Related conditions


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Portal hypertension

Congestive heart failure

Budd-Chiari syndrome

Peritoneal metastases

1. Description of the problem

Ascites is the accumulation of fluid in the peritoneal cavity. It is commonly related to portal hypertension resulting from cirrhosis. Less common etiologies include cardiac failure, hepatic venous outflow obstruction and peritoneal metastases.

1. Symptoms: abdominal distention, abdominal discomfort, weight gain, shortness of breath, peripheral edema

2. Signs: distended abdomen with positive shifting dullness with or without a fluid thrill

3. Signs related to underlying etiology:

a. Cirrhosis – muscle mass loss, icteric sclera, spider angioma, palmar erythema, pedal edema, gynecomastia, prominent abdominal wall veins (caput medusae), palpable firm liver, palpable spleen

b. Heart failure – distended jugular veins, palpable thrills and murmurs, enlarged & pulsatile liver; constrictive pericarditis – pulsus paradoxus

c. Peritoneal malignancy – emaciation, palpable thickened omentum or mass

1. Establish diagnosis:

a. Check blood counts, liver profile, renal functions

b. Perform ultrasound imaging of liver and hepatic vessels

c. Determine ascitic fluid total protein, albumin, cell count and culture

2. Establish etiology:

a. Determine serum ascites albumin gradient (SAAG); if SAAG ≥1.1, evaluate for portal hypertension or cardiac failure; if <1.1, investigate for other causes.

b. CT or MRI abdomen with contrast if renal functions normal

c. Consider upper gastrointestinal endoscopy to evaluate for varices.

3. Treatment

a. Dietary salt restriction to a maximum of 2 gm sodium per day

b. Diuretics – combination of a loop diuretic (furosemide) and a potassium-sparing diuretic (spironolactone); maximize dosage and add thiazide or metolazone, if suboptimal response

c. Monitor serum electrolytes, BUN and creatinine; reduce diuretic dosage or hold if pre-renal failure develops.

d. Large-volume paracentesis if ascites intractable (persistent ascites despite maximization of diuretic dosages, development of severe hyponatremia or pre-renal failure); intravenous salt-poor albumin is infused if >5 liters of fluid are removed

e. Consider transjugular portosystemic shunt (TIPS) placement in patients with Child’s A/B cirrhosis with a low MELD score, if frequent paracentesis required despite dietary and diuretic compliance.

f. Treat underlying etiology of ascites (heart failure, hepatic outflow obstruction, malignancy, etc.).

2. Emergency Management

Emergency measures are required for large, tense ascites that causes dyspnea, hypoxia and/or severe abdominal discomfort. Such patients benefit from emergent large-volume paracentesis. Hypoxia in some patients is exacerbated by a hydrothorax that is often right-sided and is occasionally without significant ascites. Measures required include:

1. Correct hypoxia with inhaled oxygen via nasal cannulae or facial mask; endotracheal intubation is generally not needed except if patient has advanced hepatic encephalopathy.

2. Perform large-volume paracentesis; drain ascites continually if patient has no hemodynamic instability or pre-renal failure.

3. infuse intravenous salt-poor albumin if >5 liters of fluid drained or if there is associated renal insufficiency.

4. Perform thoracentesis if there is a large hydrothorax associated with collapse of the lung.

5. Evaluate ascitic fluid for spontaneous bacterial peritonitis by performing cell count and culture.

Drugs and dosages

Furosemide (Lasix): initial dose 40 mg daily by mouth to a maximum of 120 mg daily

Spironolactone (Aldactone); initial dose 100 mg daily to a maximum of 300 mg daily

Metolazone: 2.5-10 mg daily

Intravenous salt-poor albumin: 6-8 gms per liter of ascitic fluid removed

3. Diagnosis

The diagnosis is established by a combination of clinical evaluation, laboratory and imaging studies and possibly hepatic vein catheterization and a transjugular liver biopsy.

1. Determine presence of ascites by clinical evaluation via history and physical examination.

2. Confirm by abdominal ultrasound.

3. Perform diagnostic paracentesis and determine SAAG.

4. Determine etiology by performing laboratory and imaging studies.

5. Evaluate for other etiologies if there are no features of cirrhosis.

Diagnostic tests

1. Blood studies: Hb, white cell and platelet counts, creatinine, electrolytes, total and direct bilirubin, ALT, AST, alkaline phosphatase, gamma GTP, total protein, albumin, viral hepatitis and autoimmune serologies, alfa1-antitrypsin, ceruloplasmin and ferritin levels

2. Ultrasound abdomen with Doppler studies of hepatic vessels

3. Chest X-ray

4. CT or MRI abdominal scan with intravenous contrast, triphasic

5. Upper gastrointestinal endoscopy

6. Hepatic vein catheterization for portal pressure gradient measurement

7. Transjugular liver biopsy

8. Echocardiogram

9. Laparoscopy with peritoneal biopsies


The pathophysiology of ascites is dependent on the underlying cause. Sinusoids, the functional capillary unit of the liver, are characterized by highly permeable and fenestrated endothelium. Fluid homeostasis is normally maintained by a fine balance between the intravascular and extravascular hydrostatic and oncotic pressures.

The loss of hepatic architecture associated with cirrhosis results in intrasinusoidal hypertension, whereas hypoalbuminemia reduces intravascular oncotic pressure. In addition, nitric oxide release causes systemic and splanchnic vasodilation that enhances the renin-angiotensin-aldosterone system and also triggers ADH release, causing increased fluid retention.

These factors favor a net transfer of fluid into the peritoneal cavity until a new level of homeostasis is reached. Cardiac failure and hepatic outflow obstruction cause post-sinusoidal hypertension with similar consequences. Ascites secondary to infections and malignancy is a direct result of peritoneal inflammation and possible lymphatic outflow obstruction with a characteristically low SAAG of <1.1. The pathophysiology of ascites associated with conditions such as hypothyroidism and hemodialysis is poorly understood.


Chronic liver disease is the twelfth leading cause of death in the United States according to the Centers for Disease Control. In 2007, the age-adjusted death rate from liver disease per 100,000 population was noted to be 9.7. In comparison, the death rate from cardiac disease and malignant neoplasms was 204 and 187, respectively, and the death rate from all diseases was 804.

Ascites is the most common complication of cirrhosis and the most frequent reason for hospital admission among such patients. Over a period of 10 years, almost 50% of patients with well-compensated cirrhosis develop ascites. Once ascites develops, almost 50% would die or require liver transplantation by 5 years.

Special considerations for nursing and allied health professionals.


What’s the evidence?

Xu, JQ, Kochanek, KD, Murphy, SL, Tejada-Vera, B. “Deaths: Final data for 2007”. National vital statistics reports. vol. vol 58. 2010.