PARACENTESIS-INDUCED CIRCULATORY DYSFUNCTION - MECHANISM AND EFFECT ON HEPATIC HEMODYNAMICS IN CIRRHOSIS

Citation
L. Ruizdelarbol et al., PARACENTESIS-INDUCED CIRCULATORY DYSFUNCTION - MECHANISM AND EFFECT ON HEPATIC HEMODYNAMICS IN CIRRHOSIS, Gastroenterology, 113(2), 1997, pp. 579-586
Citations number
26
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
113
Issue
2
Year of publication
1997
Pages
579 - 586
Database
ISI
SICI code
0016-5085(1997)113:2<579:PCD-MA>2.0.ZU;2-2
Abstract
Background & Aims: Therapeutic paracentesis may be associated with a c irculatory dysfunction, manifested by a marked increase of the plasma renin activity and plasma norepinephrine. The aim of the study was to characterize the systemic and hepatic hemodynamic changes associated w ith paracentesis-induced circulatory dysfunction, Methods: Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hep atic hemodynamics were assessed 1 hour and 6 days after complete mobil ization of ascites in 37 patients treated by total paracentesis plus i ntravenous dextran-70 infusion. Results: Paracentesis-induced circulat ory dysfunction occurred in 10 patients (renin and norepinephrine incr eased from 9.0 +/- 10.5 to 28.8 +/- 19.0 ng.mL(-1).h(-1) and from 752. 0 +/- 364.0 to 1223.0 +/- 294.0 pg/mL, respectively) and was associate d with significant reduction in systemic vascular resistance (-13.0% /- 2.6%; P < 0.05) and increase in hepatic venous pressure gradient (f rom 19.5 +/- 1.5 to 22.5 +/- 2.4 mm Hg; P < 0.01), In the remaining 27 patients, mobilization of ascites also induced a significant but smal ler reduction in systemic vascular resistance (-5.0% +/- 1.6%; P < 0.0 5) without significant changes in renin, norepinephrine, and hepatic v enous pressure gradient, Conclusions: Paracentesis-induced circulatory dysfunction is predominantly caused by an accentuation of the arterio lar vasodilation already present in untreated cirrhotic patients with ascites. The homeostatic activation of endogenous vasoactive systems m ay account for the increased intrahepatic vascular resistance associat ed with this condition.