Ascites
From Medical-Wiki
Ascites is basically an abnormal accumulation of fluid within the abdominal cavity.
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The physiology of ascites
The most recent theory explaining the physiology of ascites is termed the peripheral arterial vasodilation hypothesis. This theory includes elements of two prior theories — underfilling and overflow — and suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume.
As the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. The expansion of intravascular fluid leads to an overflow of fluid into the peritoneal cavity. Thus, the underfilling theory is operative early and the overflow theory is operative late.
The factors that have been well documented and are not debated are elevated circulating levels of epinephrine and norepinephrine. In addition, hypoalbuminemia reduces plasma oncotic pressure promoting the extravasation of fluid. Ascites is rarely present unless there is both portal hypertension and hypoalbuminemia.
Clinical presentation of ascites
When patients present, they typically will have been aware of increasing abdominal girth for but a short period of time. Histories associated with risk factors include heavy alcohol use, chronic viral hepatitis, intravenous drug use, sexual promiscuity, sexual orientation, transfusions before 1980 (hepatitis C exposure), tattoos, habitation or origination from an area endemic for hepatitis.
If alcohol plays a role in the etiology of liver disease, ascites may occur in a waxing and waning pattern following the patient’s drinking pattern.
Factors associated with metabolic syndrome are now known to place patients at risk for nonalcoholic liver disease—and subsequent cirrhosis. [1]
Physical findings
Physical examination should focus on the signs of portal hypertension and liver disease. If there is a significant amount of ascitic fluid, the liver may be difficult to palpate. The puddle sign indicates that as little as 120 mL of fluid is present. Two physical signs for demonstrating larger amounts of ascites are shifting dullness and bulging flanks. [2]
Other classic physical findings have been used as being indicative of intra-abdominal pathology. With the advent of highly accurate imaging, these findings may not be as quite as relevant, but they are still of interest.
An elevated jugular venous pulse suggests cardiac involvement in the origin of ascitic fluid.
A Sister Mary Joseph nodule in the umbilicus suggests peritoneal carcinomatosis originating from gastric, pancreatic, or hepatic primary malignancy.
A Virchow node is a left-sided supraclavicular node that suggests an upper abdominal malignancy.
Anasarca is total body edema caused by cardiac disease or nephrotic syndrome. [3]
Treatment of ascites
In 2003, the International Ascites Club released guidelines for treatment of ascites. It concluded that mild to moderate ascites should be treated with fluid and salt restriction and diuresis with spironolactone. Diuretics may then be added in a step-wise fashion.
Gross ascites should be treated with therapeutic paracentesis followed by colloid volume expansion. Diuretics should then be added to the regimen.
Refractory ascites should be managed by repeated large volume paracentesis or through the insertion of transjugular intrahepatic portosystemic stent shunt (TIPS). This procedure improves quality of life and renal function but there is no evidence that it prolongs survival.
The only completely effective treatment is liver transplant.
