What Is Ascites?

Ascites is the presence of excess fluid in the peritoneal cavity. It is a common clinical finding with a wide range of causes, but develops most frequently as a part of the decompensation of previously asymptomatic chronic liver disease.

Pathogenesis

The pathogenesis of ascites formation has several contributing factors that are listed below.

Pathogenic Mechanisms in Ascites Formation

A) Increased hydrostatic pressure

1. Cirrhosis
2. Hepatic vein occlusion (Budd-Chiari syndrome)
3. Inferior vena cava obstruction
4. Constrictive pericarditis
5. Congestive heart failure

B) Decreased colloid osmotic pressure

1. End-stage liver disease with poor protein synthesis
2. Nephrotic syndrome with protein loss
3. Malnutrition
4. Protein-losing enteropathy

C) Increased permeability of peritoneal capillaries

1. Tuberculous peritonitis
2. Bacterial peritonitis
3. Malignant disease of the peritoneum

D) Leakage of fluid into the peritoneal cavity

1. Bile ascites
2. Pancreatic ascites(secondary to a leaking pseudocyst)
3. Chylous ascites
4. Urine ascites

E) Miscellaneous causes

1. Myxedema
2. Ovarian disease(Meigs’ syndrome)
3. Chronic hemodialysis

Clinical Manifestations and Diagnosis

The clinical manifestations of ascites can vary from an asymptomatic patient to patients complaining of increased abdominal girth, early satiety, and respiratory distress depending on the amount of fluid accumulated in the abdomen. On physical examination presence of ascites is suggested by the following findings:.

• Abdominal distension
• Bulging flanks
• Tympany of the top
• Fluid wave
• Shifting dulness
• Puddle sign

Ultrasonography can be peformed to detect or exclude the presence of fluid if the physical examination is not definitive, since abdominal USG can detect small amounts of fluid as 100 mL.

Abdominal Paracentesis

Abdominal paracentesis with analysis of the ascitic fluid should be done in patients with new onset ascites, those requiring hospitalization because of ascites and those whose condition deteriorates during hospitalization.

Analysis of Ascitic Fluid

The ascitic fluid should be analyzed for:

1. The serum-ascitic albumin gradient (SAAG) is calculated by subtracting the albumim concentration of the ascitic fluid from the albumin concentration of a serum specimen obtained on the same day.
2. The amylase concentration which is elevated in pancreatic ascites.
3. The triglyceride concentration which is elevated is chylous ascites.
4. White cell count when greater than 350/microliter is suggestive of infection. If most cells are polymorphonuclear, bacterial infection should be suspected. When mononuclear cells predominated , tuberculosis or fungal infection is likely.
5. Red cell count When greater than 50.000/microliter denotes hemorrhagic ascites, which usually is due to malignancy, tuberculosis or trauma.
6. Gram stain and culture which can confirm the diagnosis of bacterial infection.
7. pH when less than 7 suggests bacterial infection
8. Cytology can be positive in malignancy.

The serum-ascitic albumin gradient correlates directly with portal pressure, and patients with gradients greater than or equal to 1.1 g/dl have portal hypertension (transudative ascites) and patients with gradients lesser than 1.1 g/dl do not (exudative ascites). The total protein concentration of ascitic fluid and LDH activity has been traditionally used to classify ascitic fluid in exudate or transudate but they are not so accurate as SAAG. See table 2 with the classification of types of ascites according to the level of the serum-ascites albumin gradient.

table 2. Types of Ascites according to the level of the serum-ascites albumin gradient

High Gradient ( > or = 1.1 g/dl)

Cirrhosis
Alcoholic Hepatitis
Cardiac Failure
Fulminant Hepatic Failure
Portal-vein Thrombosis

Low Gradient

Peritoneal Carcinomatosis
Pancreatic ascites
Biliary ascites
Peritoneal Tuberculosis
Nephrotic Syndrome
Serositis
Bowel obstruction or infarction

Treatment

Monitoring

The treatment of ascites depends on it’s cause. In the majority of patients, cirrhosis leading to portal hypertension is the major cause. A particular value of recognizing portal hypertension as a cause of ascites is that medical management using diuretics and salt restriction is often effective in portal hypertensive patients. Conversely, ascites due to peritoneal inflammation or malignancy alone does not respond to salt restriction and diuretics.
The treatment can be attempted in an outpatient setting. However hospitalization may be necessary in three situations:

1. For investigations of the cause of liver disease;
2. Intensive education of the patient in preparing a diet limited to 88 mmol of sodium per day;
3. Careful monitoring of serum and urine electrolytes and serum concentration of urea nitrogen and creatinine.

At the hospital it’s important to monitoring body weight and the intake and output of fluids. Fluid restriction is only necessary if the serum sodium concentration drops below 120 mmol per liter. It is also important to determine the sodium balance which can be approximated by monitoring intake(diet, sodium-containing medications and intravenous solutions) and urinary excretion because, a negative sodium balance is a predictor of weight loss.

A reasonable goal for a patient without peripheral edema is a negative sodium balance with a weight loss of 0.5 Kg per day.

Drugs

Most patient with cirrhotic ascites respond to dietary sodium restriction and diuretics. The combination of spironolactone and furosemide is the most effective regimen for rapid diminution of ascites. The starting dose is 100 mg of Spironolactone and 40 mg of Furosemide together in the morning. If there is no decrease in body weight or increase in urinary sodium excretion after two or three days, the doses of both drugs should be increased. The doses of medication can be increased to 400 mg of Spironolactone per day and 160 mg of Furosemide per day.

Only 10% of patients do not respond to this medical approach (diuretics plus dietary sodium restriction) and in those who respond no other treatment for ascites is needed as long as it continues to be effective.

Diuretic-Resistant Ascites

Treatment options for ascites resistant to medical therapy include:

• Therapeutic Paracentesis
• LeVeen or Denver(peritoneovenous) shunt
• Liver transplantation
• Extracorporeal ultrafiltration of ascitic fluid with reinfusion
• Transjugular intrahepatic portosystemic stent shunt

Therapeutic Paracentesis

Paracentesis of up to 1 L of fluid may provide relief of acute respiratory embarrassment secondary to tense ascites. Removal of greater volumes and total paracentesis (largest reported volume, 22,5 L) are subject of discussion since some authors advocate the replacement of 10 g of albumin intravenously for each 1 L of ascitic fluid removed in order to prevent a reduction in plasma volume, abnormalities of electrolytes and creatinine. However it is not clear if the use of albumin or others volume expanders such as Dextran affects the morbidity and mortality.

 

References

Runyon BA : Care of patients with ascites. New England Journal of Medicine 330:337, 1994.

Runyon BA, Montano AA, Akriviadis EA et al : The serum-ascites gradient is superior to the exsudate-transudate concept in differential diagnosis of ascites. Ann Intern Med 117:215, 1992.

Diseases of the peritoneum, mesentery and omentum. In Wynngaarden JB, Smith LH, Bennet JC(eds): Cecil Textbook of Medicine, 20th edition. W B Saunders Company, 1996.

Cirrhosis of the liver and its major sequelae. In Wynngaarden JB, Smith LH, Bennet JC(eds): Cecil Textbook of Medicine, 20th edition. W B Saunders Company, 1996.

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