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[Natural course and physiopathology of ascites in the cirrhotic patient].
Ann Ital Med Int. 1996 Oct; 11 Suppl 2:30S-38S.AI

Abstract

Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death.

Authors+Show Affiliations

Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Università degli Studi di Bologna.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

ita

PubMed ID

9004818

Citation

Bernardi, M, et al. "[Natural Course and Physiopathology of Ascites in the Cirrhotic Patient]." Annali Italiani Di Medicina Interna : Organo Ufficiale Della Societa Italiana Di Medicina Interna, vol. 11 Suppl 2, 1996, 30S-38S.
Bernardi M, Colantoni A, Caraceni P, et al. [Natural course and physiopathology of ascites in the cirrhotic patient]. Ann Ital Med Int. 1996;11 Suppl 2:30S-38S.
Bernardi, M., Colantoni, A., Caraceni, P., Sica, G., & Trevisani, F. (1996). [Natural course and physiopathology of ascites in the cirrhotic patient]. Annali Italiani Di Medicina Interna : Organo Ufficiale Della Societa Italiana Di Medicina Interna, 11 Suppl 2, 30S-38S.
Bernardi M, et al. [Natural Course and Physiopathology of Ascites in the Cirrhotic Patient]. Ann Ital Med Int. 1996;11 Suppl 2:30S-38S. PubMed PMID: 9004818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Natural course and physiopathology of ascites in the cirrhotic patient]. AU - Bernardi,M, AU - Colantoni,A, AU - Caraceni,P, AU - Sica,G, AU - Trevisani,F, PY - 1996/10/1/pubmed PY - 1996/10/1/medline PY - 1996/10/1/entrez SP - 30S EP - 38S JF - Annali italiani di medicina interna : organo ufficiale della Societa italiana di medicina interna JO - Ann Ital Med Int VL - 11 Suppl 2 N2 - Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death. SN - 0393-9340 UR - https://www.unboundmedicine.com/medline/citation/9004818/[Natural_course_and_physiopathology_of_ascites_in_the_cirrhotic_patient]_ L2 - https://medlineplus.gov/cirrhosis.html DB - PRIME DP - Unbound Medicine ER -