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Ascites (/stiz/) (from Greek asktes, "baglike")[1] is

a gastroenterological term for an accumulation of fluid in the peritoneal


cavity that exceeds 25 mL.[2]
Although most commonly due to cirrhosis, severe liver disease or metastatic
cancer, its presence can be a sign of other significant medical problems, such
as BuddChiari syndrome. Diagnosis of the cause is usually with blood tests,
an ultrasound scan of the abdomen, and direct removal of the fluid by needle
or paracentesis (which may also be therapeutic). Treatment may be with
medication (diuretics), paracentesis, or other treatments directed at the cause.

Mild ascites is hard to notice, but severe ascites leads to abdominal


distension. Patients with ascites generally will complain of progressive
abdominal heaviness and pressure as well as shortness of breath due to
mechanical impingement on thediaphragm.
Ascites is detected on physical examination of the abdomen by visible bulging
of the flanks in the reclining patient ("flank bulging"), "shifting dullness"
(difference in percussion note in the flanks that shifts when the patient is
turned on the side) or in massive ascites with a "fluid thrill" or "fluid wave"
(tapping or pushing on one side will generate a wave-like effect through the
fluid that can be felt in the opposite side of the abdomen).
Other signs of ascites may be present due to its underlying cause. For
instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the
liver) patients may also complain of leg swelling,
bruising, gynecomastia, hematemesis, or mental changes due
to encephalopathy. Those with ascites due to cancer (peritoneal
carcinomatosis) may complain of chronic fatigue or weight loss. Those with
ascites due to heart failure may also complain of shortness of breath as well
as wheezing and exercise intolerance.

Causes[edit]
Causes of high SAAG ("transudate") are:[3]

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 (childhood protein-energy malnutrition)

Causes of low SAAG ("exudate") are:

Cancer (metastasis and primary peritoneal carcinomatosis) - 10%

Infection: Tuberculosis - 2% or Spontaneous bacterial peritonitis

Pancreatitis - 1%

Serositis

Nephrotic syndrome[4]

Hereditary angioedema[5]

Other rare causes:

Meigs syndrome

Vasculitis

Hypothyroidism

Renal dialysis

Peritoneum mesothelioma

Abdominal tuberculosis

Diagnosis[edit]

Ascites in a person with abdominal cancer as seen on ultrasound

Liver cirrhosis with ascites

Routine complete blood count (CBC), basic metabolic profile, liver enzymes,
and coagulation should be performed. Most experts recommend a
diagnostic paracentesis be performed if the ascites is new or if the patient with
ascites is being admitted to the hospital. The fluid is then reviewed for its
gross appearance, protein level, albumin, and cell counts (red and white).
Additional tests will be performed if indicated such as microbiological
culture, Gram stain and cytopathology.[3]
The serum-ascites albumin gradient (SAAG) is probably a better discriminant
than older measures (transudate versus exudate) for the causes of ascites.[6] A
high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A
low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive etiology.
Ultrasound investigation is often performed prior to attempts to remove fluid
from the abdomen. This may reveal the size and shape of the abdominal
organs, and Doppler studies may show the direction of flow in the portal vein,
as well as detecting Budd-Chiari syndrome(thrombosis of the hepatic vein)
and portal vein thrombosis. Additionally, the sonographer can make an
estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be
drained under ultrasound guidance. An abdominal CT scan is a more accurate
alternate to reveal abdominal organ structure and morphology.[citation needed]

Classification[edit]
Ascites exists in three grades:[7]

Grade 1: mild, only visible on ultrasound and CT

Grade 2: detectable with flank bulging and shifting dullness

Grade 3: directly visible, confirmed with the fluid wave/thrill test

Pathophysiology[edit]
Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to
35 liters are possible.
Roughly, transudates are a result of increased pressure in the hepatic portal
vein (>8 mmHg, usually around 20 mmHg[8]), e.g. due to cirrhosis, while
exudates are actively secreted fluid due to inflammation or malignancy. As a
result, exudates are high in protein, high in lactate dehydrogenase, have a
low pH (<7.30), a low glucose level, and morewhite blood cells. Transudates
have low protein (<30 g/L), low LDH, high pH, normal glucose, and fewer than
1 white cell per 1000 mm. Clinically, the most useful measure is the difference
between ascitic and serum albumin concentrations. A difference of less than 1
g/dl (10 g/L) implies an exudate.[3]
Portal hypertension plays an important role in the production of ascites by
raising capillary hydrostatic pressure within the splanchnic bed.
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, notablyaldosterone. 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 hepatorenal syndrome. Other complications of ascites include spontaneous
bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic
fluid such as complement.

Treatment[edit]

Diagram showing ascites being drained

Ascites is generally treated while an underlying etiology is sought, in order to


prevent complications, relieve symptoms, and prevent further progression. In
patients with mild ascites, therapy is usually as an outpatient. The goal is
weight loss of no more than 1.0 kg/day for patients with both ascites
and peripheral edema and no more than 0.5 kg/day for patients with ascites
alone.[9] In those with severe ascites causing a tense abdomen, hospitalization
is generally necessary for paracentesis.[10][11]
Treatments in high SAAG ("transudate") are:

Diet[edit]
Salt restriction is the initial treatment, which allows diuresis (production of
urine) since the patient now has more fluid than salt concentration. Salt
restriction is effective in about 15% of patients.[12] Water restriction is needed
if serum sodium levels drop below 130 mmol L1.[13]

Diuretics[edit]
Since salt restriction is the basic concept in treatment, and aldosterone is one
of the hormones that acts to increase salt retention, a medication that
counteracts aldosterone should be sought. Spironolactone (or other distaltubule diuretics such as triamterene oramiloride) is the drug of choice since
they block the aldosterone receptor in the collecting tubule. This choice has
been confirmed in a randomized controlled trial.[14] Diuretics for ascites should
be dosed once per day.[15] Generally, the starting dose is oral spironolactone
100 mg/day (max 400 mg/day). 40% of patients will respond to
spironolactone.[12] For nonresponders, a loop diuretic may also be added and
generally, furosemide is added at a dose of 40 mg/day (max 160 mg/day), or
alternatively (bumetanide or torasemide). The ratio of 100:40 reduces risks of

potassium imbalance.[15] Serum potassium level and renal function should be


monitored closely while on these medications.[13]
Monitoring diuresis: Diuresis can be monitored by weighing the patient daily.
The goal is weight loss of no more than 1.0 kg/day for patients with both
ascites and peripheral edema and no more than 0.5 kg/day for patients with
ascites alone.[9] If daily weights cannot be obtained, diuretics can also be
guided by the urinary sodium concentration. Dosage is increased until a
negative sodium balance occurs.[15] A random urine sodium-to-potassium ratio
of > 1 is 90% sensitivity in predicting negative balance (> 78-mmol/day sodium
excretion).[16]
Diuretic resistance: Diuretic resistance can be predicted by giving 80 mg
intravenous furosemide after 3 days without diuretics and on an 80 mEq
sodium/day diet. The urinary sodium excretion over 8 hours < 50 mEq/8 hours
predicts resistance.[17]
If a patient exhibits a resistance to or poor response to diuretic
therapy, ultrafiltration or aquapheresis may be needed to achieve adequate
control of fluid retention and congestion. The use of such mechanical methods
of fluid removal can produce meaningful clinical benefits in patients with
diuretic resistance and may restore responsiveness to conventional doses of
diuretics.[18][19]

Paracentesis[edit]
Main article: Paracentesis
In those with severe (tense) ascites, therapeutic paracentesis may be needed
in addition to medical treatments listed above.[10][11] As this may deplete serum
albumin levels in the blood, albumin is generally administered intravenously in
proportion to the amount of ascites removed.

Surgery[edit]
Ascites that is refractory to medical therapy is considered an indication
for liver transplantation. In the United States, the MELD score (online
calculator)[20] is used to prioritize patients for transplantation.
In a minority of people with advanced cirrhosis that have recurrent ascites,
shunts may be used. Typical shunts used are portacaval

shunt, peritoneovenous shunt, and thetransjugular intrahepatic portosystemic


shunt (TIPS). However, none of these shunts has been shown to extend life
expectancy, and are considered to be bridges to liver transplantation. A metaanalysis of randomized controlled trials by the international Cochrane
Collaboration concluded that "TIPS was more effective at removing ascites as
compared with paracentesis...however, TIPS patients develop hepatic
encephalopathy significantly more often".[21]

Low SAAG[edit]
Exudative ascites generally does not respond to manipulation of the salt
balance or diuretic therapy. Repeated paracentesis and treatment of the
underlying cause is the mainstay of treatment.
Complications[edit]

Spontaneous bacterial peritonitis[edit]


Main article: Spontaneous bacterial peritonitis

Hepatorenal syndrome[edit]
Main article: Hepatorenal syndrome

Thrombosis[edit]
Complications involve portal vein thrombosis and splenic vein thrombosis:
clotting of blood affects the hepatic portal vein or varices associated with
splenic vein. This can lead to portal hypertension and reduction in blood flow.
When a liver cirrhosis patient is suffering from thrombosis, it is not possible to
perform a liver transplant, unless the thrombosis is very minor. In case of
minor thrombosis, there are some chances of survival using cadaveric liver
transplant.

Society and culture[edit]


It has been suggested that ascites was seen as a punishment especially
for oath-breakers among the Proto-Indo-Europeans.[22] This proposal builds on
the Hittite military oath as well as various Vedic hymns (RV 7.89, AVS 4.16.7).
A similar curse dates to the Kassite dynasty (12th century BC), threatening
oath-breakers: "May Marduk, king of heaven and earth, fill his body
with dropsy, which has a grip that can never be loosened".[citation
needed]
Comparable is also Numbers 5:11ff, where a confirmed adulteress is
punished with swelling of the abdomen.

References[edit]
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