Colloidosmotic pressure

In liver diseases involving elevated hydrostatic pressure (e.g. as a result of portal hypertension), the inflow of fluid into the interstitium is increased, whereas the return of fluid into the vascular bed is decreased due to the depressed colloidosmotic pressure (e.g. as a result of hypalbuminaemia). Likewise, a boost in capillary permeability leads to an outflow of fluid into the interstitial tissue. (2, 5, 8, 12)... 

Reduction in colloidosmotic pressure The colloidosmotic pressure in the plasma is lower in hver cirrhosis patients. This results from (1.) restriction in the synthesis of albumin (which is, however, only clinicaUy manifest after 3 or 4 weeks due to the half-life of plasma albumin), (2.) greater loss of protein-rich fluid in the abdominal cavity, and (3.) dilution of the vascular volume. A critical concentration of albumin in the plasma is deemed to be about 3 g/100 ml (ca. 435 pmol/1). Below this albumin value, there is a clear correlation between portal hypertension and the formation of ascites. The coexistence of portal hypertension and hypalbuminaemia (critical concentration 2.5—3.0 gldl) is an important prerequisite for the formation of ascites. 

Sinusoidal portal hypertension with increased hydrostatic pressure and decreased colloidosmotic pressure are of considerable, probably paramount importance for the onset of ascites formation. Further influencing factors could be the growing imbalance between the augmented lymph production and drainage as well as the higher degree of capillary permeability. 

However, the significance of the decreased colloidosmotic (oncotic) pressure is not as great as has been hitherto assumed. Nevertheless, when the hydrostatic pressure is raised at the same time, incongruity between these two Starling forces is created, and fluid escapes into the abdominal cavity. This process is greatly furthered by the disparity between lymph production and lymph transport. Tliese mechanical factors (s. tab. 16.3) may effect the formation of ascites, yet they cannot produce large quantities of ascitic fluid. Such a development, however, can be expected if the capillary permeability is additionally heightened due to toxic or inflammatory causes. 

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