Ascites

Define :  Ascites refers to the excessive accumulation of free fluid in the peritoneal cavity.

• Small amount of ascites are asymptomatic.
• But with larger accumulations of fluid (> IL) there is abdominal distension, fullness of the flanks, shifting dullness on percussion.
• When the ascites is marked, a fluid thrill present.

Causes of ascites:

A) Common causes:

1. Chronic liver disease & liver cirrhosis.
2. Malignant disease: Hepatic, peritoneal.
3. Congestive cardiac failure.

B) Other causes :

1. Hypoproteinaemia: Nephrotic syndrome, protein-losing enteropathy, malnutrition
2. Pancreatitis
3. Lymphatic obstruction
4. Infection: Tuberculosis, spontaneous bacterial peritonitis (SBP)
5. Hepatic venous occlusion: Budd-Chiari syndrome, veno-occlusive disease.

C) Rare causes:

1). Meigs syndrome.

2) Hypothyroidism

Types of ascites :

1) Exudative:

• Ascites protein concentration above 25 gm/l.
• Serum ascites albumin gradient of less than 11 gm/1.

2) Transudative:

• Ascites protein concentration below 25 gm/l.
• Serum ascites albumin gradient of more than 11 gm/1.

Important causes of ascites with pedal oedema.

Ascites with pedal oedema:

1. Liver cirrhosis
2. Congestive cardiac failure.
3. Nephrotic syndrome
4. PEM (Kwashiorkor)
5. IVC obstruction
6. Hypothyroidism

Ascitic fluid (appearance & analysis):

• Cirrhosis: Clear, straw-coloured or light green.
• Malignant disease: Bloody.
• Infection: Cloudy.
• Biliary communication: Heavy bile staining.
• Lymphatic obstruction: Milky-white (chylous).

Management of Ascites:

History:

• Onset and progression of symptoms.
• Past history of jaundice, haematemesis, tuberculosis, rheumatic heart disease etc.
• Personal history-Alcoholism
• Family history-e.g. cirrhosis, Wilson’s disease, haemochromatosis.
• History of heart disease and renal disease.

Clinical examination:

General examination:

1. Hepatic facies.
2. Higher cerebral functions: Confusion, disorientation, disturbed sleep pattern.
3. Puffiness of face with periorbital oedema: Nephrotic syndrome.
4. Lymphadenopathy: Tuberculosis, malignancy, collagen vascular disorders.
5. Raised JVP & cyanosis: Heart failure.
6. Clubbing of fingers.
7. Stigmata of CLD: Spider naevi, gynaecomastia, testicular atrophy, loss of axillary and pubic hair etc.
8. Palmar erythema.
9. Pedal oedema.
10. Signs of nutritional deficiency: Angular stomatitis, cheilosis, anaemia, atrophy of tongue, muscle wasting and pigmentation of tongue and mucous membranes.

Abdominal findings:

1) Abdominal distension with fullness in the flanks.

2) Dilated superficial abdominal veins.

3) Eversion of the umbilicus.

4) Abdominal striae.

5) Shifting dullness on percussion

6) When the ascites is marked, a fluid thrill is present.

7) Associated features of ascites:

• Distortion or eversion of the umbilicus.
• Herniae
• Abdominal striae.
• Divancation of the recti and scrotal oedema
• Pleural effusions are found in about 10% of patients
• Splenomegaly
• Hepatomegaly

Investigations of ascites:

1) Ascitic fluid analysis:

• Appearance (discussed above).
• Ascitic albumin (plus serum albumin)
• White cell count.
• Cytology for malignant cells.
• Microscopy and culture.
• Ascitic amylase (mcreased in ascites due to pancreatitis).

2) Serum albumin & total protein.

3) USG of the whole abdomen.

4) Liver function tests (if CLD suspected).

5) CBC with ESR for detecting infection.

6) Chest X ray for TB, cardiomegaly, chronic constrictive pericarditis.

7) CT or MRI for detection of any growth or mass.

Treatment of Ascites : 

1) Sodium and water restriction:

• Daily sodium intake less than 100 mmol.
• No added salt.
• Restriction of water intake to 1-1.5 L/day.
• Na+ retaining drug (NSAIDs, corticosteroid) should be avoided.

2) Diuretic drugs:

• Spironolactone (100-400 mg/day) is the drug of choice for long-term therapy because it is a powerful aldosterone antagonist but it can cause painful gynaecomastia and hyperkalaemia.
• Some patients will also require powerful loop diuretics; eg furosemide.

3) Paracentesis: 3-5 litres daily is safe, provided the circulation is supported by giving intravenous colloid such as human albumin (6-8 gm per litre of ascites removed) or another plasma expander.

4) Peritoneo-venous (LeVeen) shunt:  The peritoneo-venous shunt is a long tube with a non- return valve running subcutaneously from the peritoneum to the internal jugular vein in the neck, which allows ascitic fluid to pass directly into the systemic circulation

5) Transjugular intrahepatic portosystemic stent shunt (TIPSS).

B) Specific treatment:  According to diagnosis. Read also more about Ascites.

Some Important information about ascites.

Ascitic fluid is sent in three departments:

• Bio-chemistry department for biochemical examination (protein, sugar, ADA).
• Pathology department for cytological examination (WBC counts, malignant cells).
• Microbiology department for staining (Gram & AFB), culture and sensitivity.

Refractory ascites: Patients who do not respond to doses of 400 mg spironolactone and 160 mg furosemide are considered to have refractory or diuretic-resistant ascites and should be treated by other therapeutic measures.

Drugs containing relatively large amount of sodium or causing sodium retention:

High sodium content:

• Antacids
• Alginates.
• Antibiotics.
• Phenytoin.
• Sodium valproate
• Effervescent preparations; e.g. Aspirin, Calcium, Paracetamol.

Sodium retention : 

• Corticosteroids
• NSAIDs.
• Oestrogens.
• Metoclopramide
• Carbenoxolone.