Ascites: Encyclopedia II - Ascites - Pathophysiology

Ascites - Pathophysiology

Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 litres are fully possible.

Roughly, transudates are a result of increased pressure on the portal vein (>8 mmHg), 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 mg/dl implies an exudate.

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 the feared hepatorenal syndrome.

Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement. Many acutely ill ascitic patients have SBP and require antibiotic treatment.

If portal hypertension is the cause, complications can be fulminant, such as bleeding esophageal varices.

Adapted from the Wikipedia article "Pathophysiology", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki