1.

2 ASCITIES
Ascites (also known as peritoneal cavity fluid, peritoneal fluid excess,
hydroperitoneum or more archaically as abdominal dropsy) is the accumulation of
fluid (usually serous fluid which is a pale yellow and clear fluid) in the peritoneal
cavity. The accumulation of fluid is caused by an imbalance of plasma flow into and
out of the blood and lymphatic vessels.
ETIOLOGY AND PATHOPHYSIOLOGY
Table 1.2a ETIOLOGY OF ASCITIES
Liver Non-liver
• Hepatitis B cirrhosis • Malignancy
• Hepatitis C cirrhosis • Congestive heart failure
• Cryptogenic cirrhosis • Nephrotic syndrome
• Hepatoma • Peritoneal tuberculosis

(Timm EG, Stragand JJ.2005)

PATHOPHSIOLOGY
• CIRRHOSIS:
The most common cause of Ascites is advanced liver disease or cirrhosis.
Approximately 80% of the Ascites cases are thought to be due to cirrhosis. Most
theories suggest portal hypertension as the main contributor. The increase in portal
blood pressure and decrease in albumin may be responsible in forming the pressure
gradient and resulting in abdominal ascites. Regardless of the cause, sequestration of
fluid within the abdomen leads to additional fluid retention by the kidneys due to
stimulatory effect on blood pressure hormones, notably aldosterone. The sympathetic
nervous system is also activated, and renin production is increased due to decreased
perfusion of the kidney.Extreme disruption of the renal blood flow can lead to the
feared hepatorenal syndrome
• SALT AND RETENTION:
Salt and water retention may contribute to Ascites. The circulating blood volume may
be perceived low by the sensors in the kidneys as the formation of Ascites, may
deplete some volume from the blood. This signals the kidneys to reabsorb more salt
and water to compensate for the volume loss.
• CONGESTIVE HEART FAILURE:
Ascites related to increased pressure gradient are congestive heart failure and
advanced kidney failure due to generalized retention of fluid in the body
• OBSTRUCTION OF THE PORTAL VESSEL:
In rare cases, increased pressure in the portal system can be caused by internal or
external obstruction of the portal vessel, resulting in portal hypertension without
cirrhosis. Examples of this can be a mass pressing on the portal vessels from inside
the abdominal cavity or blood clot formation in the portal vessel obstructing the
normal flow and increasing the pressure in the vessel (for example, the Budd-Chiari
syndrome).

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 • MALIGNANT ASCITES:
Ascites formation as a result of cancers, called malignant ascites. These types of
ascites are typically manifestations of advanced cancers of the organs in the
abdominal cavity, such as, colon cancer, pancreatic cancer, stomach cancer, breast
cancer, lymphoma, lung cancer, or ovarian cancer.

• PANCREATIC ASCITES:
Pancreatic Ascites can be seen in people with chronic pancreatitis.The most common
cause of chronic pancreatitis is prolonged alcohol abuse. Pancreatic ascites can also
be caused by acute pancreatitis as well as trauma to the pancreas. (Timm EG,
Stragand JJ.2005)

Cirrhosis/portal hypertension

↑Nitric oxide

Systemic/ Splanchinic vasodilatation

↓Effective arterial blood volume

Activation of renin-angiotensin aldosterone

system

Hyper dynamic circulation Sodium and water retention Renal vasoconstriction

ASCITES
FIGURE 1.2a. Pathogenesis of ascites.

TYPES AND CLASSIFICATION OF ASCITIES

1. UNCOMPLICATED ASCITES
Ascites that is not infected and which is not associated with the development of the
hepatorenal syndrome. Ascites can be graded as follows:
• Grade 1 (mild): Ascites is only detectable by ultrasound examination.
• Grade 2 (moderate): Ascites causing moderate symmetrical distension of the
abdomen.
• Grade 3 (tense): Ascites causing marked abdominal distension.

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 2. REFRACTORY ASCITES
Ascites that cannot be mobilised or early recurrence of which (that is, after
therapeutic paracentesis) cannot be satisfactorily prevented by medical therapy.
This includes two different subgroups.
• Diuretic resistant ascites: ascites that is refractory to dietary sodium
restriction and intensive diuretic treatment (spironolactone 400 mg/day and
frusemide 160 mg/day for at least one week, and a salt restricted diet of less
than 90 mmol/day (5.2 g of salt/day).
• Diuretic intractable ascites: ascites that is refractory to therapy due to the
development of diuretic induced complications that preclude the use of an
effective diuretic dosage

BASED ON THE AMOUNT OF PROTEIN FOUND IN THE

FLUID
Ascites is divided into 2 types based on protein content;
• Transudative are a result of increased pressure in the portal vein (>8 mmHg,
usually around 20 mmHg, e.g. due to cirrhosis, Transudates have low protein
(<30g/L), low LDH, high pH, normal glucose, and less than 1 white cell per
1000 mm³.
• Exudative are actively secreted fluid due to inflammation or malignancy.
exudates are high in protein, high in lactate dehydrogenase, have a low pH
(<7.30), a low glucose level, and more white blood cells.

BASED ON THE SERUM ASCITES ALBUMIN GRADIENT or

SAAG

That is amount of albumin in the ascitic fluid compared to the serum albumin (albumin
measured in the blood). (Moore KP, Wong F, Gines P,et al.2003)
Table 1.2b TYPES AF ASCITIES AND SAAG (Serum ascites-albumin gradient)
ASCITIES RELATED TO PORTAL SAAG VALUE
HYPERTENSION
• Cirrhosis
• Congestive heart failure, Generally greater than 1.1.
• Budd-Chiari
• Nephrotic syndrome
ASCITIES RELATED TO OTHER REASONS
• Malignant Is lower than 1.1.
• Pancreatitis
• Tuberculosis

RISK FACTORS FOR ASCITIES

Many of the risk factors for developing ascites and cirrhosis are similar including
• Hepatitis B
• Hepatitis C

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 • Long standing alcohol abuse.
• Other are related to the other underlying conditions, such as congestive heart
failure, malignancy, and kidney disease
CLINICAL FEATURES OF ASCITIES
• Abdominal pain, discomfort, and bloating are also frequently seen as ascites
becomes larger.
• Complain of progressive abdominal heaviness and pressure as well as
shortness of breath with large ascites due to increased pressure on the
diaphragm and the migration of the fluid across the diaphragm causing
pleural effusions (fluid around the lungs).
• Mild ascites is hard to notice, but severe ascites leads to abdominal distension
• A cosmetically disfiguring large belly, due to ascites, is also a common
concern of some patients.
There may be no symptoms associated with ascites especially if it is mild (usually
less than about 100 – 400 ml in adults). (Timm EG, Stragand JJ, 2005)
LAB FINDINGS
In patients with new-onset ascites of unknown origin, peritoneal fluid should be sent
for cell count, albumin level, culture, total protein, Gram stain, and cytology. (Shah
R, Fields JM. 2009)
Table 1.2c : LAB FINDING
• Inspection Most ascitic fluid is transparent and tinged yellow. A minimum of
10,000 red blood cells/µL is required for ascitic fluid to appear
pink, and more than 20,000 red blood cells/µL will produce
distinctly blood-tinged fluid.
• Cell count Normal ascitic fluid contains fewer than 500 leukocytes/µL and
fewer than 250 polymorphonuclear leukocytes (PMNs)/µL. Any
inflammatory condition can cause an elevated white blood cell
count. A PMN count of greater than 250 cells/µL is highly
suggestive of bacterial peritonitis. In tuberculous peritonitis and
peritoneal carcinomatosis, lymphocytes usually predominate.
• SAAG The SAAG is the best single test for classifying ascites into portal
hypertensive (SAAG >1.1 g/dL) and non–portal hypertensive
(SAAG <1.1 g/dL) causes. Calculated by subtracting the ascitic
fluid albumin value from the serum albumin value, it correlates
directly with portal pressure.
• Total protein An elevated SAAG and a high protein level are observed in most
cases of ascites due to hepatic congestion. The combination of a
low SAAG and a high protein level is characteristic of malignant
ascites.
• Culture/Gram Culture has a 92% sensitivity for the detection of bacteria in
stain: ascitic fluid
• Cytology Sensitive for detection of malignant ascites
• Imaging • Chest and plain abdominal films
studies • Ultrasonography

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 • Other Tests • Laparoscopy Computed tomography (CT) scanning

Table 1.2d: DIFFERENTIAL DIAGONOSIS OF ASCITIES AND SAAG

INTERPRETATION (Runyon BA, Montano AA, Akriviadis EA,et al.1992)
Gradient ≥1.1 g/dl (portal Gradient <1.1 g/dl
hypertension)
• Cirrhosis
• Alcoholic hepatitis
• Cardiac ascites
• Portal-vein thrombosis
• Budd–Chiari syndrome
• Liver metastases
Causes of high SAAG ("transudate")
• Cirrhosis - 81% (alcoholic
in 65%, viral in 10%,
cryptogenic in 6%)
• Heart failure - 3%
• Hepatic Venous occlusion:
• Budd-Chiari syndrome or
• Veno-occlusive disease
• Constrictive pericarditis
• Kwashiorkor
• Peritoneal carcinomatosis
• Tuberculous peritonitis
• Pancreatic ascites
• Biliary ascites
• Nephrotic syndrome
• Liver metastases Serositis
Causes of low SAAG ("exudate”)
• Cancer (primary peritoneal
carcinomatosis and metastasis) -
10%
• Infection: Tuberculosis - 2% or
Spontaneous bacterial peritonitis
• Pancreatitis - 1%
• Serositis
• Nephrotic syndrome or Protein
losing enteropathy
• Hereditary angioedema

COMPLICATIONS
• Spontaneous Bacterial Peritonitis
• Hepatorenal Syndrome
• Complications Of Paracentesis
(Bataller R, Gines P, 2005)

MANAGEMENT
Ascites is generally treated while an underlying etiology is sought, in order to
prevent complications, relieve symptoms, and prevent further progression.
Table 1.2e TREATMENT OF ASCITIES IN CASE OF
1.HIGH SAAG 2.LOW SAAG
Medical Care • Exudative ascites generally does
• Salt restriction not respond to manipulation of the
• Diuretics salt balance or diuretic therapy.
• Water restriction • Repeated paracentesis and
• Paracentesis treatment of the underlying cause is
• Surgical care the mainstay of treatment
• Liver transplantation
• Shunting

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NON PHARMACOLOGICAL TREATMENT
• Bed rest is not recommended for the treatment of ascites.
• Dietary salt should be restricted to a no added salt diet of 90 mmol salt/day
(5.2 g salt/day).
PHARMACOLOGICAL TREATMENT
Table 1.2f :GENERAL PHARMACOLOGICAL TREATMENT
Hyponatremia • Serum sodium 126–135 mmol/L, normal serum creatinine.
Continue diuretic therapy, but observe serum electrolytes. Do
not restrict water.
• Serum sodium 121–125 mmol/L, normal serum creatinine.
International opinion is to continue diuretic therapy, our
opinion is to stop diuretic therapy or adopt a more cautious
approach. Serum sodium 121–125 mmol/L, serum creatinine
elevated 150 mmol/L diuretics and give volume expansion.
• Serum sodium 120 mmol/L, stop diuretics. The management
of these patients is difficult and controversial. We believe that
most patients should undergo volume expansion with colloid
(haemaccel, gelofusine, or voluven) or saline. However, avoid
increasing serum sodium by .12 mmol/L per 24 hours
• Firstline treatment of ascites should be spironolactone alone,
Diuretics increasing from 100 mg/day to a dose of 400 mg/day.
• If this fails to resolve ascites, frusemide should be added in a
dose of up to 160 mg/day but this should be done with careful
biochemical and clinical monitoring.
• Therapeutic paracentesis is the first line treatment for patients
Therapeutic with large or refractory ascites.
paracentesis • Paracentesis of 5 litre of uncomplicated ascites should be
followed by plasma expansion with a synthetic plasma
expander (150–200 ml of gelofusine or haemaccel), and does
not require volume expansion with albumin.
• Large volume paracentesis should be performed in a single
session with volume expansion being given once paracentesis
is complete, preferably using 8 g albumin/l of ascites removed
(that is 100 ml of 20% albumin/3 l ascites).
TIPS procedure TIPS could be used for the treatment of refractory ascites requiring
frequent therapeutic paracentesis or thepatic hydrothorax with
appropriate assessment of risk benefit ratio.
Liver • Liver transplantation should be considered in patients with
transplantation cirrhotic ascites.
• All patients with SBP should be considered for referral for
liver transplantation.

(Garcia-Tsao G, Lim Joseph .2009)

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FOR REFRACTORY ASCITES
Table 1.2g MANAGEMENT STRATEGY FOR REFRACTORY ASCITES
Definitions • Ascites that is not eliminated even with maximum diuretic
therapy
• Ascites that is not eliminated because maximum dosages of
diuretics cannot be attained, given the development of diuretic-
induced complications
Recommended • Total paracentesis + i.v. albumin (6 – 8 g /L of ascites removed)
therapy • If < 5 L of ascites is removed, a synthetic plasma volume
expander may be used instead of albumin
• Continue with salt restriction and diuretic therapy as tolerated
Alternative • TIPS for patients who require frequent paracentesis (every 1 – 2
therapy weeks) and whose CTP score is <11
• Peritoneovenous shunt for patients who are not TIPS or
transplant candidates
CTP, Child – Turcotte – Pugh; i.v., intravenous; TIPS, transjugular intrahepatic portosystemic shunt.

FOR UNCOMPLICATED ASCITES

Table 1.2h : MANAGEMENT STRATEGY IN UNCOMPLICATED ASCITES
• Treat ascites once other complications have been treated
General • Avoid NSAIDs
management • Norfloxacin prophylaxis (400 mg p.o. q.d.) in patients with an
ascites protein level of < 1.5 g / dl, impaired renal function
(serum creatinine level ≥ 1.2 mg / dl, BUN ≥ 25 mg / dl, serum
sodium level ≤ 130 mEq / l), or severe liver failure (CTP score ≥
9 points with serum bilirubin level ≥ 3 mg / dl)
Salt restriction • Liberalize if restriction results in poor food
Specific 1 – 2 g / day
intake
management Diuretics • Spironolactone alone (start at 50 – 100 mg
Spironolactone based
q.d., single morning dose)
• Or Spironolactone (50 – 100 mg q.d.) +
frusemide (start at 20 – 40 mg q.d., single
morning dose
• Use as initial therapy only in patients with
LVP
tense ascites; administer intravenous
albumin (6 – 8 g / l of ascites removed)

FOLLOW-UP AND GOALS

• Adjustment of diuretic dosage should be performed every 4 – 7 days
• Patient should be weighed at least weekly and BUN, creatinine, and
electrolytes measured every 1 – 2 weeks while adjusting dosage
• Double dosage of diuretics if: Weight loss < 4 lb (2 kg) a week and BUN,
creatinine, and electrolytes are stable
• Halve the dosage of diuretics or discontinue if: Weight loss ≥ 1 lb (0.5 kg /
day) or if there are abnormalities in BUN, creatinine, or electrolytes

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• Maximum diuretic dosage is spironolactone (400 mg q.d.) and frusemide
(160 mg q.d.)

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