Ascites pathophysiology

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

Cirrhosis results in elevation of portal blood pressure because of fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature. The pathophysiologic abnormalities that cause it result in the commonly encountered problems of ascites, portal hypertension and esophageal varices, HE, and coagulation disorders. 

The signals necessary to activate or increase the formation of a substance or a regulatory system depend on the point in time and intensity of a specific pathophysiological situation as well as on the respective liver disease and the developmental phase of the ascites. 

As early as 1964 and in later publications, it was possible to demonstrate the significance of glycoproteins (hexosamine, fucose, sialic acid [34], etc.) and cholinesterase for the detection of non-inflammatory, inflammatory or malignant disease and their follow-up as well as for the distinction between transudate and exudate in a so-called phlogogram (E. Kuntz, 1964). (see footnote p.298) Because of the significance and pathophysiological features of the mucopolysaccharides, appropriate biochemical parameters are likely to be of further interest. In addition, elevated values of hyaluronic acid have been found in the ascitic fluid of cirrhotic patients. 

In pathophysiological and prognostic terms, even ascites that can only be identified by ultrasonic methods is a sign of decompensation - either decompensation which is still latent, yet unstable, or decompensation which is slowly increasing by itself This latter condition ultimately calls for much more severe measures (also involving more side effects) than merely moderate and cautious efforts to restore the patient to a stable state of recompensation, which should then be as lasting as possible. 

Probably the first surgical step was hepatopexy, which was performed by Ch. Th. Billroth in 1894. After the first omentopexy (or epiplopexy) was carried out by D. Drummond et al. in 1896 (243) and by S. Talma in 1898 (259), attention continued to focus on surgical ways to treat ascites. With regard to the pathophysiological aspects, the techniques described can be categorized into six groups ... 

Angeli, P., Caregaro, L., Menon, R, Sacerdoti, D., deToni, R., Merkel, C., Gatta, A. Variability of atrial natriuretic peptide plasma levels in ascitic cirrhotics pathophysiological and clinical implications. Hepatology 1992 16 1389-1394... 

C. A pathophysiological interpretation of unresponsiveness to spironolactone in a stepped-care approach to the diuretic treatment of ascites in nonazotemic cirrhotic patients. Hepatology 1991 14 231-236... 

Hepatorenal syndrome, functional renal failure in the setting of cirrhosis in the absence of intrinsic renal disease, occurs in patients with cirrhosis as a result of intense vasoconstriction within the renal cortical vasculature. It is common and develops in approximately 40% of patients with cirrhosis and ascites within 5 years. The resultant reduction in blood supply to the kidneys causes avid sodium retention and oliguria. The vasoconstriction that occurs in the kidneys is in stark contrast to the state of systemic vasodilation that is characteristic of chronic liver failure. The pathophysiologic mechanism responsible for these effects is unknown, but is linked to the systemic vasodilation, hypovolemia, and hyperkinetic circulation seen in chronic liver failure. ... 

Runyon B. Ascites and spontaneous bacterial peritonitis. In Eeldman M, Scharschmidt BE, Sleisenger MH, eds. Sleisenger and Eordtran s Gastrointestinal and Liver Disease Pathophysiology/Diagnosis/Treatment, 6th ed. Philadelphia, Saunders, 1998 1310-1333. 

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