CLINICAL MEDICINE

Ascites : Diagnosis and Management

Rita Sood*

Abstract
Ascites, the collection of fluid in the peritoneal cavity, occurs with a variety of disease states. It is one of the earliest and most
common complication of chronic liver disease. In cirrhosis, it is associated with circulatory dysfunction characterized by
arterial vasodilatation, high cardiac output and stimulation of vasoactive systems.
As appropriate treatment depends on accurate diagnosis, paracentesis should be performed in every patient with new onset
ascites to determine the cause and to detect potential complications. The treatment of ascites due to causes other than
chronic liver disease is based on the underlying disease. In ascites associated with chronic liver disease, a combination of low
sodium diet and the administration of diuretics remains the mainstay of therapy. Large volume paracentesis along with
infusion of albumin is the preferred treatment for refractory ascites. The recently introduced technique of transjugular
intrahepatic portosystemic shunt for the management of refractory ascites needs further evaluation.

Introduction
In clinical practice, the term ascites refers to the
detectable and pathologic collection of fluid in the
peritoneal cavity. Usually it is a clinical finding and
can be confirmed by a diagnostic paracentesis.
Subclinical amount of fluid (i.e., less than 1.5 litre)
can be detected using ultrasonography or computed
tomography of the abdomen.

Aetiology
Chronic liver disease with portal hypertension,
congestive cardiac failure, tuberculosis and
malignancy are important causes of ascites. However,
it can occur secondary to a number of pathological
conditions. Various causes of ascites are shown in
Table I1
Table I : Causes of Ascites
Venous hypertension
Cirrhosis of liver
Congestive cardiac failure
Constrictive pericarditis
Hepatic venous outflow obstruction
Acute portal vein thrombosis
Hypoalbuminemia
Cirrhosis of liver
Nephrotic syndrome
Malnutrition
Infections
Tuberculosis
Parasitic (strongyloidosis, entamoeba)

* Additional Professor, Department of Medicine

All India Institute of Medical Sciences,
New Delhi-110 029

Malignancies
Peritoneal carcinomatosis
Lymphomas and leukaemias
Primary mesothelioma
Miscellaneous
Chylous ascites
Systemic lupus erythematosus
Ovarian disease
Pancreatic ascites
Pseudomyxoma peritonei

Pathogenesis
In a large number of patients, cirrhosis of liver is the
cause of ascites. Several factors contribute to the
development of ascites in chronic liver disease. Kidney
plays a central role and is responsible for sodium
and water retention, through complex mechanisms.
The mechanism by which the diseased liver affects
renal function is not fully understood. The peripheral
arterial vasodilatation hypothesis proposed in 1988
is based on the presence of characteristic circulatory
abnormalities seen in cirrhotic patients2. These
patients show manifestations of increased cardiac
output, arterial hypotension, decreased peripheral
vascular resistance and splanchnic vasodilatation.
Possible causes for vasodilatation include
portosystemic shunting and/or impaired clearance of
vasodilator substances like nitric oxide, endotoxins,
prostacyclin, glucagon and adenosine. This peripheral
and splanchnic vasodilatation is perceived as
reduction in effective plasma volume. The effective
hypovolumia brings into play the baroreceptor
mediated activation of renin - angiotensin aldosterone system and sympathetic nervous system
which produce renal vasoconstriction and salt and

water retention (Fig. 1)2,3.

Cirrhosis
t
t

Portal hypertension

Deranged liver function

Portal-systemic shunt
t

Accumulation of vasodilator substances

(NO, Prostacyclin, Adenosine, Endotoxins)
Cytokines
t

Peripheral and splanchnic vasodilatation

t

Effective hypovolumia
t

Renin - angiotensin - aldosterone system

Antidiuretic hormone secretion
Sympathetic nervous activity
t
t

Renal
vasoconstriction

Sodium and
water retention

t
t

Increased
renal
prostaglandin
synthesis

Impaired
renal
prostaglandin
synthesis
(e.g. due to drugs)

Ascites formation

Preservation of
renal
haemodynamics

Renal failure

Figure 1 : Factors involved in initiation and maintenance of sodium retention

and renal dysfunction in patients with cirrhosis.

In patients with ascites, renal secretion of

prostaglandins, particularly PGE 2 may help to
preserve renal function by maintaining glomerular
filtration and free water clearance. When this renal
PGE2 production falls, perhaps due to renal deficiency
of the precursor arachidonic acid, renal function
deteriorates. Drugs which inhibit prostaglandin
synthetase e.g., NSAIDs may lead to deterioration of
renal function and should be avoided in these
patients. Other factors that contribute to ascites
formation in cirrhosis are:

82

decreased oncotic pressure of plasma due to

impaired albumin production by the liver;

portal hypertension which localizes the fluid within
the peritoneal cavity; and

an increased production of hepatic lymph due to
post-sinusoidal obstruction by the hepatic
nodules1.

In ascites associated with other conditions, the

pathogenesis depends on the cause. In congestive
cardiac failure, elevation of right sided cardiac
pressures results in the congestion of hepatic sinusoids
and leakage of fluid from the surface of liver. In
addition, reduction in effective blood volume leads
to sodium and water retention by the kidney4. In
ascites associated with non-hepatic malignant
disease, the pathogenesis depends on the type and
location of tumour5. In peritoneal carcinomatosis, the
most common cause of malignant ascites, the leakage
of protein rich fluid from the malignant cells causes
exudation of extracellular fluid into the peritoneal
cavity. Large liver tumours pressing on or growing
into the portal or hepatic veins can cause portal
hypertension and ascites. Infiltration of lymphatic
channels by malignant disease especially lymphoma
may lead to rupture of lymphatics and thereby
produce chylous ascites. Chylous ascites can also
occur after transection of lymphatics, such as after
abdominal surgery6. Filarasis is another uncommon
but important cause of chylous ascites.
Pancreatic ascites results from rupture of the
pancreatic duct or leakage of the pancreatic secretions
from a pseudocyst. Irritation of the peritoneum by
the pancreatic secretions can cause accumulation of
protein rich exudate in the peritoneal cavity. Biliary
ascites forms by similar mechanism. In infections such
as tuberculosis, the mechanism is similar to that in
carcinomatosis. There is leakage of protein rich fluid
into the peritoneal cavity by the inflamed peritoneum.
The mechanism of ascites in nephrotic syndrome and
dialysis associated ascites is unclear but is probably
related to volume expansion and abnormal peritoneal
permeability. Hypoalbuminaemia also contributes to
ascites in nephrotic syndrome.

Diagnosis
History
Ascitic fluid may accumulate rapidly or gradually
depending upon the cause. Mild ascites may not

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auscultatory percussion for detecting ascites has been

assessed using ultrasound of abdomen as gold
standard. It was observed that auscultatory percussion
has a greater sensitivity (66% Vs 45%) but a lower
specificity (48% Vs 68%) than the puddle sign8.

produce any symptoms. Moderate ascites may just

produce an increase in abdominal girth and weight
gain. Large amounts of fluid can produce abdominal
discomfort, appearance of hernias particularly
umbilical hernias and hinder the mobility of the
patient. Elevation of diaphragm and restriction of its
movements can produce breathlessness.

Physical examination can provide clues to the cause

of ascites in a given patient. Signs of chronic liver
disease, e.g., palmar erythema, spider naevi,
jaundice, etc. should be looked for. Presence of
splenomegaly and large collateral veins may suggest
portal hypertension. Patients with cardiac causes of
ascites may show engorged jugular veins. Collaterals
in the back may indicate an obstruction of the inferior
vena cava. Presence of enlarged lymph nodes may
suggest tuberculosis or lymphoma.

In many patients, a diagnosis of liver disease might

have been established earlier, as ascites develops later
when there is decompensation. However, ascites can
be the first sign of liver disease. Thus, it is important
to obtain a history of risk factors for liver disease like
alcohol consumption, drug abuse, blood transfusions
or hepatitis in the past. Sudden development of ascites
in a previously stable patient of cirrhosis should raise
the suspicion of hepatoma.

Investigations

A history of heart failure and pericardial disease

should make one suspect cardiac ascites. A history
suggestive of malignancy elsewhere, e.g., breast,
gastrointestinal tract, ovaries or lymphoma may
suggest malignant ascites. In India, tuberculosis as a
cause of ascites should be suspected if there is history
of fever, constitutional symptoms and in the presence
of known extra-abdominal tuberculosis. In patients
with pancreatic ascites there is usually a history
suggestive of chronic pancreatitis. The same patient
may have more than one disease predisposing to
ascites.

Abdominal paracentesis and analysis of ascitic

fluid
Abdominal paracentesis and a careful analysis of
ascitic fluid is the single most important procedure
and should be an early step in evaluating a patient
with ascites. It should be performed in all patients
with new onset ascites and whenever deterioration
occurs in a patient with known ascites. Paracentesis
can be performed easily and within minutes. The
procedure has been found to be safe with about 1
percent risk of abdominal wall haematoma9. This was
despite the fact that two-thirds of the patients, most
of whom had cirrhosis, had prolonged prothrombin
time. Therefore, it is unnecessary to routinely
administer fresh frozen plasma or platelets to cirrhotic
patients who have a coagulopathy before performing
paracentesis. Concerns regarding the introduction of
bacterial peritonitis are also unfounded9. As the midline caudal to the umbilicus is a relatively avascular
area, this site is recommended for paracentesis9,10.
Either of the lower quadrants may be used if there is
a surgical scar in the mid line. The bowel may adhere
to the abdominal wall near surgical scars and a
needle inserted close to a scar may enter the intestine.

Physical examination
Ascites needs to be differentiated from abdominal
distension due to other causes like gross obesity,
gaseous distention, bowel obstruction, abdominal
cysts or masses. The diagnosis may be obvious in
patients with massive ascites, but when only a small
or moderate amount of fluid is present, the accuracy
of physical assessment is only about 50%, even by
experienced gastroenterologists7. Flank dullness which
is present in about 90% of patients, is the most
sensitive physical sign. Shifting dullness on percussion
is more specific but less sensitive than flank dullness
for detection of ascites. A fluid thrill or wave may be
demonstrable in cases of tense ascites. Occasionally
massive ovarian or hydatid cysts and pregnancy with
hydramnios can masquerade as ascites as they can
also be associated with fluid thrill. The puddle sign,
reported to detect as little as 120 ml of fluid clinically
requires the patient to be in knee-elbow position
during examination. The utility of puddle sign and

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Analysis of the ascitic fluid is useful in the differential

diagnosis of ascites. The gross appearance of the
fluid may be helpful in determining the pathologic
process. In ascites due to portal hypertension or
hypoalbuminaemia, the fluid is clear and straw
coloured; turbid ascites may indicate infection.
Chylous ascites typically has a milky appearance.

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Blood stained fluid is usually due to malignancy but

may occur with tuberculosis, pancreatitis, hepatic vein
thrombosis, recent abdominal punctures or due to a
traumatic tap. Dark brown fluid may indicate the
presence of bile. The tests of ascitic fluid that are
frequently performed are shown in Table II. Routine
tests are performed on all the specimens. Optional
tests are performed on specimens for patients with
suspected infection of ascitic fluid, suspected
tuberculosis or malignant ascites.

The cell count is the single most important test

performed on the ascitic fluid. It provides immediate
information about the possible bacterial infection.
Samples with a predominance of neutrophils and an
absolute neutrophil count of > 250 per cubic mm
should be presumed to be infected. An elevated ascitic
fluid WBC count is seen in all inflammatory processes
and malignant ascites. Lymphocytes predominate in
tuberculosis. Cytological examination may reveal
malignant cells in malignant ascites.

Table II : Tests of Ascitic Fluid

Table III : Classification of types of ascites

according to the level of serum-ascites albumin
gradient (SAAG)

Routine Tests

Optional tests

Total protein

Grams stain & culture

Albumin

AFB smear & culture

Cell count

Cytology
Amylase
Lactate dehydrogenase (LDH)
Glucose

The total protein concentration of ascitic fluid has

traditionally been used to classify samples into the
broad categories of exudate or transudate. Low
protein ascites with total protein concentration of less
than 2.5 g per decilitre is called transudative ascites
and usually occurs with portal hypertension or
hypoalbuminaemia. A higher protein ascites with total
protein concentration of more than 2.5 g per decilitre
is called exudative ascites and is usually associated
with tuberculosis, malignancy, pancreatitis,
myxoedema, etc. However, a total protein
concentration of greater than 2.5 g per decilitre has
recently been shown to have an accuracy of only 56
percent in detecting an exudate11. The serum-ascites
albumin gradient (SAAG) has been found to be
superior to the ascites total protein concentration for
the differential diagnosis of ascites11,12. The gradient
is calculated by substracting the ascitic fluid albumin
level from the serum level obtained on the same day.
A gradient of more than 1.1 g per decilitre indicates
presence of portal hypertension with an accuracy of
97 percent. The SAAG correlates directly with portal
pressure13. An increasing hydrostatic pressure between
the portal vasculature and ascitic fluid is balanced by
corresponding difference in oncotic forces. In patients
with mixed causes of ascites, the SAAG tended to
resemble that in uncomplicated transudative ascites12.
A classification of the types of ascites according to
the level of serum-ascites albumin gradient is shown
in Table III14.

84

High gradient
(> 1.1 g/dl)

Low gradient
(< 1.1. g/dl)

Cirrhosis

Peritoneal tuberculosis

Alcoholic hepatitis

Peritoneal carcinomatosis

Cardiac failure

Pancreatic ascites

Massive liver metastasis

Biliary ascites

Fulminant hepatic failure

Nephrotic syndrome

Budd-Chiari syndrome

Serositis

Portal vein thrombosis

Bowel obstruction or infarction

Veno-occlusive disease
Fatty liver of pregnancy
Myxoedema
Mixed ascites
Adapted from Runyon 14

Culture of the ascitic fluid for bacteria should be

obtained routinely in patients with cirrhotic ascites,
in whom spontaneous bacterial peritonitis (SBP) can
occur. For optimal results, 10 ml of ascitic fluid
should be inoculated at the bedside into a blood
culture bottle15. Gram staining is useful in detecting
secondary peritonitis due to gut perforation but is
only about 10 percent sensitive in detecting bacteria
early in SBP16. In tuberculous peritonitis, the smear
for acid-fast bacilli (AFB) is rarely positive and
culture is positive only in about 50% of cases17.
Ascitic fluid glucose can drop significantly in severe
infections like secondary peritonitis or late stage
of SBP. Low glucose can also be found in malignant
ascites. Measurement of ascitic fluid amylase is
useful when there is suspicion of pancreatic ascites.
Chylous ascites may show Sudan staining fat
globules on microscopic examination and an
increased triglyceride content by chemical
examination. Triglyceride levels are low in

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74% of cases23. This procedure is rarely needed to detect

peritoneal carcinomatosis because of the sensitivity of
the cytology5.

pseudochylous ascites which can occur due to the

presence of large number of degenerating
malignant or inflammatory cells. Alkali will dissolve
cellular proteins and thus reduce turbidity in
pseudochylous fluid whereas extraction with ether
will lead to clearing if turbidity is due to lipid 18.
Rarely, fluid may be mucinous in character
suggesting pseudomyxoma peritonei.

Complications of Ascites
Umbilical hernia
Some patients may develop or may show an increase
in the size of already existent umbilical hernia . Most
hernias recur after surgical repair unless the ascites
is controlled.

Role of imaging
Radiologic studies are useful in detecting small amounts
of ascitic fluid as well as helpful in assessing the
aetiology of ascites19. Abdominal sonography may
detect as little as 100 ml of intraperitoneal fluid20.
Although sonography is more cost-effective than
computed tomography (CT), CT detects even smaller
amounts of ascitic fluid. The appearance of liver may
suggest cirrhosis. Pancreatic pseudocyst, intraabdominal tumours can be visualized. Doppler
sonography can detect thrombosis of the portal or
hepatic veins. In patients with tuberculous peritonitis,
thickening of mesentery and bowel wall, matting of
bowel loops and presence of mesenteric lymph nodes
may provide a clue21. In patients with small amount of
ascites, adhesions from previous surgery or where ascites
is compartmentalised, sonography can be an invaluable
guide for localising a safe and useful site for
paracentesis. CT may provide information that may be
difficult to obtain on ultrasonography. In patients with
carcinomatosis or inflammatory peritonitis, a contrast
enhanced CT scan may demonstrate enhancement of
the peritoneal lining. Similar results with peritoneal
abnormalities have recently been reported for magnetic
resonance imaging using gadolinium22. In patients with
pancreatic ascites alone or associated with liver cirrhosis,
endoscopic retrograde pancreatography with
fluoroscopy can demonstrate leakage of pancreatic juice
from the pancreatic duct. In patients with cirrhosis and
large hydrothorax, scintigraphy with Technetium sulfur
colloid or radiolabelled albumin can be used to
diagnose the intraperitoneal origin of the thoracic fluid.

Hydrothorax
Pleural effusion, particularly on the right side can
develop in some patients with ascites. It occurs due
to passage of fluid through small holes in the
diaphragm. These effusions may be very large.
Spontaneous bacterial peritonitis (SBP)
SBP is defined as the spontaneous bacterial infection
of the ascitic fluid without any apparent intraabdominal source. Most cases are seen in patients
with cirrhotic ascites. The risk for SBP is 15% within
the first 3 years after the onset of ascites24. SBP is
thought to occur as a result of prolonged bacteraemia
due to impaired host-defense mechanisms and
decreased bactericidal activity in the ascitic fluid.
Bactericidal activity parallels the total protein
concentration in the fluid. Prospective studies have
shown that SBP is 10 times more likely to develop in
patients with protein concentrations lower than 1 g/
dl during hospitalisation than in those with
concentration higher than 2 g/dl24.
Symptoms and signs of SBP can be very subtle and
non-specific. The most common features are fever
and abdominal pain, but patients may present with
hypotension or hepatic encephalopathy. SBP should
be suspected whenever sudden deterioration occurs
in a patient with ascites. Definitive diagnosis requires
bacterial culture of ascitic fluid. However, culture
negative SBP is common. The most important finding
in the ascitic fluid is an elevated neutrophil count. A
count of 250 cells/mm 3 or more is considered
diagnostic25. Most of the episodes are due to single
gram-negative enteric bacteria. Secondary bacterial
peritonitis should be suspected if the infection is
polymicrobial or if a patient with presumed SBP does
not respond to antibiotic therapy. Patients suspected
to have SBP should be treated empirically with

Laparoscopy
With the availability of new imaging techniques, the
need for laparoscopy in determining the cause of ascites
has decreased. However, if the diagnosis remains
unclear, laparoscopy with direct visualization of the
peritoneum may be indicated. Typical peritoneal
tubercles are found in most patients with tuberculous
peritonitis and peritoneal biopsies detect the disease in
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antibiotics without awaiting culture results, as they

can deteriorate rapidly. Cefotaxime, a third generation
cephalosporin, is the best studied antibiotic for treating
SBP. A 5-7 day course of parenteral antibiotics seems
to be sufficient. Aminoglycosides should be avoided
because of increased risk of nephrotoxicity in patients
with cirrhosis. Seventy percent of patients have another
episode of SBP within 1 year and the 1-year survival
rate is 38%26.
Strategies have been developed to prevent hospitalacquired SBP among susceptible patients, by selective
intestinal decontamination using oral antibiotics like
norfloxacin. It is recommended that SBP prophylaxis
with antibiotics should be restricted to cirrhotic patients
at high risk, including bleeding cirrhotic patients, those
with a past history of SBP, and those with low protein
content in the ascitic fluid27. However, prophylatic
treatment with antibiotics may prevent recurrence but
has not been proven to prolong survival28.

Treatment of Ascites
Ascites due to causes other than chronic liver
disease
Treatment of non-cirrhotic ascites is to be directed at
the underlying cause. Appropriate chemotherapy is
needed for infective causes. The management of
chylous ascites will depend upon the underlying cause.
However, a low fat diet with medium chain
triglycerides substituted for the normal long chain
triglycerides may help decrease the triglycerides
content of the ascitic fluid. Treatment of pancreatic
ascites is controversial. Some patients may respond
to conservative measures like salt restriction, diuretics
and IV hyperalimentation. Somatostatin infusion may
help by reducing the pancreatic exocrine secretion29.
Occasionally surgical or endoscopic intervention may
be needed.
The management of malignant ascites is an important
clinical problem when ascites causes severe
symptoms. Repeated therapeutic paracentesis is
required. If malignant cells are present in the ascitic
fluid and there are no intra-abdominal tumour
masses, palliation may be achieved in some patients
with chemosensitive malignancies by intraperitoneal
injection of the appropriate cytotoxic drug. In patients
without malignant cells in the ascitic fluid, a
peritoneovenous shunt may be of value in the control
of resistant ascites1.

86

Ascites due to liver disease

Ascites in cirrhosis generally occurs within 10 years
of diagnosis in about 50 % of patients. Patients
may present with moderate ascites, tense ascites,
refractory ascites, hyponatraemia, or with
hepatorenal syndrome. A thorough search should
be made for precipitating factors in patient with
recent onset or worsening ascites. The general
approach to management includes determining the
baseline body weight, serum electrolytes, urea and
creatinine and sodium concentration in a random
urine sample.
Sodium restriction, bed rest and use of diuretics are
the mainstay of therapy. The upright posture in
patients with cirrhosis and ascites has been reported
to be associated with marked activation of reninangiotensin-aldosterone and sympathetic nervous
system, reduction of glomerular filtration rate (GFR)
and sodium excretion and a decreased response to
loop diuretics 30. Thus, strict bed rest is often
recommended because of improved renal clearance
in supine position.
Sodium intake needs to be restricted to about 8001000 mg (2g NaCl) in order to induce a negative
sodium balance and permit diuresis. The factors
favourable to respond to bed rest and salt restriction
include recent onset ascites, a reversible liver disease,
correctable precipitating factor, high urinary sodium
excretion and normal renal function. In about 20%
of cirrhotics with ascites, urinary sodium
concentrations are relatively high. In these patients,
restriction of sodium and bed rest alone may result
in disappearance of ascites2. Fluid restriction is not
necessary unless hyponatraemia is present. In majority
of patients, a negative sodium balance can only be
achieved by increasing the urinary sodium excretion
with diuretics.
For a patient with mild to moderate ascites, therapy
can be undertaken as an outpatient and should be
gradual and incremental. The goal of diuretic
treatment is a loss of weight of not more than 1.0
kg/day if both ascites and edema are present and
not more than 0.5 kg/day in patients with ascites
alone3. Spironolactone, an aldosterone antagonist is
preferred as the initial diuretic. It decreases sodium
reabsorption in the distal tubule. The recommended
starting daily dose is 50 to 100 mg/day and a
maximum of upto 400 mg/day may be given in one
or more doses. Spironolactone may not provide
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effective than albumin in prevention of post

paracentesis circulatory dysfuction, particularly in
patients in whom more than 5 litres of ascitic fluid is
removed34. When these patients are discharged from
the hospital, they should be put on salt restriction and
diuretics to prevent reaccumulation of the fluid.

effective diuresis in all ascitic cirrhotic patients even

in adequate doses. The most important factor
determining the unresponsiveness to aldosterone
antagonists is the presence of renal failure. Addition
of a loop diuretic (furosemide) to spironolactone
potentiates the effect of both drugs and reduces the
risk of developing hyperkalaemia. A useful therapeutic
approach may be to add 40 mg of furosemide for
100 mg of spironolactone. The maximum dose of
diuretics recommended is a combination of
spironolactone 400 mg/day with furosemide 160 mg/
day.31 These patients should be monitored for weight
reduction, electrolytes, urea and creatinine. If a patient
fails to respond to these regimens, the physician
should suspect presence of some of the responsible
factors. These are, lack of compliance with salt
restriction, use of prostaglandin inhibitors like NSAIDs,
development of SBP, or progression of the underlying
disease32.

Management of refractory ascites

In about 10% of patients, the ascites is refractory to
treatment with first line measures mentioned above.
A new definition and diagnostic criteria of refractory
ascites has been proposed recently35. Refractory
ascites is now defined as the ascites that cannot be
mobilized or early recurrence of which (i.e. after
therapeutic paracentesis) cannot be satisfactorily
prevented by medical therapy. It includes two different
subtypes: diuretic resistant ascites and diuretic
intractable ascites, i.e., development of diuretic
induced complications that preclude the use of an
effective diuretic dosage. Most of these patients with
refractory ascites have severe disturbances of systemic
haemodynamics and renal function 36 . The
development of refractory ascites usually indicates
advanced underlying disease. The therapeutic options
for this group of patients are discussed below.

Thirty to fifty percent of patients develop complications

with diuretic therapy. These include hyponatraemia,
renal failure due to depletion of intravascular volume
and hepatic encephalopathy. Other side-effects
related to the use of spironolactone in cirrhotics are
decreased libido, impotence and gynaecomastia in
men, and menstrual irregularities in women. Muscle
cramps may often be present.

Repeated large volume paracentesis at intervals

of 2-3 weeks depending upon the severity of sodium
retention and the amount of fluid removed each time.
Many centres routinely perform total paracentesis on
such patients 36. This can be performed on an
outpatient basis. Ascites recirculation with removal,
concentration and reinfusion of peritoneal fluid has
been explored in USA and Japan. Technical problems
and life threatening complications like infection and
coagulopathy led to its unpopularity. The procedure
has been performed at some centres as the standard
therapy in diuretic refractory ascites37.

Patients with severe or tense ascites who are refractory

to diuretics should be treated with large volume
paracentesis. Five or more litres of fluid should be
removed to relieve dyspnoea, decrease early satiety,
and prevent pressure related leakage from the site of
paracentesis. Therapeutic paracentesis is
haemodynamically beneficial in patients with tense
ascites, contrary to the popular belief. Several
randomized controlled clinical trials have
demonstrated that large volume paracentesis with
intravenous albumin infusion induces a lower
incidence of complications than diuretic therapy.
Paracentesis associated with intravenous albumin
infusion (about 8 g of albumin per litre of ascitic fluid
removed) is considered to be the treatment of choice
in patients with tense ascites33. Albumin infusion is
required to prevent reduction in effective intravascular
volume. A cheaper alternative is to use dextran or
synthetic gelatins which are effective but may be
followed by slight circulatory disturbances. A
randomized controlled trial using the three substances
as plasma expanders after large volume paracentesis
has shown that dextran-70 or polygeline are less
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Peritoneovenous shunt (PVS) or LeVeen shunt was

introduced especially for the treatment of patients with
refractory ascites38. One limb of the shunt lies in the
peritoneal cavity and the other in the superior vena
cava close to the entrance of right atrium. A valve at
the venous end prevents backflow of blood into the
tubing. Flow is maintained by the peritoneovenous
pressure gradient. This technique produces a marked
increase in plasma volume and inhibits renin,
aldosterone, noradrenaline and anti-diuretic hormone
(ADH) concentrations leading to an increase in
diuresis, natriuresis and free water clearance. In
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addition, the procedure is also followed by an increase

in renal blood flow and GFR. However, despite these
positive effects of PVS, there are a large number of
complications which may occur early in the
postoperative period or at any time during follow up.
Serious complications include sepsis, peritonitis,
disseminated intravascular coagulation, and variceal
haemorrhage which could occur due to rise in portal
pressure. However, obstruction of the prosthesis is the
most common complication and occurs in 40-60%
of patients during first year of follow up39.
In a recently conducted multicentric controlled clinical
trial in cirrhotics with refractory ascites in which PVS
was compared to therapeutic paracentesis, it was
demonstrated that PVS is better than paracentesis in
the long-term control of ascites. However, it also
showed that PVS does not reduce the total hospital
stay and does not increase survival. Therefore,
paracentesis with intravenous albumin should be a
better alternative to PVS in the management of
refractory ascites40.
Surgical portosystemic shunts in which the portal
vein is used as an outflow tract (side to side portacaval
and mesocaval shunt). They relieve portal
hypertension and are effective in clearing ascites.
However, because of high incidence of hepatic
encephalopathy and of high surgical mortality in
patients with advanced liver disease, they are seldom
used nowadays41.
Transjugular intrahepatic portosystemic shunt
procedure (TIPS) which is a non-surgical portocaval
anastomosis and behaves like a side-to-side
portacaval shunt, has recently been proposed as an
effective treatment for refractory ascites42,43. In this
procedure, a tract is created between branches of
hepatic and portal veins, resulting in an intrahepatic
portosystemic shunt with a concomitant reduction in
portal pressure. The procedure is most commonly
used for the treatment of recurrent oesophageal
variceal bleeding. Its main advantage over the
traditional surgical shunts is a decrease in morbidity
and mortality related with the procedure. Experience
with TIPS procedure in treating ascites is still limited.
There are few published reports and most are
preliminary. Various studies have assessed the effects
of TIPS in patients with refractory ascites42,43. These
studies have shown that the insertion of TIPS is
associated with marked suppression of antinatriuretic

88

systems and an improvement in renal function and

in renal response to diuretics. However, TIPS may also
impair hepatic function and induce severe
encephalopathy44. Moreover, this procedure has an
additional problem of a high rate of shunt malfunction
due to stenosis of the stent or the hepatic vein segment
connecting with the prosthesis. Other technical
complications that can occur with TIPS include
haemobilia and biliary vascular fistula, liver
haematoma, stent migration and intra-abdominal
bleeding45. A randomized trial comparing TIPS with
paracentesis showed lower survival among patients
treated with TIPS46. At present, TIPS should be used
for refractory ascites only as a part of randomized
trials3.
Liver transplantation can cure ascites by replacing
the cirrhotic liver by a normal one. Overall, one year
survival after liver transplantation exceeds 75%47.
Patients with refractory ascites who are otherwise good
candidates for transplantation should be considered
for liver transplantation.

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