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The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid collection within the abdominal cavity. Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle. This article focuses only on ascites associated with cirrhosis.

See the image below.

Pathophysiology

The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation.

The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.

The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia.

The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis.

Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites.

Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.

Epidemiology

Mortality/Morbidity

Ambulatory patients with an episode of cirrhotic ascites have a 3-year mortality rate of 50%. The development of refractory ascites carries a poor prognosis, with a 1-year survival rate of less than 50%.^[1]

Sex

Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle.

History

See the list below:

• Patients with ascites often state that they have recently noticed an increase in their abdominal girth.
• Because most cases of ascites are due to liver disease, patients with ascites should be asked about risk factors for liver disease. These include the following:
• Long-term heavy alcohol use
• Chronic viral hepatitis or jaundice
• Intravenous drug use
• Multiple sexual partners
• Homosexual activity with a male partner, or heterosexual activity with a bisexual male
• Transfusion with blood not tested for hepatitis virus: in the United States, screening of donated blood for hepatitis B virus (HBV) began in 1972; reliable testing of the blood supply for hepatitis C virus (HCV) began in 1992 in developed countries
• Tattoos
• Living or birth in an area endemic for hepatitis
• Patients with alcoholic liver disease who alternate between heavy alcohol consumption and abstention (or light consumption) may experience ascites in a cyclic fashion.
• When a patient with a very long history of stable cirrhosis develops ascites, the possibility of superimposed hepatocellular carcinoma (HCC) should be considered.
• Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.
• Patients with a history of cancer, especially gastrointestinal cancer, are at risk for malignant ascites. Malignancy-related ascites is frequently painful, whereas cirrhotic ascites is usually painless.
• Patients who develop ascites in the setting of established diabetes or nephrotic syndrome may have nephrotic ascites.

Physical

The physical examination in a patient with ascites should focus on the signs of portal hypertension and chronic liver disease.

• Physical findings suggestive of liver disease include jaundice, palmar erythema, and spider angiomas.
• The liver may be difficult to palpate if a large amount of ascites is present, but if palpable, the liver is often found to be enlarged. The puddle sign may be present when as little as 120 mL of fluid is present. When peritoneal fluid exceeds 500 mL, ascites may be demonstrated by the presence of shifting dullness or bulging flanks. A fluid-wave sign is notoriously inaccurate.
• Elevated jugular venous pressure may suggest a cardiac origin of ascites. A firm nodule in the umbilicus, the so-called Sister Mary Joseph nodule, is not common but suggests peritoneal carcinomatosis originating from gastric, pancreatic, or hepatic primary malignancy.
• A pathologic left-sided supraclavicular node (Virchow node) suggests the presence of upper abdominal malignancy.
• Patients with cardiac disease or nephrotic syndrome may have anasarca.

Causes

See the list below:

• Normal peritoneum
• Portal hypertension (serum-ascites albumin gradient [SAAG] >1.1 g/dL)
• Hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome
• Liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure, massive hepatic metastases
• Hypoalbuminemia (SAAG < 1.1 g/dL)
• Nephrotic syndrome
• Protein-losing enteropathy
• Severe malnutrition with anasarca
• Miscellaneous conditions (SAAG < 1.1 g/dL)
• Chylous ascites
• Pancreatic ascites
• Bile ascites
• Nephrogenic ascites
• Urine ascites
• Ovarian disease
• Diseased peritoneum (SAAG < 1.1 g/dL)
• Infections
• Bacterial peritonitis
• Tuberculous peritonitis
• Fungal peritonitis
• Human immunodeficiency virus (HIV)-associated peritonitis
• Malignant conditions
• Peritoneal carcinomatosis
• Primary mesothelioma
• Pseudomyxoma peritonei
• Hepatocellular carcinoma
• Other rare conditions
• Familial Mediterranean fever
• Vasculitis
• Granulomatous peritonitis
• Eosinophilic peritonitis

Medical Care

Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard medical management for ascites and are effective in approximately 95% of patients.

• Water restriction is used only if persistent hyponatremia is present (see Diet, below).
• More recent research has focused on the treatment of refractory ascites with aquaretics—vasopressin V2-receptor antagonists that promote excretion of electrolyte-free water and thus might be beneficial in patients with ascites and hyponatremia.^[5] Although study results have been promising,^[6] aquaretics still await approval by the Food and Drug Administration (FDA).
• In a multicenter study that assessed the safety and efficacy of an automated pump system for the treatment of refractory ascites in 40 patients at 9 centers, Bellot et al reported the automated pump was an efficacious tool to remove ascites from the peritoneal cavity to the bladder.^[7] During the 6-month follow-up period, 90% of the ascites was removed with the pump system; there was also a significant reduction in the monthly median number of large volume paracentesis as well as a reduction in the number of cirrhosis-related adverse events.^[7]
• Therapeutic paracentesis may be performed in patients who require rapid symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid are removed, saline alone is an effective plasma expander.^[8] The removal of 5 L of fluid or more is considered large-volume paracentesis. Total paracentesis, that is, removal of all ascites (even >20 L), can usually be performed safely.
• Supplementing 5 g of albumin per each liter over 5 L of ascitic fluid removed decreases complications of paracentesis, such as electrolyte imbalances and increases in serum creatinine levels secondary to large shifts of intravascular volume. Note: The AASLD indicates that postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L ((class I, level C recommendation); however, for large-volume paracenteses, an albumin infusion of 6-8 g per liter of fluid removed appears to improve survival and is recommended (class IIa, level C recommendation).^[4]
• To avoid exposing patients to blood products, the use of terlipressin (eg, 1 mg every 4 hours for 48 hours) rather than albumin has been proposed for prevention of circulatory dysfunction after large-volume paracentesis. Initial studies suggest that terlipressin is as effective as albumin for this purpose.^{[9, 10]}
• Repeated therapeutic paracentesis can be used to treat refractory ascites (class I, level C recommendation).^[4] For palliative care in patients with advanced cancer, an alternative to serial paracenteses is placement of an indwelling peritoneal catheter; ascitic fluid can then be removed by continuous drainage^[11] or intermittent drainage with a proprietary system utilizing vacuum bottles, which can be performed in the patient’s home.^[12] Preservation of good nutrition status is important.^[13]
• The transjugular intrahepatic portosystemic shunt (TIPS) is an interventional radiologic technique that reduces portal pressure and may be the most effective treatment for patients with diuretic-resistant ascites. In the procedure, which is performed with the patient under conscious sedation or general anesthesia, an interventional radiologist places a stent percutaneously from the right jugular vein into the hepatic vein, thereby creating a connection between the portal and systemic circulations. TIPS is gradually becoming the standard of care in patients with diuretic-refractory ascites.

Diuretics

Diuretic agents are the mainstay of medical therapy in ascites.

Spironolactone (Aldactone)

For the management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions. The peak effect of Aldactone is approximately 3 d.

Furosemide (Lasix)

Increases the excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Dose must be individualized to patient.
Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until the desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until a satisfactory effect is achieved.

Amiloride (Midamor)

A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Metolazone (Mykrox, Zaroxolyn)

Helps treat edema in congestive heart failure. Increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be more effective in those with impaired renal function.

Mannitol (Osmitrol)

Inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular filtrate. Increases urinary output.

Differential Diagnoses

·         Acute Liver Failure

·         Alcoholic Hepatitis

·         Biliary Disease

·         Budd-Chiari Syndrome

·         Cirrhosis

·         Dilated Cardiomyopathy

·         Familial Mediterranean Fever

·         Hepatocellular Adenoma

·         Hepatorenal Syndrome

·         Nephrotic Syndrome

·         Portal Hypertension

·         Primary Biliary Cirrhosis

·         Protein-Losing Enteropathy

·         Restrictive Cardiomyopathy

·         Viral Hepatitis

Ascites

Ascites

The abdomen of a person with cirrhosis showing massive ascites and prominent superficial veins

Ascites (/əˈsaɪtiːz/ ə-SY-teez, from Greek askites, "baglike")^[1] is a gastroenterological term for an accumulation of fluid in the peritoneal cavity. The medical condition is also known as peritoneal cavity fluid, peritoneal fluid excess, hydroperitoneum or more archaically as abdominal dropsy. 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 Budd–Chiari 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.

Signs and symptoms

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 the diaphragm.
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

Causes of high SAAG ("transudate") are:^[2]

• 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^[3]
• Hereditary angioedema^[4]

Other Rare causes:

• Meigs syndrome
• Vasculitis
• Hypothyroidism
• Renal dialysis
• Peritoneum mesothelioma
• Abdominal tuberculosis

Diagnosis

Ascites in a person with abdominal cancer as seen on ultrasound

Routine complete blood count (FBC), 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.^[2]
The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.^[5] 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

Ascites exists in three grades:^[6]

• 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

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^[7]), 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 more white blood cells. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³. 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.^[2]
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, 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 hepatorenal syndrome. Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement.

Treatment

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.^[8] In those with severe ascites causing a tense abdomen, hospitalization is generally necessary for paracentesis.^[9][10]
Treatments in high SAAG ("transudate") are:

Diet

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.^[11] Water restriction is needed if hyponatremia < 130 mmol per liter develops.^[12]

Diuretics

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 distal-tubule diuretics such as triamterene or amiloride) 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.^[13] Diuretics for ascites should be dosed once per day.^[14] Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). 40% of patients will respond to spironolactone.^[11] 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.^[14] Serum potassium level and renal function should be monitored closely while on these medications.^[12]
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.^[8] 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.^[14] A random urine sodium-to-potassium ratio of > 1 is 90% sensitivity in predicting negative balance (> 78-mmol/day sodium excretion).^[15]
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.^[16]
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.^[17][18]

Paracentesis

Main article: Paracentesis

In those with severe (tense) ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above.^[9][10] As this may deplete serum albumin levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed.

Surgery

Ascites that is refractory to medical therapy is considered an indication for liver transplantation. In the United States, the MELD score (online calculator)^[19] 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 the transjugular 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 meta-analysis 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"^[20]

Low SAAG

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

Spontaneous bacterial peritonitis

Main article: Spontaneous bacterial peritonitis

Hepatorenal syndrome

Main article: Hepatorenal syndrome

Thrombosis

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

It has been suggested that ascites was seen as a punishment especially for oath-breakers among the Proto-Indo-Europeans.^[21] 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.

Ascites

• Manifestations of Liver Disease
• Overview of Liver Disease
• Ascites
• Cholestasis
• Fatty Liver
• Hepatic Encephalopathy
• Jaundice in Adults
• Liver Failure
• Portal Hypertension

Ascites is the accumulation of protein-containing (ascitic) fluid within the abdomen.

·         Many disorders can cause ascites, but the most common is high blood pressure in the veins that bring blood to the liver ( portal hypertension), which is usually due to cirrhosis.

·         If large amounts of fluid accumulate, the abdomen becomes very large, sometimes making people lose their appetite and feel short of breath and uncomfortable.

·         Analysis of the fluid can help determine the cause.

·         Usually, a low-sodium diet and diuretics can help eliminate excess fluid.

Ascites tends to occur in long-standing (chronic) rather than in short-lived (acute) disorders. It most commonly results from

·         Portal hypertension—high blood pressure in the portal vein (the large vein that brings blood from the intestine to the liver) and its branches

Portal hypertension usually results from cirrhosis (severe scarring of the liver), which is commonly caused by consumption of large amounts of alcohol or by viral hepatitis.
Ascites may occur in other liver disorders, such as severe alcoholic hepatitis without cirrhosis, chronic hepatitis, and obstruction of the hepatic vein ( Budd-Chiari syndrome).
Ascites can also occur in disorders unrelated to the liver, such as cancer, heart failure, kidney failure, inflammation of the pancreas (pancreatitis), and tuberculosis affecting the lining of the abdomen.
In people with a liver disorder, ascitic fluid leaks from the surface of the liver and intestine and accumulates within the abdomen. A combination of factors is responsible. They include the following:

·         Portal hypertension

·         Fluid retention by the kidneys

·         Alterations in various hormones and chemicals that regulate body fluids

Also, albumin usually leaks from blood vessels into the abdomen. Normally, albumin, the main protein in blood, helps keep fluid from leaking out of blood vessels. When albumin leaks out of blood vessels, fluid also leaks out.
Spontaneous bacterial peritonitis (infection of the ascitic fluid that develops for no apparent reason) sometimes occurs. This infection is common among people with ascites and cirrhosis, especially alcoholics.

Symptoms of Ascites

Small amounts of fluid within the abdomen usually cause no symptoms. Moderate amounts may increase the person's waist size and cause weight gain. Massive amounts may cause abdominal swelling (distention) and discomfort. The abdomen feels taut, and the navel is flat or even pushed out.
The swollen abdomen puts pressure on the stomach, sometimes leading to loss of appetite, and pressure on the lungs, sometimes leading to shortness of breath.
In some people with ascites, the ankles swell because excess fluid accumulates there (causing edema).
If spontaneous bacterial peritonitis develops, people usually have abdominal discomfort, and the abdomen may feel tender. People may have a fever and feel generally unwell. They may become confused, disoriented, and drowsy. Untreated, this infection can be fatal. Survival depends on early treatment with appropriate antibiotics.

Diagnosis of Ascites

·         A doctor's evaluation

·         Sometimes an imaging test such as ultrasonography

·         Sometimes analysis of ascitic fluid

When a doctor taps (percusses) the abdomen, the fluid makes a dull sound. However, a doctor may not be able to detect ascitic fluid unless the volume is about a quart or more.
If doctors are uncertain whether ascites is present or what is causing it, they may do ultrasonography or computed tomography (CT).In addition, a small sample of ascitic fluid can be withdrawn by inserting a needle through the wall of the abdomen—a procedure called diagnostic paracentesis. Laboratory analysis of the fluid can help determine the cause.

Treatment of Ascites

·         A low-sodium diet and bed rest

·         Diuretics

·         Removal of ascitic fluid (therapeutic paracentesis)

·         Sometimes surgery to reroute blood flow (portosystemic shunting) or liver transplantation

·         For spontaneous bacterial peritonitis, antibiotics

The basic treatment for ascites is a low-sodium diet and bed rest.
If diet is ineffective, people are usually also given drugs called diuretics (such as spironolactone). Diuretics make the kidneys excrete more sodium and water into the urine.
If ascites makes breathing or eating difficult, the fluid may be removed through a needle inserted into the abdomen—a procedure called therapeutic paracentesis. The fluid tends to reaccumulate unless people also follow a low-sodium diet and take a diuretic. Because a large amount of albumin is usually lost from the blood into the abdominal fluid, albumin may be given intravenously.
If large amounts of fluid accumulate frequently or if other treatments are ineffective, a portosystemic shunt or liver transplantation may be needed. The portosystemic shunt connects the portal vein or one of its branches with a vein in the general circulation and thus bypasses the liver. However, placement of the shunt is an invasive procedure and can cause problems, such as deterioration of brain function ( hepatic encephalopathy) and deterioration of liver function.
If spontaneous bacterial peritonitis is diagnosed, people are given antibiotics such as cefotaxime. Because this infection often recurs within a year, a different antibiotic (such as norfloxacin) is given after the initial infection resolves to prevent the infection from recurring.