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==Overview== | ==Overview== | ||
Revision as of 13:24, 26 January 2018
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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]
Overview
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).
Historical Perspective
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".
Classification
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.
Pathophysiology
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.
Causes
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.
Differentiating Ascites from Other Diseases
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).
Epidemiology and Demographics
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.
Risk Factors
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.
Screening
There is insufficient evidence to recommend routine screening for ascites.
Natural History, Complications, and Prognosis
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%.
Diagnosis
History and Symptoms
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
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.
Laboratory Findings
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.
Electrocardiogram
There are no ECG findings associated with ascites.
X-ray
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.
CT scan
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).
MRI
There are no MRI findings associated with ascites.
Ultrasound
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).
Other Imaging Findings
There are no other imaging findings associated with ascites.
Other Diagnostic Studies
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.
Treatment
Medical Therapy
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
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.
Primary Prevention
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.
Secondary Prevention
Effective measures for the secondary prevention of ascites include water and sodium intake restriction, diuretic use, and antibiotic prophylaxis for spontaneous bacterial peritonitis (SBP).