesis. Initial studies suggest that terlipressin is as effective as albumin for this purpose.7,8
  • Repeated therapeutic paracentesis can be used to treat refractory ascites.3 For palliative care in patients with advanced cancer, an alternative to serial paracenteses is placement of an indwelling peritoneal catheter; ascitic fluid can then be removed by continuous drainage9 or intermittent drainage with a proprietary system utilizing vacuum bottles, which can be performed in the patient’s home.10
  • The transjugular intrahepatic portosystemic shunt (TIPS) is an interventional radiologic technique that reduces portal pressure and may be the most effective treatment for patients with diuretic-resistant ascites. In the procedure, which is performed with the patient under conscious sedation or general anesthesia, an interventional radiologist places a stent percutaneously from the right jugular vein into the hepatic vein, thereby creating a connection between the portal and systemic circulations. TIPS is gradually becoming the standard of care in patients with diuretic-refractory ascites.

Surgical Care


Peritoneovenous shunt.

Peritoneovenous shunt.

[ CLOSE WINDOW ]
Peritoneovenous shunt.

Peritoneovenous shunt.


The peritoneovenous shunt is an alternative for patients with medically intractable ascites (see Image 2 or above). This is a megalymphatic shunt that returns the ascitic fluid to the central venous system. Beneficial effects of these shunts include increased cardiac output, renal blood flow, glomerular filtration rate, urinary volume, and sodium excretion and decreased plasma renin activity and plasma aldosterone concentration. Although it has largely been supplanted by TIPS, peritoneovenous shunting has been shown to improve short-term survival (compared with paracentesis) in cancer patients with refractory malignant ascites.11 The AASLD suggests considering peritoneovenous shunting for patients with refractory ascites who are not candidates for paracentesis or TIPS (Grade I).3

The AASLD recommends that patients with cirrhosis and ascites be considered for liver transplantation.3

Consultations

Consultation with a gastrointestinal specialist and/or hepatologist should be considered for all patients with ascites, particularly if the ascites is refractory to medical treatment.

Diet

Sodium restriction of 500 mg/d (22 mmol/d) is feasible in a hospital setting; however, it is unrealistic in most outpatient settings. A more appropriate sodium restriction is 2000 mg/d (88 mmol). Indiscriminate fluid restriction is inappropriate. Fluids need not be restricted unless the serum sodium level drops below 120 mmol/L.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with ascites.

Diuretics

Diuretic agents are the mainstay of medical therapy in ascites.


Spironolactone (Aldactone)

For the management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions. The peak effect of Aldactone is approximately 3 d.

Adult

25-200 mg/d PO qd or divided bid

Pediatric

1.5-3.5 mg/kg/d PO in divided doses q6-24h

May decrease the effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity

Documented hypersensitivity; anuria; renal failure; hyperkalemia

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with renal and hepatic impairment; may cause gynecomastia and impotence in men


Furosemide (Lasix)

Increases the excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Dose must be individualized to patient.

Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until the desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until a satisfactory effect is achieved.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h

1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases concentrations; interferes with the hypoglycemic effect of antidiabetic agents and antagonizes the muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides, hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter.


Amiloride (Midamor)

A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Adult

5-20 mg PO qd

Pediatric

Not established

Concomitant therapy with potassium supplementation may increase serum potassium levels; if concomitant use of these agents is indicated because of demonstrated hypokalemia, use caution and monitor serum potassium level frequently; generally, lithium should not be administered with diuretics because this may reduce renal clearance and add a high risk of lithium toxicity; administration of NSAIDs can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics; when used concomitantly, observe patients closely to determine if the desired effect of the diuretic is obtained.

Indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels; consider the potential effects on potassium kinetics and renal function.

Documented hypersensitivity; elevated serum potassium levels (>5.5 mEq/L); impaired renal function, acute or chronic renal insufficiency, and evidence of diabetic nephropathy; monitor electrolytes closely if evidence of renal functional impairment is present, BUN is >30 mg/100 mL, or serum creatinine level is >1.5 mg/100 mL

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Potassium retention associated with use of an antikaliuretic agent is accentuated in the presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level; mild hyperkalemia is usually not associated with abnormal ECG findings.


Metolazone (Mykrox, Zaroxolyn)

Helps treat edema in congestive heart failure. Increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be more effective in those with impaired renal function.

Adult

5-20 mg/dose PO q24h

Pediatric

Administer as in adults.

Thiazides may decrease the effect of anticoagulants, sulfonylureas, and gout treatments; anticholinergics and amphotericin B may increase the toxicity of thiazides; the effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, or methenamine; when administered concurrently, thiazides increase the toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants.

Documented hypersensitivity; hepatic coma or anuria

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with hepatic or renal disease, diabetes mellitus, gout, or lupus erythematosus


Mannitol (Osmitrol)

Inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular filtrate. Increases urinary output.

Adult

0.5-2 g/kg IV over 30-60 min as a 15-25% solution; repeat q6-8h

Pediatric

Not established

May decrease serum lithium levels

Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate patient's cardiovascular status before rapid administration, because a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination; when blood is given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood.

More on Ascites

Overview: Ascites
Differential Diagnoses & Workup: Ascites
Treatment & Medication: Ascites
Follow-up: Ascites
Multimedia: Ascites
References
Further Reading
[ CLOSE WINDOW ]

References

  1. [Best Evidence] Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results?. JAMA. Mar 12 2008;299(10):1166-78. [Medline].

  2. Han CM, Lee CL, Huang KG, et al. Diagnostic laparoscopy in ascites of unknown origin: Chang Gung Memorial Hospital 20-year experience. Chang Gung Med J. Jul-Aug 2008;31(4):378-83. [Medline]. [Full Text].

  3. American Association for the Study of Liver Diseases. Management of adult patients with ascites due to cirrhosis. National Guideline Clearinghouse. Available at http://www.guideline.gov/summary/summary.aspx?doc_id=5259&nbr=003590&string=ascites.. Accessed March 20, 2009.

  4. Gines P, Cardenas A. The management of ascites and hyponatremia in cirrhosis. Semin Liver Dis. Feb 2008;28(1):43-58. [Medline].

  5. Ginès P, Wong F, Watson H, et al, for the HypoCAT Study Investigators. Effects of satavaptan, a selective vasopressin V(2) receptor antagonist, on ascites and serum sodium in cirrhosis with hyponatremia: a randomized trial. Hepatology. Jul 2008;48(1):204-13. [Medline].

  6. Sola-Vera J, Minana J, Ricart E, et al. Randomized trial comparing albumin and saline in the prevention of paracentesis-induced circulatory dysfunction in cirrhotic patients with ascites. Hepatology. May 2003;37(5):1147-53. [Medline]. [Full Text].

  7. Lata J, Marecek Z, Fejfar T, Zdenek P, et al. The efficacy of terlipressin in comparison with albumin in the prevention of circulatory changes after the paracentesis of tense ascites--a randomized multicentric study. Hepatogastroenterology. Oct-Nov 2007;54(79):1930-3. [Medline].

  8. Singh V, Kumar R, Nain CK, Singh B, Sharma AK. Terlipressin versus albumin in paracentesis-induced circulatory dysfunction in cirrhosis: a randomized study. J Gastroenterol Hepatol. Jan 2006;21(1 pt 2):303-7. [Medline].

  9. Mercadante S, Intravaia G, Ferrera P, Villari P, David F. Peritoneal catheter for continuous drainage of ascites in advanced cancer patients. Support Care Cancer. Aug 2008;16(8):975-8. [Medline].

  10. Courtney A, Nemcek AA Jr, Rosenberg S, et al. Prospective evaluation of the PleurX catheter when used to treat recurrent ascites associated with malignancy. J Vasc Interv Radiol. Dec 2008;19(12):1723-31. [Medline].

  11. Seike M, Maetani I, Sakai Y. Treatment of malignant ascites in patients with advanced cancer: peritoneovenous shunt versus paracentesis. J Gastroenterol Hepatol. Dec 2007;22(12):2161-6. [Medline].

  12. Wallerstedt S, Olsson R, Simren M, et al. Abdominal tenderness in ascites patients indicates spontaneous bacterial peritonitis. Eur J Intern Med. Jan 2007;18(1):44-7. [Medline].

  13. Albornoz L, Motta A, Alvarez D, et al. Nitric oxide synthase activity in the splanchnic vasculature of patients with cirrhosis: relationship with hemodynamic disturbances. J Hepatol. Oct 2001;35(4):452-6. [Medline].

  14. Amadon MN, Arroyo V. Ascites and spontaneous bacterial peritonitis. In: Schiff ER, Sorrell MF, Maddrey WC, eds. Schiff's Diseases of the Liver. 8th ed. Philadelphia, Pa: Lippincott Raven; 1999:503-44.

  15. Cardenas A, Bataller R, Arroyo V. Mechanisms of ascites formation. Clin Liver Dis. May 2000;4(2):447-65. [Medline].

  16. [Best Evidence] D'Amico G, Luca A, Morabito A, Miraglia R, D'Amico M. Uncovered transjugular intrahepatic portosystemic shunt for refractory ascites: a meta-analysis. Gastroenterology. Oct 2005;129(4):1282-93. [Medline].

  17. Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. Feb 2001;120(3):726-48. [Medline].

  18. Jeffery J, Murphy MJ. Ascitic fluid analysis: the role of biochemistry and haematology. Hosp Med. May 2001;62(5):282-6. [Medline].

  19. Oguntona SA, Alebiosu CO. Current concepts in the management of refractory cirrhotic ascites. Niger J Med. Jul-Sep 2006;15(3):197-202. [Medline].

  20. Pauly RP, Sood MM, Chan CT. Management of refractory ascites using nocturnal home hemodialysis. Semin Dial. Jul-Aug 2008;21(4):367-70. [Medline].

  21. Reynolds TB. Ascites. Clin Liver Dis. Feb 2000;4(1):151-68, vii. [Medline].

  22. Runyon B. Approach to the patient with ascites. In: Yamada T, Alpers DH, Laine L, Owyang C, Powell DW, eds. Textbook of Gastroenterology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999:966-91.

  23. Wong F, Blendis L. Hepatorenal failure. Clin Liver Dis. Feb 2000;4(1):169-89. [Medline].

[ CLOSE WINDOW ]

Further Reading

Related eMedicine Topics

Clinical Trials

National Guideline Clearinghouse

[ CLOSE WINDOW ]

Keywords

ascites, fluid collection, fluid accumulation, fluid retention, distended abdomen, portal hypertension, hypoalbuminemia, hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome, liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure, massive hepatic metastases,

nephrotic syndrome, protein-losing enteropathy, severe malnutrition, anasarca, chylous ascites, pancreatic ascites, bile ascites, nephrogenic ascites, urine ascites, ovarian disease, bacterial peritonitis, tuberculous peritonitis, fungal peritonitis, HIV-associated peritonitis, malignancy, peritoneal carcinomatosis, primary mesothelioma, pseudomyxoma peritonei, hepatocellular carcinoma, HCC,

familial Mediterranean fever, vasculitis, granulomatous peritonitis, eosinophilic peritonitis, alcohol use, chronic viral hepatitis, jaundice, intravenous drug use, blood transfusions, alcoholic liver disease, obesity, hypercholesterolemia, type 2 diabetes mellitus, nonalcoholic steatohepatitis, gastrointestinal cancer, malignant ascites, cirrhotic ascites, nephrotic ascites, palmar erythema, spider angiomas, puddle sign, Sister Mary Joseph nodule, gastric malignancy, pancreatic malignancy, hepatic primary malignancy, left-sided supraclavicular node, Virchow node

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Rahil Shah, MD, Consulting Staff, Department of Gastroenterology, University Medical Center
Rahil Shah, MD is a member of the following medical societies: American College of Gastroenterology and American Society for Gastrointestinal Endoscopy
Disclosure: Takeda Consulting fee Speaking and teaching; Santarus Consulting fee Speaking and teaching

Coauthor(s)

Janice M Fields, MD, Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, William Beaumont Hospital, St. John Macomb-Oakland Hospital
Janice M Fields, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and National Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Robert J Fingerote, MD, MSc, BSc, FRCPC, Consultant, Clinical Evaluation Division, Biologic and Gene Therapies, Directorate Health Canada; Consulting Staff, Department of Medicine, Division of Gastroenterology, York Central Hospital, Richmond Hill, Ontario
Robert J Fingerote, MD, MSc, BSc, FRCPC is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.