Ascites

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Ascites is defined as fluid accumulation of more than 25 mL in the peritoneal cavity. Ascites may be classified according to etiology into four groups include portal hypertension, hypoalbuminemia, peritoneal disease, and other diseases. Ascites is also classified based on the Serum-ascites albumin gradient (SAAG) as two subtypes include transudate – SAAG > 1.1 g/dL and exudate – SAAG < 1.1 g/dL. Ascites is excess accumulation of fluid in the peritoneal cavity. The fluid can be defined as a transudate or an exudate. Amounts of up to 25 liters are fully possible. Roughly, transudates are a result of increased pressure in the portal vein (> 8 mmHg), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy. The most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1.1 g/dl (10 g/L) implies an exudate. There is no genetic background for ascites. On gross pathology, clear to pale yellow fluid accumulation in peritoneal space are characteristic findings of ascites under normal condition, but it may be chylous, psudochylous, or bloody. Paracentesis is sampling ascites fluid through abdominal wall with overall complication rate of not more than 1%. The sampled fluid will be surveyed upon total protein concentration, neutrophil count, and inoculation into blood culture bottles. The mainstays of first-line treatment of patients with cirrhosis and ascites include (1) education regarding dietary sodium restriction (2000 mg per day [88 mmol per day]) and (2) oral diuretics. Medical therapy is based on different grades of ascites. Medical therapy would inhibit different processes in pathophysiology of ascites. First-line treatment of patients with cirrhosis and ascites consists of sodium restriction (88 mmol per day [2000 mg per day], diet education), and diuretics (oral spironolactone with or without oral furosemide).

About 20 BC, Aulus Cornelius Celsus (A.D. 30), a Roman encyclopedist explained in his book “De Medicina” three different types of fluid accumulation under the skin; which was called hydrops by Greeks. Celsus postulated that ascites is mostly secondary to quartan fever (malaria) in Rome. The principles of treatment for ascites were explained as thirst, rest, and abstinence. Drinking less fluid and sweating more, not with exercise, but with heated sand, or in the sweating-room, or with a dry oven and such- like were the other alternative therapies. In 1827, Ludwig van Beethoven involved in ascites and underwent large volumes of paracenteses. His physician write about him as “Beethoven had almost immediate relief, and when he saw the stream of water [during paracentesis], cried out that the operation made him think of Moses, who struck the rock with his staff and made the water gush forth“.

Ascites may be classified according to etiology into four groups include portal hypertension, hypoalbuminemia, peritoneal disease, and other diseases. Ascites is also classified based on the Serum-ascites albumin gradient (SAAG) as two subtypes include transudate – SAAG > 1.1 g/dL and exudate – SAAG < 1.1 g/dL.

Ascites is excess accumulation of fluid in the peritoneal cavity. The fluid can be defined as a transudate or an exudate. Amounts of up to 25 liters are fully possible. Roughly, transudates are a result of increased pressure in the portal vein (> 8 mmHg), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy. The most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1.1 g/dl (10 g/L) implies an exudate. There is no genetic background for ascites. On gross pathology, clear to pale yellow fluid accumulation in peritoneal space are characteristic findings of ascites under normal condition, but it may be chylous, psudochylous, or bloody.

Life threatening causes of ascites are acute liver failure, hepatic failure, and hepatorenal syndrome. Common causes of ascites are Budd-Chiari syndrome, malignancy, and cirrhosis. Less common causes of ascites are the conditions which may lead to fetal ascites, neonatal ascites, and infantile ascites.

Diseases that cause ascites should differentiate from each others, such as cirrhosis, Alcoholic hepatitis, Budd-Chiari syndrome, Constrictive pericarditis, Heart failure, Myxedema, Cancer, Nephrotic syndrome, Pancreatitis, Serositis, and Tuberculosis. The ascites may be transudate (serum-ascites albumin gradient [SAAG] ≥ 1.1 g/dL) or exudate (serum-ascites albumin gradient [SAAG] < 1.1 g/dL).

The incidence of ascites is approximately 60,000 per 100,000 individuals with cirrhosis worldwide. The incidence of ascites is approximately 75,000 per 100,000 cirrhotic individuals with a mortality rate of 50%, within 3 years. Patients of all age groups may develop ascites. Cirrhotic ascites usually affects individuals of the non-Hispanic blacks and Mexican Americans race. Males are more commonly affected by cirrhotic ascites than females. The male to female ratio is approximately 2.5 to 1.

The most potent risk factor in the development of ascites is cirrhosis. Other risk factors include malignancy, heart failure, and tuberculosis. Common risk factors in the development of asctes include acute liver failure, hepatorenal syndrome, liver fibrosis, Budd-Chiari syndrome, constrictive pericarditis, nephrotic syndrome, pancreatitis, and serositis.

There is insufficient evidence to recommend routine screening for ascites.

More than half of the patients with cirrhosis would involve with ascites during the disease. If left untreated, 11.4% of patients with cirrhotic ascites may progress to develop hepatorenal syndrome during 5 years. Common complications of ascites include spontaneous bacterial peritonitis (SBP), dilutional hyponatremia, and hepatorenal syndrome. Prognosis is generally poor, and the 5-year survival rate of patients with cirrhotic ascites is approximately 56.6%.

The hallmark of ascites is abdominal distention. A positive history of cirrhosis and liver failure is suggestive of ascites. The most common symptoms of ascites include abdominal discomfort, shortness of breath, and weight gain.

Physical examination of patients with ascites is usually remarkable for flank dullness, shifting dullnes, and fluid wave. The presence of decreased breath sounds or dull percussion in lower chest on physical examination is diagnostic of pleural effusion beside ascites.

The only diagnostic laboratory finding associated with ascites is serum-ascites albumin gradient (SAAG). SAAG is defined as the difference between albumin level in serum and ascites. Other diagnostic laboratory findings may reveal the underlying causes of ascites. Cirrhosis, as the most common cause of ascites, reveals elevated liver enzymes, creatinine, international normalized ratio (INR) along with decreased albumin, platelet count, hemoglobin (anemia), and white blood cell (WBC) count.

There are no ECG findings associated with ascites.

An abdominal X-ray may be helpful in the diagnosis of ascites. Findings on an abdominal X-ray suggestive of ascites include increased density in abdomen diffusely, lack of shadow differentiation between different soft tissues in abdomen, displacement of intestines and viscera medially, and flank bulging.

Abdominal CT scan may be helpful in the diagnosis of ascites. Findings on CT scan suggestive of ascites include fluid accumulation within abdominal cavity, defined as transudate (same density as water), exudate (more density than water), and hemoperitoneum (density as ~45 HU).

There are no MRI findings associated with ascites.

Ultrasound may be helpful in the diagnosis of ascites. Findings on an ultrasound diagnostic of ascites include anechoic fluid accumulation in abdominal cavity (simple transudate ascites), fluid accumulation along with floating debris (exudative, hemoperitoneum, or malignant ascites), and fluid accumulation along with septations (inflammatory or malignant ascites).

There are no other imaging findings associated with ascites.

Paracentesis is sampling ascites fluid through abdominal wall with overall complication rate of not more than 1%. The sampled fluid will be surveyed upon total protein concentration, neutrophil count, and inoculation into blood culture bottles.

The mainstays of first-line treatment of patients with cirrhosis and ascites include (1) education regarding dietary sodium restriction (2000 mg per day [88 mmol per day]) and (2) oral diuretics. Medical therapy is based on different grades of ascites. Medical therapy would inhibit different processes in pathophysiology of ascites. First-line treatment of patients with cirrhosis and ascites consists of sodium restriction (88 mmol per day [2000 mg per day], diet education), and diuretics (oral spironolactone with or without oral furosemide).

Surgery is the mainstay of treatment for refractory ascites. Refractory ascites is defined as ascites that can not be mobilized or the early recurrence of which can not be satisfactorily prevented by medical therapy. Large volume paracentesis is the choice treatment for patients with tense ascites. Transjugular intrahepatic portosystemic shunt (TIPS) would be indicated when there is frequent (> 3 times per month) need for large volume paracentesis to manage ascites. Liver transplantation is indicated for refractory ascites treatment in patients that can not be underwent TIPS.

Effective measures for the primary prevention of ascites include hepatitis B vaccination, hepatitis C vaccination, alcohol abstinence, low fat diet, low sodium diet, and water restriction.

Effective measures for the secondary prevention of ascites include water and sodium intake restriction, diuretic use, and antibiotic prophylaxis for spontaneous bacterial peritonitis (SBP).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

About 20 BC, Aulus Cornelius Celsus (A.D. 30), a Roman encyclopedist explained in his book “De Medicina” three different types of fluid accumulation under the skin; which was called hydrops by Greeks. Celsus postulated that ascites is mostly secondary to quartan fever (malaria) in Rome. The principles of treatment for ascites were explained as thirst, rest, and abstinence. Drinking less fluid and sweating more, not with exercise, but with heated sand, or in the sweating-room, or with a dry oven and such- like where the other alternative therapies. In 1827, Ludwig van Beethoven involved in ascites and underwent large volumes of paracenteses. His physician write about him as “Beethoven had almost immediate relief, and when he saw the stream of water [during paracentesis], cried out that the operation made him think of Moses, who struck the rock with his staff and made the water gush forth.”

• About 20 BC, Aulus Cornelius Celsus (A.D. 30), a Roman encyclopedist explained in his book “De Medicina” three different types of fluid accumulation under the skin; which was called hydrops by Greeks. Celsus postulated that ascites is mostly secondary to quartan fever (malaria) in Rome.^[1]
  • Very tense belly with frequent noise of the wind movement sound – called tympanites.
  • Uneven swelling and rising up in the body – called leukophlegmasia or hyposarca.
  • The fluid gathering all together in the belly with visible movement along with the movements of body – called ascites.
• In 25 BC, Philip of Epirus, promised to cure the certain friend of king Antigonus with ascites. Philip cured the patient with devouring poultices and drinking his own urine. The basis of his treatment was thirst, rest, and abstinence.^[1]
• 2000 years ago, Celsus, the Roman encyclopedist explain the first treatment procedure for ascites. He described a bronze tube with a specific collar to drain the abdominal fluid.^[2]
• In 1906, Frederick Maberly reported large amounts of fluid drained from ascites patient abdomen for the first time. The procedure was consisted of simultaneous paracentesis while patients sit on adjacent shoeshine chairs.^[3]
• In 1935, Daniel Darrow, an American pediatrician, suggested the role of sodium restriction in the treatment of ascites.^[4]
• In 1936, Robert Alexander McCance, a British biochemist, found the passive nature of water movement and the the importance of sodium ion in ascites.^[5]
• In 1947, John Layne, an American physician, described 20 patients with ascites which were treated by low sodium acid-ash diet.^[6]
• In 1939, Hugh Butt, an American biochemist, postulated possible relation between serum albumin level and volume overload in patients with ascites.^[7]
• In 1944, Charles Janeway, an American pathologist, suggested “high-salt” (300 mmol/L) albumin products as ascites treatment.^[8]
• In 1945, George Thorn, an American biochemist, suggested “low-salt” (15 mmol/25 g) albumin products for volume overload treatment.^[9]
• In 1949, William Faloon, an American biochemist, found that mercurial diuretics can increase the urinary sodium output dramatically, so can alleviate the fluid overload in ascites patients.^[10]
• In 1957, Kagawa, an American biologist, discovered aldosterone.^[11]
• In 1958, John Laragh, an American physician, discovered chlorothiazide diuretic as a potential treatment for ascites. Laragh proved complete cure of ascites in three out of nine patients, but they finally involved in hypokalemic hypochloremic alkalosis, though.^[12] Various diuretics have been studied in treatment of ascites until now.
• In 1949, Thomas Chalmers, an American research fellow, mentioned that complete bed rest had an important role in the management of chronic liver diseases and ascites.^[13]
• In 1949, Alexander Leaf, an American internist, revealed that passive contribution of water to fluid overload was the basis to introduce the fluid restriction as a treatment option for ascites.^[14]
• From 1896 that Drummond and Morrison, British surgeons, reported the first surgical procedure of treatment of ascites, various surgical options were suggested for these patients.^[15]
• In 1898, Talma, a German surgeon, evaluated the “omentopexy” procedure in a patient with ascites. In this procedure some adhesion were induced around the liver and portal system to prevent ascites formation. The patient was cured and lived until 2 years after surgery.^[16]
• In 1943, Charles Fergusen, an American urologist, invented a surgical procedure in which a right nephrectomy was done first and then the peritoneum anastomosis with renal pelvis was performed. In this procedure the ascites fluid continuously drained via bladder and there was no need to frequent paracentesis.^[17]
• In 1946, Crosby and Cooney, American surgeons, suggested the glass collar-button shaped instrument called “Crosby-Cooney button” to be placed in abdominal wall, allowing continuous drainage of ascites into subcutaneous tissues.^[18]
• In 1966, Marshall Orloff, an American surgeon, first described side to side porto-caval shunt for treatment of ascites.^[19]
• In 1974, Harry LeVeen, an American surgeon, suggested the “Peritoneo-venous shunt” procedure for treatment of ascites through drainage of fluid overload into the veins.^[20]
• In 1982, Colapinto, a Canadian radiologist, first presented the transjugular intrahepatic portosystemic shunt (TIPS) for ascites treatment.^[21]
• In 1967, Thomas Strazl, a British surgeon, performed the first liver transplant with more than 1 year surveillance in a patient with cirrhosis and ascites.^[22]

• About 20 BC, Aulus Cornelius Celsus (A.D. 30), a Roman encyclopedist explained in his book “De Medicina” mentioned that ascites was relieved in slaves more easily than freemen. Because slaves can endure thirst, hunger, and other troublesome more than unserviceable freedom.
• The principles of treatment for ascites were explained as thirst, rest, and abstinence. Drinking less fluid and sweating more, not with exercise, but with heated sand, or in the sweating-room, or with a dry oven and such- like where the other alternative therapies.
  • Pills composed of wormwood two parts and myrrh one part were given on an empty stomach to treat refractory types of ascites.
  • Various remedies for ascites were postulated as the followings:
    • Iris root
    • Spikenard
    • Saffron
    • Cinnamon
    • Cassia
    • Myrrh
    • Balsam
    • Galbanum
    • Ladanum
    • Oenanthe
    • Opopanax
    • Cardamon
    • Ebony
    • Cypress seeds
    • Taminian grape (Greeks call staphisagra)
    • Southern wood
    • Rose leaves
    • Sweet flag root
    • Bitter almonds
    • Goat’s marjoram
    • Styrax
  • The quantity of fluid input and output had to be measured and recorded daily.
  • Abdomen circumference was also measured on a daily basis.^[23]

• In 1827, Ludwig van Beethoven involved in ascites and underwent large volumes of paracenteses. His physician write about him as “Beethoven had almost immediate relief, and when he saw the stream of water [during paracentesis], cried out that the operation made him think of Moses, who struck the rock with his staff and made the water gush forth.”
  • 2 days later Beethoven died and autopsy showed cirrhosis and splenomegaly as “shrunken liver to half its normal volume…it was beset with knots the size of a bean…the spleen was double its proper size and dark colored and firm.”^[24]
• The cirrhotic ascites, secondary to chronic alcohol and drug use, decreased lifespan in jazz musicians; result in dramatic influence on the history of jazz music.^[25]
  • Charlie Parker died from cirrhotic ascites at 35 years of age in 1955.
  • John Coltrane (inventor of avant-garde jazz) died with ascites secondary to hepatitis B and hepatocellular carcinoma at 41 years of age in 1967.
  • Stan Getz in 1990 and Steve Lacy in 2004, both saxophone stylists, died from hepatocellular carcinoma.
  • Bill Evans, a lyrical pianist, died of cirrhotic complications.
  • The famous Four Brothers from the Woody Herman band (Stan Getz, Al Cohn, Serge Chaloff, and Zoot Sims) all died from cirrhosis complications.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Ascites may be classified according to etiology into four groups include: portal hypertension associated, hypoalbuminemia associated, peritoneal disease associated, and other diseases associated. Ascites is also classified based on the serum-ascites albumin gradient (SAAG) as two subtypes include transudate – SAAG > 1.1 g/dL and exudate – SAAG < 1.1 g/dL.

Ascites may be classified according to etiology into four groups:^[1]

• Portal hypertension
• Hypoalbuminemia
• Peritoneal disease
• Other diseases

Ascites is also classified based on the serum-ascites albumin gradient (SAAG) as two subtypes:^[2]

• Transudate – SAAG > 1.1 g/dL
• Exudate – SAAG < 1.1 g/dL

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Ascites is the excess accumulation of fluid in the peritoneal cavity. The fluid can be defined as transudate or exudate. Amounts of up to 25 liters are fully possible. Roughly, transudates are a result of increased pressure in the portal vein (> 8 mmHg), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy. The most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1.1 g/dl (10 g/L) implies an exudate. There is no genetic background for ascites. On gross pathology, clear to pale yellow fluid accumulation in peritoneal space are characteristic findings of ascites under normal condition, but it may be chylous, psudochylous, or bloody.

• Ascites is the excess accumulation of fluid in the peritoneal cavity. The fluid can be defined as a transudate or an exudate. Amounts of up to 25 liters are fully possible.^[1]
• Roughly, transudates are a result of increased pressure in the portal vein (> 8 mmHg), such as cirrhosis; while exudates are actively secreted fluid due to inflammation or malignancy.
• Exudates:
  • High protein
  • High lactate dehydrogenase (LDH)
  • Low pH (< 7.30)
  • Low glucose level
  • High white blood cells count
• Transudates:
  • Low protein (< 30 g/L)
  • Low lactate dehydrogenase (LDH)
  • High pH
  • Normal glucose
  • Fewer than 1 white blood cell per 1000 mm³

• The most useful measure is the difference between ascitic and serum albumin concentrations.
• A difference of less than 1.1 g/dl (10 g/L) implies an exudate.

• The main pathophysiology of ascites in cirrhotic patients consists of three interrelated mechanisms, include:^[2]
  • Portal hypertension
  • Vasodilation
  • Hyperaldosteronism
• There is a nitric oxide overload in cirrhotic patients from an unknown source. Therefore, they involved in hypovolemia secondary to the systemic vasodilation.^[3]
• The vasodilation induced by nitric oxide would trigger the stimulation of juxta-glumerular system to upregulate antidiuretic hormone (ADH) and sympathetic drive.^[4] Excess ADH causes water retention and volume overload.^[5]
• Despite the normal physiology of vessels, angiotensin would not cause vasoconstriction in cirrhotic patients and vasodilation becomes perpetuated.^[6]
• Portal hypertension leads to more production of lymph, to the extend of lymphatic system overload. Then, the lymphatic overflow will directed into to peritoneal cavity, forming ascites.^[7]

• Peritoneal malignancy produces some protein factors into the peritoneum, which may lead to osmotic drainage of water and fluid accumulation. Tuberculosis and other forms of ascites are induced through the same mechanism and osmotic fluid shift.^[8]
• Pancreatic and biliary ascites are induced through leakage of pancreatic secretions or bile into the peritoneal cavity, which may lead to inflammatory fluid shift and accumulation.

• There is no genetic background for ascites.
• Ascites syndrome, also called pulmonary hypertension, is in fact a genetic disorder in broilers and poultry.^[9]

Associated conditions with ascites are as following:^[10]

• Cirrhosis
• Heart failure
• Portal hypertension
• Kwashiorkor
• Viral hepatitis
• Pancreatic disease
• Biliary disease

• On gross pathology, clear to pale yellow fluid accumulation in peritoneal space are characteristic findings of ascites under normal condition.^[11]

• Chylous ascites gross pathology is milky presentation of ascites fluid, which is reflective of high amounts of chylomicrons.^[12]
• On gross pathology, milky appearance of ascitic fluid is characteristics of the followings:^[13]
  • Cirrhosis
  • Infections (parasitic and tuberculosis)
  • Malignancy
  • Congenital defects
  • Trauma
  • Inflammatory processes
  • Nephropathies
  • Cardiopathies

• Pseudochylous is the condition in which on gross pathology the ascitic fluid appearance is cloudy and/or turbid.
• The following conditions can lead to pseudochylous:^[14]
  • Bacterial infection
  • Peritonitis
  • Pancreatitis
  • Perforated bowel

• On gross pathology, bloody appearance of ascitic fluid is characteristics of the followings:^[15]
  • Benign or malignant tumors
  • Hemorrhagic pancreatitis
  • Perforated ulcer

• On microscopic histopathological analysis, characteristic findings of cirrhosis, as the most common cause of ascites, are based on Robbins definition (all three is needed for diagnosis):^[17]
  • Bridging fibrosis
  • Nodule formation
  • Disruption of the hepatic architecture

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2], M.Umer Tariq [3], Carlos A Lopez, M.D. [4]

Life-threatening causes of ascites are acute liver failure, hepatic failure, and hepatorenal syndrome. Common causes of ascites are Budd-Chiari syndrome, malignancy, and cirrhosis. Less common causes of ascites are the conditions which may lead to fetal ascites, neonatal ascites, and infantile ascites.

• Acute liver failure
• Hepatic failure
• Hepatorenal syndrome
• Liver fibrosis
• Liver cirrhosis

• Budd-Chiari syndrome
• Cancer
• Cirrhosis
• Constrictive pericarditis
• Heart failure
• Nephrotic syndrome
• Pancreatitis
• Serositis
• Tuberculosis

• Gastrointestinal disorders
  • Meconium peritonitis
  • Intestinal malrotation
  • Small intestinal or colonic atresia
  • Intussusception
  • Volvulus
  • Cystic fibrosis
  • Biliary atresia
  • Portal venous malformations
• Infection
  • Parvovirus
  • Syphilis
  • Cytomegalovirus
  • Toxoplasmosis
  • Acute maternal hepatitis
• Genitourinary disorders
  • Hydronephrosis
  • Polycystic kidney disease
  • Urinary obstruction
  • Ovarian cyst
  • Persistent cloaca
• Chylous ascites
• Cardiac disorders
  • Arrhythmia
  • Heart failure
• Chromosomal abnormalities
  • Trisomy
  • Turner syndrome
• Neoplasm
• Hematologic
  • Hemolytic anemia
  • Neonatal hemochromatosis
• Metabolic disease
  • Niemann-Pick type C
  • Congenital disorders of glycosylation
  • Wolman disease
  • Lysosomal storage disease
• Other
  • Maternal/fetal abuse
  • Idiopathic

• Hepatobiliary disorders
  • Cirrhosis
  • Alpha-1-antitrypsin deficiency
  • Congenital hepatic fibrosis
  • Viral hepatitis
  • Budd-Chiari syndrome
  • Biliary atresia
  • Bile duct perforation
  • Portal venous malformation
  • Ruptured mesenchymal hamartoma
• Gastrointestinal disorders
  • Intestinal malrotation
  • Intestinal perforation
  • Acute appendicitis
  • Intestinal atresia
  • Pancreatitis
• Chylous ascites
• Parenteral nutrition extravasation
• Metabolic disease
• Genitourinary disorders
  • Obstructive uropathy
    • Posterior urethral valves
    • Ureterocele
    • Lower ureteral stenosis
    • Ureteral atresia
    • Imperforate hymen
    • Bladder rupture
  • Bladder injury from umbilical artery catheterization
  • Nephrotic syndrome
  • Ruptured corpus luteum cyst
• Cardiac
  • Arrhythmia
  • Heart failure
• Hematologic
  • Neonatal hemochromatosis
• Other
  • Cutis marmota telangictatica congenita
  • Intravenous vitamin E
  • Pseudo-ascites
    • Small bowel duplication
  • Abdominal trauma
  • Idiopathic

• Hepatobiliary disorders
  • Cirrhosis
  • Congenital hepatic fibrosis
  • Acute hepatitis
  • Budd-Chiari syndrome
  • Bile duct perforation
  • Liver transplantation
• Gastrointestinal disorders
  • Acute appendicitis
  • Intestinal atresia
  • Pancreatitis
  • Pyloric duplication
• Serositis
  • Crohn disease
  • Eosinophilic enteropathy
  • Henoch-Schonlein purpura
• Chylous ascites
  • Intestinal lymphangiectasia
  • Lymphatic duct obstruction
  • Lymphatic duct trauma
• Parenteral nutrition extravasation
• Neoplasm
  • Lymphoma
  • Wilm tumor
  • Clear cell renal sarcoma
  • Glioma
  • Germ cell tumor
  • Ovarian tumor
  • Mesothelioma
  • Neuroblastoma
• Metabolic disease
• Genitourinary disorders
  • Nephrotic syndrome
  • Peritoneal dialysis
• Cardiac
  • Heart failure
• Pseudo-ascites
  • Celiac disease
  • Cystic mesothelioma
  • Omental cyst
  • Ovarian cyst
• Other
  • Systemic lupus erythematosus
  • Ventriculoperitoneal shunt
  • Vitamin A toxicity
  • Chronic granulomatous disease
  • Nonaccidental trauma
  • Idiopathic

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Diseases that cause ascites should differentiate from each others, such as cirrhosis, Alcoholic hepatitis, Budd-Chiari syndrome, Constrictive pericarditis, Heart failure, Myxedema, Cancer, Nephrotic syndrome, Pancreatitis, Serositis, and Tuberculosis. The ascites may be transudate (serum-ascites albumin gradient [SAAG] ≥ 1.1 g/dL) or exudate (serum-ascites albumin gradient [SAAG] < 1.1 g/dL).

• Diseases that cause ascites should differentiate from each others, such as cirrhosis, Alcoholic hepatitis, Budd-Chiari syndrome, Constrictive pericarditis, Heart failure, Myxedema, Cancer, Nephrotic syndrome, Pancreatitis, Serositis, and Tuberculosis.
• The ascites may be transudate (serum-ascites albumin gradient [SAAG] ≥ 1.1 g/dL) or exudate (serum-ascites albumin gradient [SAAG] < 1.1 g/dL).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

The incidence of ascites is approximately 60,000 per 100,000 individuals with cirrhosis worldwide. The incidence of ascites is approximately 75,000 per 100,000 cirrhotic individuals with a mortality rate of 50%, within 3 years. Patients of all age groups may develop ascites. Cirrhotic ascites usually affects individuals of the non-Hispanic blacks and Mexican Americans race. Males are more commonly affected by cirrhotic ascites than females. The male to female ratio is approximately 2.5 to 1.

• The incidence of ascites is approximately 60,000 per 100,000 individuals with cirrhosis worldwide.^[1]
• Among patients with ascites 8,000 to 35,000 per 100,000 individuals would involve in spontaneous bacterial peritonitis (SBP).^[2]
• The incidence of chylous ascites is approximately 5 per 100,000 individuals worldwide.^[3]

• The prevalence of ascites is approximately 75,000 per 100,000 individuals with cirrhosis in Western countries.^[4]
• The prevalence of cirrhosis, malignancy, heart failure, tuberculosis, and nephrotic syndrome is approximately 81,000, 10,000, 3,000, 2,000, and 1,000 per 100,000 individuals with ascites worldwide, respectively.^[5]

• The incidence of ascites is approximately 75,000 per 100,000 cirrhotic individuals with a mortality rate of 50%, within 3 years.^[6]
• Survival from ascites majorly depends on severity of portal hypertension, liver failure, and circulation dysfunction.^[4]

• Patients of all age groups may develop ascites.

• There is no racial predilection to ascites.
• Cirrhotic ascites usually affects individuals of the non-Hispanic blacks and Mexican Americans race.^[7]

• Ascites affects men and women equally.
• Males are more commonly affected by cirrhotic ascites than females. The male to female ratio is approximately 2.5 to 1.^[7]

• Cirrhotic ascites is a common disease that tends to affect people below the poverty and with low education level.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

The most potent risk factor in the development of ascites is cirrhosis. Other risk factors include malignancy, heart failure, and tuberculosis. Common risk factors in the development of asctes include acute liver failure, hepatorenal syndrome, liver fibrosis, Budd-Chiari syndrome, constrictive pericarditis, nephrotic syndrome, pancreatitis, and serositis.

• The most potent risk factor in the development of ascites is cirrhosis. Other risk factors include malignancy, heart failure, and tuberculosis.

• Common risk factors in the development of asctes include acute liver failure, hepatorenal syndrome, liver fibrosis, Budd-Chiari syndrome, constrictive pericarditis, nephrotic syndrome, pancreatitis, and serositis.

• Common risk factors in the development of cirrhosis include:^[1]
  • Acute liver failure
  • Hepatic failure
  • Hepatorenal syndrome
  • Liver fibrosis
  • Liver cirrhosis
  • Budd-Chiari syndrome
  • Cancer
  • Cirrhosis
  • Constrictive pericarditis
  • Heart failure
  • Nephrotic syndrome
  • Pancreatitis
  • Serositis
  • Tuberculosis

• Less common risk factors in the development of ascites include:^[2]
  • Amebiasis
  • Ascariasis
  • Brucellosis
  • HIV infection
  • Pelvic inflammatory disease
  • Pseudomembranous colitis
  • Salmonellosis
  • Whipple’s disease
  • Amyloidosis
  • Castleman’s syndrome
  • Extramedullary hematopoiesis
  • Hemophagocytic syndrome
  • Histiocytosis X
  • Leukemia
  • Lymphoma
  • Mastocytosis
  • Multiple myeloma
  • Abdominal pregnancy
  • Crohn’s disease
  • Endometriosis
  • Gaucher’s disease
  • Lymphangioleiomyomatosis
  • Myxedema
  • Ovarian hyperstimulation syndrome
  • POEMS syndrome
  • Systemic lupus erythematosus
  • Ventriculoperitoneal shunt
  • Chlamydia peritonitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

There is insufficient evidence to recommend routine screening for ascites.

• There is insufficient evidence to recommend routine screening for ascites.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

More than half of the patients with cirrhosis would involve with ascites during the disease. If left untreated, 11.4% of patients with cirrhotic ascites may progress to develop hepatorenal syndrome during 5 years. Common complications of ascites include spontaneous bacterial peritonitis (SBP), dilutional hyponatremia, and hepatorenal syndrome. Prognosis is generally poor, and the 5-year survival rate of patients with cirrhotic ascites is approximately 56.6%.

Ascites may contribute to three grades:^[1]

• Grade 1: Mild accumulation of fluid in abdomen, which is only visible on ultrasound.
• Grade 2: Moderate accumulation of fluid in abdomen, which is detectable with flank bulging and shifting dullness.
• Grade 3: Severe accumulation of fluid in abdomen, which is directly visible with fluid thrill.

• More than half of the patients with cirrhosis would involve with ascites during the disease.
• The symptoms of refractory ascites typically develop in 11.3% of patients during 5 years of cirrhosis.
• If left untreated, 37.1% of patients with cirrhotic ascites may progress to develop dilutional hyponatremia during 5 years.
• If left untreated, 11.4% of patients with cirrhotic ascites may progress to develop hepatorenal syndrome during 5 years.^[2]

• Common complications of ascites include:^[3]
  • Spontaneous bacterial peritonitis (SBP)
  • Dilutional hyponatremia
  • Hepatorenal syndrome
  • Weight loss and protein malnutrition
  • Hepatic encephalopathy

• Prognosis is generally poor, and the 5-year survival rate of patients with cirrhotic ascites is approximately 56.6%.
• The presence of spontaneous bacterial peritonitis (SBP), dilutional hyponatremia, and hepatorenal syndrome is associated with a particularly poor prognosis among patients with cirrhotic ascites.^[2]

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