Ascites overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Ascites is defined as fluid accumulation of more than 25 mL in the peritoneal cavity.
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.