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Ascites, in cirrhosis

La Villa, G., Raggi, V.C. Medical treatment of ascites in cirrhosis. Gastroenterol. Internat. 1993 6 26-32... [Pg.319]

Gines, E, Uriz, J., Calahorra, B., Garcia-Tsao, G., Kamath, P.S., Rnlz-del-Arbol, L., Planas, R., Bosch, J., Arroyo, V., Rodes, J. Transjugular intrahepatic portosystemic shunting versus paracentesis plus albumin for refractory ascites in cirrhosis. Gastroenterology 2002 123 ... [Pg.320]

Smadja, C., Franco, D. The LeVeen shunt in the elective treatment of intractable ascites in cirrhosis. A prospective study on 140 patients. Ann. Surg. 1985 201 488 - 493... [Pg.321]

R, Gassull, M.A., Teres, X, Arroyo, V., Rodes, X Impact of shunt surgery for variceal bleeding in the natural history of ascites in cirrhosis a retrospective study. Hepatology 1994 20 584-591... [Pg.369]

Moore K, Wong F, Gines P, Bernard M, Ochs A, Salerno F, et al. The management of ascites in cirrhosis Report on the consensus conference of the International Ascites Club. Hepatology 2003 38 258-66. [Pg.1838]

Gines P, Fernandez-Espatrach G, Arroyo V, et al. Pathogenesis of ascites in cirrhosis. Semin Liver Dis 1997 17 175-189. [Pg.710]

The target in treating ascites is to effect a fluid loss of approximately 0.5 L per day.22 Because ascites equilibrates with vascular fluid at a much slower rate than does peripheral edema, aggressive diuresis is associated with intravascular volume depletion and should be avoided unless patients have concomitant peripheral edema. Patients with peripheral edema in addition to ascites may require increasing furosemide doses until euvolemia is achieved intravenous diuretics are often necessary.22 Diuretic therapy in cirrhosis is typically lifelong. [Pg.333]

Dexamethasone Testing of adrenal cortical hyperfunction cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Tnamc/no/one Treatment of pulmonary emphysema where bronchospasm or bronchial edema plays a significant role, and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome) in conjunction with diuretic agents to induce a diuresis in refractory CHF and in cirrhosis of the liver with refractory ascites and for postoperative dental inflammatory reactions. [Pg.254]

Hepatic cirrhosis and ascites In these patients, sudden alterations of electrolyte balance may precipitate hepatic encephalopathy and coma. Do not institute therapy until the basic condition is improved. [Pg.689]

Hypokalemia Hypokalemia prevention requires particular attention to the following Patients receiving digitalis and diuretics for CHF, hepatic cirrhosis, and ascites in aldosterone excess with normal renal function potassium-losing nephropathy certain diarrheal states or where hypokalemia is an added risk to the patient (eg, history of ventricular arrhythmias). [Pg.690]

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. [Pg.1330]

Spironolactone, an aldosterone antagonist, is the drug of choice since secondary hyperaldosteronism often coexists in patients with hepatic ascites. Aldosterone is usually metabolised by the liver and is highly protein bound, therefore the free aldosterone levels are raised in cirrhosis. Spironolactone competes with aldosterone for receptor sites in the distal tubule, resulting in potassium retention and sodium and water loss. The initial dose of spironolactone is 100-200 mg and can be slowly increased according to response. There is a lag of 3-5 days between the beginning of spironolactone treatment and the onset of the natriuretic effect. [Pg.351]

Indications for prophylactic antibiotics for prevention of SBP in cirrhosis with ascites ... [Pg.51]

Gines A, Escorsell A, Gines P, Salo J, Jimenez W, Inglad a L, Navasa M, Claria J, Mimola A, Arroyo V, Rodes J. Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites. Gastroenterology 1993 105 229-36. [Pg.86]

About 50% of patients with cirrhosis develop ascites within 10 years of diagnosis and 50% of these will die within 2 years. The process by which ascites forms in cirrhosis is not fully understood but appears to involve the accumulation of vasodilator substances, activation of the renin-angiotensin-aldosterone system (causing renal retention of sodium and water), and the production of antidiuretic hormone (causing hyponatraemia due to dilution, not deficiency, of plasma sodium). [Pg.656]

It is not clearly understood why in some cases oedema without ascites and in other cases ascites without oedema as well as ascites together with oedema or even pleural effusion without ascites occur. Ascites develops most frequently during the course of liver disease (= hepatogenic ascites), in particular in chronic liver diseases with portal hypertension (= portal ascites), (s. tab. 16.7) Various mechanical, biochemical and neural disorders overlap in their effects and pathways, depending on the underlying liver disease. Only rarely is ascites found in diseases with presinusoidal localization of portal hypertension (such as portal vein thrombosis) or with minor restrictions in the synthesis of albumin (as in biliary cirrhosis). Formation of ascites occurs in about 50% of all cirrhotic patients within 10 years of... [Pg.296]

Hepatic hydrothorax (C.S. Morrow et al., 1958) is evident during the course of liver cirrhosis with ascites in 0.4-12% of cases. The mean frequency is about 6%, although in two-thirds of the cases, a right-sided effusion (with the author s own patients a bilateral effusion) was ascertained. (66) (s. fig. 16.8) Hepatic hydrothorax is a transudate cell count protein concentration <2.5 g/dl, total protein effusion to serum ratio <0.5, LDH effusion to serum ratio <2.3, serum to pleural fluid albumin gradient >1.1 g/dl. (s. also fig. 16.9) (17, 37, 47, 52 - 54, 66)... [Pg.298]

Even if pathogenesis has still not been fully resolved, it is generally attributed to various regulatory defects in the immune system (so-called acquired immune defect syndrome in cirrhosis) (1.) reduction in the opsonic and bactericidal activity of the ascitic fluid, (2.) impaired function of the RES phagocytosis system, and (3.) leukocytic functional deficiency. A decrease in C3 concentration in the ascitic fluid (<20 mg/dl) reduced the bacterial content and, according to the literature, led to the occurrence of SBP in 47% of cases within a short space of time. [Pg.303]

In decompensated liver cirrhosis or gastrointestinal bleeding, the use of antibiotics is recommended for the primary prevention of SBP as well as to avert a relapse. This is especially true if predisposing factors for SBP are present. In cirrhosis with ascites, for example, SBP occurs in about 80% of hospitalized patients within the first week. For this reason, SBP is deemed to be a nosocomial infection (H.o. Conn, 1987) although other investigators regard the domestic surroundings as the most... [Pg.303]

Fig. 16.13 Enonnous refractory ascites in alcoholic cirrhosis. Bilateral inguinal hernia with scrotal oedema. Muscular atrophy. Hepatic encephalopathy (II—III) (same patient as in fig. 16.14)... Fig. 16.13 Enonnous refractory ascites in alcoholic cirrhosis. Bilateral inguinal hernia with scrotal oedema. Muscular atrophy. Hepatic encephalopathy (II—III) (same patient as in fig. 16.14)...
Lieberman, F.L., Denison, E.K., Reynolds, T.B. The relationship of plasma volume, portal hypertension, ascites, and renal sodium retention in cirrhosis the overflow theory of ascites formation. Ann. N. Y Acad. Sci. 1970 170 202-206... [Pg.317]

Rector, W.G., Ibarra, F., Openshaw, K., Hoefs, J.C. Ascites kinetics in cirrhosis relationship to plasmaoncotic balance and intensity of renal sodium retention. J. Lab. Clin. Med. 1986 107 412-419... [Pg.317]

Ring-Larsen, H., Henriksen, J.H., Christensen, N.J. Sympathetic nervous regulation in the pathogenesis of fluid retention and ascites in patients with cirrhosis. Gastroenterol. Internal. 1992 5 231 -236... [Pg.317]

Llach, J., Rimola, A., Navasa, M., Gines, R, Salmeron, J.M., Gines, A., Arroyo, V., Rodes, J. Incidence and predictive factors of first episode of spontaneous bacterial peritonitis in cirrhosis with ascites relevance of ascitic fluid protein concentration. Hepatology 1992 16 724-727... [Pg.318]

Descos, L., Gauthier, A., Levy, V.G., Michel, H., Qnlnton,A., Rneff, B., Fermanian, J., Fromhonne, E., Durbec, J.P. Comparison of six treatments of ascites in patients with liver cirrhosis. A clinical trial. Hepato-Gastroenterol. 1983 30 15-20... [Pg.319]

Santos, J., Planas, R., Pardo, A., Durandez, R., Cabre, E., Morillas, R.M., Granada, MX., Jimene J.A., Quintero, E., Gassull, M.A. Spironolactone alone or in combination with furosemide in the treatment of moderate ascites in nonazotemic cirrhosis. A randomized comparative study of efficacy and safety. J. Hepatol. 2003 39 187-192... [Pg.319]

Fasslo, E., Terg, R., Landelra, G., Abecasls, R., Salemne, M., Podesta, A., Rodriguez, R, Levi, D., Kravetz, D. Paracentesis with dextran 70 vs. paracentesis with albumin in cirrhosis with tense ascites. Results of a randomized study. J. Hepatol. 1992 14 310-316... [Pg.319]

Gerbes, A.L., Giilberg, V., Waggershauser, T., Holl, J., Reiser, M. Renal effects of transjugular intrahepatic portosystemic shunt in cirrhosis comparison of patients with ascites, with refractory ascites, or without ascites. Hepatology 1998 28 683-688... [Pg.321]


See other pages where Ascites, in cirrhosis is mentioned: [Pg.213]    [Pg.342]    [Pg.317]    [Pg.213]    [Pg.342]    [Pg.317]    [Pg.55]    [Pg.204]    [Pg.525]    [Pg.350]    [Pg.106]    [Pg.290]    [Pg.291]    [Pg.299]    [Pg.312]    [Pg.319]    [Pg.320]    [Pg.330]   
See also in sourсe #XX -- [ Pg.324 , Pg.326 , Pg.326 , Pg.330 , Pg.331 , Pg.332 , Pg.333 ]

See also in sourсe #XX -- [ Pg.1820 ]

See also in sourсe #XX -- [ Pg.693 , Pg.695 , Pg.697 , Pg.698 , Pg.703 , Pg.709 ]




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