TRANSJUGULAR INTRAHEPATIC PORTAL-SYSTEMIC SHUNT IN THE TREATMENT OF REFRACTORY ASCITES - EFFECT ON CLINICAL, RENAL, HUMORAL, AND HEMODYNAMIC PARAMETERS

Citation
J. Quiroga et al., TRANSJUGULAR INTRAHEPATIC PORTAL-SYSTEMIC SHUNT IN THE TREATMENT OF REFRACTORY ASCITES - EFFECT ON CLINICAL, RENAL, HUMORAL, AND HEMODYNAMIC PARAMETERS, Hepatology, 21(4), 1995, pp. 986-994
Citations number
38
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
21
Issue
4
Year of publication
1995
Pages
986 - 994
Database
ISI
SICI code
0270-9139(1995)21:4<986:TIPSIT>2.0.ZU;2-E
Abstract
Seventeen cirrhotics with reandactory ascites were treated with transj ugular intrahepatic portosystemic Shunt (TIPS) and followed for 15.5 /- 3.4 months. Five patients died, four within 3 months after TIPS (he patocellular failure) and one after 22 months (cholangiocarcinoma). Si x patients received transplants 1 to 10 months after the procedure. Ac tuarial sunival at 6, 12, and 24 months was 75%, 75%, and 63%, respect ively. Portosystemic venous pressure gradient decreased by 46% at 1 mo nth and by 38% at 7 to 12 months. Eight patients presented 18 stenoses 1 to 18 months after TIPS. Twelve stenoses required balloon dilatatio n. Tense ascites was present before TIPS in 100% of the patients, wher eas it was mild or absent in 56% at 1 month, in 66% at 3 to 6 months, in 57% at 7 to 12 months, and in 100% at 24 months after TIPS. Reguire ments for diuretics and paracentesis decreased after TIPS (P < .001, b oth). One month after TIPS, urinary and fractional sodium excretion in creased (P < .001, both), plasma renin activity, plasma aldosterone (P < .005, both), and plasma norepinephrine (P < .05) decreased and card iac output (P < .01) increased, systemic vascular resistances (P <.005 ) decreased, and arterial pressure did not change. Acute hepatic encep halopathy was frequent early after TIPS but was responsive to treatmen t and caused no long-term disability. In conclusion, TIPS is useful in the treatment of rehactory ascites through lowering portal pressure a nd improving renal sodium excretion. This effect could be attributable to an increase in effective blood volume causing deactivation of vaso pressor systems.