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PubMed2006

Long-term albumin infusion improves survival in patients with cirrhosis and ascites: an unblinded randomized trial.

AIM: To investigate the effects of long-term albumin administration on survival, recurrence of ascites and onset of other complications. METHODS: One hundred consecutive patients admitted for first-onset ascites were randomized to receive diuretics plus human albumin 25 g/wk in the first year and 25 g every two wk thereafter (group 1) or diuretics alone (group 2). The primary endpoint was survival without liver transplantation. Secondary endpoints were recurrence of ascites and occurrence of other complications. RESULTS: Median follow-up was 84 (2-120) mo. Albumin-treated patients had significantly greater cumulative survival rate (Breslow test=7.05, P=0.0078) and lower probability of ascites recurrence (51% versus 94%, P<0.0001). Chronic albumin infusion resulted in a mean increase in survival of 16 mo. CONCLUSION: Long-term albumin administration after first-onset ascites significantly improves patients' survival and decreases the risk of ascites recurrence.

Adult↗
PubMed2001

Minimizing ascites. Complication of cirrhosis signals clinical deterioration.

Ascites is the most common complication of cirrhosis. Its development is associated with a grave prognosis; 50% of patients die within 2 years of diagnosis. An understanding of the analysis of ascitic fluid is essential for the appropriate management of patients with liver disease and ascites. The management of patients with ascites involves a combination of dietary, medical, and surgical approaches. Furthermore, patients with ascites are at risk for ascitic fluid infections and neurohormonal dysregulation that can lead to hepatorenal syndrome. Early recognition of these complications allows therapeutic interventions that minimize further clinical deterioration in already chronically ill patients.

Ascites↗
PubMed1996

Ascites and hepatorenal syndrome: pathophysiology and management.

Ascites, a late manifestation of cirrhosis of the liver, causes increased morbidity and mortality. The renin-angiotensin-aldosterone system, the sympathetic nervous system, and arginine vasopressin are responsible for sodium and water retention in patients with cirrhosis. Fluid localizes to the peritoneal cavity mainly as a result of portal hypertension. Recent developments in the understanding of the pathophysiologic mechanisms of ascites include the role of inadequate renal prostaglandin production in the development of the hepatorenal syndrome and the possible role of nitric oxide in the pathogenesis of the renal complications of cirrhosis. The aim of medical therapy is to achieve a negative sodium balance and, consequently, fluid loss. Large-volume paracentesis is safe and effective in the management of tense ascites, but use of diuretic agents should be continued to prevent reaccumulation of ascites. Liver transplantation, transjugular intrahepatic portosystemic shunts, or LeVeen shunts should be considered in selected patients with persistent ascites. In patients with diuretic-resistant or diuretic-refractory ascites, a thorough assessment must be performed to exclude potentially reversible causes. The hepatorenal syndrome has an associated grave prognosis, especially in patients who are not candidates for liver transplantation.

Algorithms↗
PubMedDate not supplied

Current concepts in the management of refractory cirrhotic ascites.

BACKGROUND: Ascites is the pathologic accumulation of fluid within the peritoneal cavity. This condition when refractory to treatment heralds more severe complications and a poor prognosis. The aim of this paper is to review literature on the pathogenesis and current management of refractory cirrhotic ascites. METHODS: An English language literature search using Medline and PubMed (1976-2006 March) was done to assess all research/review articles on the pathogenesis and management of refractory cirrhotic ascites. RESULTS: The onset of ascites in cirrhotic patients signifies poor prognosis. Only a small percentage of patients with cirrhotic ascites develop true resistance to diuretics. Serial therapeutic paracentesis remains the available option for the majority of patients. Liver transplantation is the only definitive therapy, but the use of this method is limited by the availability of the organ and the cost of such procedure. Transjugular intrahepatic portosystemic stent shunt is a useful procedure but limited by the complication of disseminated intravascular coagulopathy. The role of other alternatives is less clearly defined. CONCLUSION: Therapeutic options in patient with cirrhotic ascites remains serial therapeutic paracentesis with or without plasma expansion. Transjugular intrahepatic portosystemic stent-shunt is a useful alternative. The unavailability of liver donors serves as a barrier to liver transplantation.

Ascites↗
PubMed1986

Cirrhotic ascites. Pathophysiology, diagnosis, and management.

Cirrhotic ascites occurs via both overflow and underfill mechanisms. Intrahepatic hypertension activates a hepatic baroreceptor reflex that enhances renal sodium absorption; plasma volume is expanded. As cirrhosis progresses, the hepatoportal Starling forces become sufficiently disturbed to sequester this "overflow" in the peritoneal cavity, which results in ascites formation. "Underfill" of the vascular system occurs and eventually dominates the clinical picture. Finally, intrahepatic hypertension also activates the renin-angiotensin system, which causes renal vasoconstriction; the increase in renal prostaglandin synthesis maintains renal blood flow. Although cirrhotic ascites is traditionally classified as a transudate, the serum-ascites albumin gradient may be a better indicator of ascites secondary to portal hypertension than other causes. General management of patients with cirrhotic ascites includes severe restriction of dietary sodium intake and bed rest; diuretics are added if spontaneous diuresis does not occur after 3 to 4 days.

Animals↗
PubMed1989

Increased lung water and ascites after massive cocaine overdosage in mice and improved survival related to beta-adrenergic blockage.

STUDY OBJECTIVE: To determine the effect of massive cocaine intoxication on lung water and ascites accumulation and the effect of beta- and alpha-adrenergic blockade on survival in massive cocaine intoxication in the mouse. DESIGN: The effect of massive cocaine intoxication on lung water, ascitic fluid accumulation, and survival following LD 100 doses of intravenous cocaine with and without alpha- and beta-adrenergic blockade was determined. INTERVENTIONS: Cocaine hydrochloride (0.15 mg/g body weight) was administered intravenously with no other interventions; with propranolol hydrochloride intravenously (0.5 mg per mouse) before and after cocaine; and with phentolamine intravenously (10.5 micrograms per mouse) before cocaine. MEASUREMENTS AND MAIN RESULTS: Intravenous cocaine hydrochloride resulted in an increase in lung water (saline controls, 4.17 +/- 1.3 [standard deviation] mg water per g mouse; cocaine hydrochloride, 5.94 +/- 0.9 mg water per g mouse; P less than 0.002). Cocaine hydrochloride always resulted in the accumulation of transudative ascitic fluid (saline controls, no measurable ascitic fluid; cocaine administration, 20.2 +/- 12.9 micrograms per mouse; ascitic fluid protein concentration, 23.5 +/- 8.5 g/L). Propranolol hydrochloride administered before or after intravenous cocaine hydrochloride resulted in a striking reduction in mortality (84 of 84 mice without propranolol died [mortality = 100%]; 7 of 39 mice with propranolol died [mortality = 18%]; P less than 0.001). CONCLUSIONS: Massive cocaine intoxication is associated with increased lung water and transudative ascites. Fluid accumulation is not prevented by either alpha- or beta-adrenergic blockers. Propranolol, administered either before or after cocaine, sharply reduces mortality. The results should be extrapolated to treatment in humans with caution.

Animals↗
PubMedDate not supplied

[Ascites as preeminent manifestation of primary hypothyroidism. Clinical case].

The case of an adult male who came to clinical evaluation because of an abundant ascites without any obvious cardiac or hepatic explanation is reported. The exudative characteristics of the ascitic fluid, the elevated serum-ascites albumin gradient, some electrocardiographic anomalies, hypercholesterolemia and a slight macrocytic anemia prompted a clinical diagnosis of probable hypothyroidism. This was also due to an anamnesis of remote antithyroid radiometabolic treatment. The serum hormone levels and the ultrasonogram of the gland confirmed the diagnosis. Hormonal substitutive therapy led to thyroid-stimulating hormone normalization and to a progressive decrease of the ascites, that eventually disappeared. This case, which involves a rare manifestation of hypothyroidism, underscores the need to consider thyroid diseases in the differential diagnosis of ascites and to include thyroid-stimulating hormone dosage among the laboratory tests to be ordered when suspicious clinical or biochemical data are present (mainly, the exudative aspect of the ascites).

Aged↗
PubMed2001

[Physical diagnosis--ascites].

The diagnosis of ascites can be made very likely by a good clinical history and a well-directed physical examination, if the patient suffers from a disease which can cause ascites. The physician should ask about recent weight gain, change in abdominal girth and ankle oedema. With a positive history, the likelihood of the presence of ascites may increase 3 to 4-fold. When the findings at physical examination are also positive, the likelihood may increase 10 to 20-fold. A fluid wave is the most specific but less sensitive symptom. Shifting dullness, bulging flanks and flank dullness are less specific but much more sensitive parameters. The presence of ascites is very unlikely if the prior probability is low and both the patient's answers and the findings at physical examination are negative. Abdominal ultrasound, the gold standard, is not strictly indicated for diagnosing ascites: if based on the trial tried: pretest probability, clinical history and physical examination, the diagnosis is very likely or very unlikely. Ultrasonography is always indicated, however, when ascites is suspected and a positive finding is of clinical relevance.

Ascites↗
PubMed2001

[Refractory ascites in hemodialysis: treatment by paracentesis- reinjection during dialysis].

Two hemodialysis patients, one male and one female, aged 46 and 54 years, were treated with preceed respectively for refractory ascites secondary to hepatic cirrhosis and for large polycystic liver. Preceed was decided because of the rapid reappearance of effusion following repeated puncture and albumin infusion, the poor tolerance to ultrafiltration (UF) and the poor nutritional status of the patients, with severe hypoalbuminemia. Abdominal paracentesis was performed on initiation of the dialysis session. Reinjection of the ascites fluid was made into the arterial line, allowing its UF and control of its flow. The procedure was performed whenever necessary, i.e., when inter-dialysis weight gain and ascites volume were high. In both cases, improvement was quickly obtained, with less rapid and less severe reappearance of the effusion and correction of albuminemia. Dialysis sessions with UF were better tolerated. No notable side effect was observed. The first patient was treated for 2 months, when he died of an unrelated cause. The other patient was treated for 6 months and then could be transferred to a dialysis center near her home. Twenty five months after start of dialysis treatment, kidney and liver transplantation were performed in this same patient. After transplantation, reappearance of moderate ascites and oedema is attributed to e degradation of renal function, without liver dysfunction. Five weeks after transplantation, improvement of renal function and ascites regression were noted. Preceed is an effective method of treating refractory ascites in the hemodialysis patient. Compared to classical paracentesis, it has the advantage of good tolerance, patient comfort and moderate cost.

Ascites↗
PubMed2001

[A case of tuberculous peritonitis diagnosed by a direct smear of ascitic fluid complicated with an active pulmonary tuberculosis and intestinal tuberculosis].

We sometimes encounter difficulties in differentiating tuberculous peritonitis from other inflammatory disorders or ascites due to carcinomatous peritonitis. Acid-fast bacilli are very rarely detected in ascites. In this study, we reported a case of tuberculous peritonitis accompanied with active pulmonary tuberculosis in which acid-fast bacilli were detected in ascites. The patient was a 37-year-old single man who had been admitted to our hospital on February 28, 2000, because acid-fast bacilli were detected in sputum, faces and ascites by a direct smear. He had a lower abdominal distention and pain. His serum CA 125 level was high, 121 U/ml. Abdominal ultrasonography showed marked ascites in Douglas pouch. However adenosine deaminase level was not high in his ascites. During treatment by the combination chemotherapy with INH, RFP, EB, and PZA, serum CA 125 level was decreased.

Adult↗
PubMed1999

[The causes of chylous ascites: a report of 22 cases].

OBJECTIVE: To review the causes and test the diagnostic accuracy of chylous ascites in 22 cases hospitalized in recent years and to compare the efficacy of current investigative procedures with those of previous decades. METHODS: 22 patients with chylous ascites were studied; they were admitted into Peking Union Medical College Hospital in 7 years (1990 - 1997). The data of the 22 patients were compared with those of 17 cases in previous 67 years (1923 - 1989) in the same hospital. Twelve of 22 patients underwent (99)Tc-labeled lymphoscintigraphy. RESULTS: Chylous ascites was diagnosed by ascites in all the 22 patients with analysis of ascitic fluid. Otherwise, the diagnosis would not be established in eight cases if examined with the naked eye. The causes of all the 22 cases were clearly diagnosed. However, the causes were not known in five cases in the 17 cases of previous years. The main causes in this group were malignant tumors (6/22), hepatic cirrhosis (5/22) and tuberculosis (4/22). Other causes included traumatic and congenital lymphatic lesions. CONCLUSION: The causes of chylous ascites can be made clear and definite by detailed comprehensive examinations, including scintigraphy. The main causes were malignant tumor, hepatic cirrhosis and tuberculosis.

Adolescent↗
PubMed1975

An infallible method for producing ascitic fluid from solid tumours.

Notwithstanding all precautions, the methods usually applied for the transformation of solid tumours into the ascitic form, frequently fail. This must certainly be ascribed to the still existing, considerably high intercellular adhesion forces despite the fact that cancer cells generally show lack of adhesiveness due to their higher electrical charge in comparison with normal cells. Hagmar recently stipulated that particularly anionic detergents increase the negative surface charge of tumour cells, while cationic detergents drastically reduce or even reverse this charge. A series of comparative experiments were undertaken by us in order to study the influence of anionic, nonionic and amphoteric detergents on the production of ascitic fluid from macerates of Yoshida sarcoma and fibrosarcoma BUSP. This latter tumour was produced and maintained in our laboratory and resisted to all our attempts to produce the ascitic form. Heparin, in concentrations of 0,2, 0,4 and 1,0 mg/ml, was used as an example of an anionic detergent; Pluronic F-68 and phosphatidylcholine, both in concentrations of 1, 2, and 5 mg/ml, represent a nonionic and an amphoteric detergent, respectively. The obtained results clearly show a most favourable action of the applied surfactants: whereas the controls, in which the detergents were not applied, failed to produce ascitic fluid in, sometimes, considerable percentages (up to 100% in the case of BUSP) of the treated animals, not a single animal remained free of ascite when the injected macerate was pre-treated with the emulsifier. It should here be mentioned, however, that heparin in the highest concentration applied (1 mg/ml) caused lysis of the tumour cells impeding, thus, whatever formations of ascitic fluid.

Animals↗
PubMed2002

[Long-term efficacy of transjugular intrahepatic portosystemic shunt for the treatment of refractory ascites].

Eighteen patients with refractory ascites (Child-Pugh score 9.9) defined by our criteria were treated with transjugular intrahepatic portosystemic shunt (TIPS). The long-term efficacy of the treatment was studied in these patients. The complete and partial response rate of refractory ascites was 73% at 6 months, 90% at 1 year and 100% at 2 years. The cumulative survival rate was 89% at 6 months, 78% at 1 year and 48% at 2 years. A statistically significant(p < 0.05) increase was observed in performance status score following TIPS: Mean performance status score prior to TIPS was 43%, as opposed to 62% at 3 months after TIPS and 85% at 2 years. Child-Pugh score and liver function tests showed no significant change. During follow-up, shunt stenosis was noted in 14 patients, requiring shunt revision. Ascites recurrence was observed in 70% of patients with shunt stenosis and shunt revision resulted in good control of ascites. Post-TIPS encephalopathy was seen in 15 patients during follow-up. In conclusion, TIPS is effective on the treatment of refractory ascites and results in an improvement in quality of life. TIPS also may improve survival of the patients with refractory ascites. However, shunt stenosis and encephalopathy are common and require careful follow-up and adequate treatment.

Adult↗
PubMed2003

Clinical and neurohumoral response to posture, physical exercise, and ascites treatment in Child-Pugh C liver cirrhosis: randomized prospective trial.

AIM: To assess clinical and neurohumoral response to posture, physical exercise, and ascites treatment in patients with Child-Pugh C liver cirrhosis and tense ascites. METHOD: Fifty patients with Child-Pugh C liver cirrhosis and tense ascites were randomly allocated into 5 groups. Thirty patients were treated with paracentesis of 6 L of acites paralleled by plasma volume expansion with 200 mL of 20% low sodium albumin (10 patients), 600 mL fresh frozen plasma (10 patients), or 900 mL solution of synthetic gelatine (10 patients), ie, doses with comparable oncotic power, and bed rest for 24 h before and after the procedure. They were compared with 10 patients treated with paracentesis of 6 L of ascites without plasma volume expansion and no bed rest, and 10 patients treated with 40 mg of furosemide IV daily and no bed rest. Mean arterial pressure, heart rate, body weight loss, urine flow rate, creatinine clearance, plasma renin activity, plasma aldosterone concentration, and plasma atrial natriuretic peptide (ANP) were measured before the procedure and 6 hours, 2, 3, and 6 days after the procedure. RESULTS: Diuretic treatment and paracentesis of 6 L of ascites without plasma volume expansion and no bed rest 24 h before and after the procedure were associated with significant hypotension (p<0.01) during 6 days of the trial, tachycardia (p<0.01) on day 1 and 2 (p=0.012), lower total body weight loss (p=0.007), increase in plasma renin activity 6 hours after the beginning of the study (p=0.025) and on day 6 (p=0.024), increase in plasma aldosterone concentration on day 6 (p=0.030), no significant change in plasma ANP levels, and decrease in creatinine clearance on day 6 (p=0.046). Albumin was superior to the other plasma expanders. Comparison between groups treated with plasma volume expansion did not show significant differences in measured parameters at any time during the study. The differences were found in the amount of needed volume of each substitute, daily sodium balance on day 1 of the trial, increase in plasma aldosterone concentration in bed rest-paracentesis-polygeline group on day 6, and the increase in plasma ANP on day 1 (p=0.077), which was proportional to the amount of infused volume. CONCLUSION: Therapeutic paracentesis of 6 L of ascites, bed rest 24 h before and after the procedure, and intravenous substitution of volume with albumin, fresh frozen plasma, and solution of synthetic gelatine were safe, rapid, and effective treatments, provided that intravascular volume was substituted simultaneously.

Adult↗
PubMedDate not supplied

The effect of beta-blocker on intractable ascites in cirrhotic patients undergoing hepatectomy for hepatocellular carcinoma.

BACKGROUND/AIMS: Intractable ascites is one of the serious complications after hepatectomy. Only little is known about their effect on postoperative ascites in patients with liver cirrhosis although beta-blockers have been used for cirrhotic complications including ascites. METHODOLOGY: Here, we report five cases of intractable ascites after hepatectomy, which were treated by propranolol (1 mg/kg/body). RESULTS: In three patients, plasma renin activity and aldosterone concentrations were markedly increased before propranolol administration, but fell to normal levels thereafter. Ascites subsided in all subjects except one, who developed cardiac dysfunction. CONCLUSIONS: Beta-blockers might be a promising drug for intractable ascites in cirrhotic patients undergoing hepatectomy.

Aged↗
PubMed2003

[Significances of plasma levels of neuropeptide Y pre- and post-treatment in patients with decompensated cirrhosis and ascites].

OBJECTIVE: To observe changes of plasma neuropeptide Y(NPY) level in ascitic patients with decompensated cirrhosis pre- and post-treatment, there fore to understand the correlation of NPY with liver function and ascitic formation. METHODS: NPY plasma levels in 20 patients with decompensated cirrhosis and ascites were detected by radioimmunological assay. RESULTS: Plasma NPY levels in patients with cirrhotic ascites were significantly lower than those in normal subjects(P < 0.01) in spite of the increases of NPY after ascites decreased (P < 0.01), which were still lower than those in normal subjects(P < 0.01). CONCLUSION: Decreased plasma NPY levels are correlated with the severity of liver damage and may be responsible for the changes of hemodynamics and ascitic formation in patients with liver cirrhosis.

Adult↗
PubMed2003

Lysophosphatidic acid is the unique platelet-activating substance in human malignant ascites.

Pathological blood platelet activation promotes thrombosis in cancer patients, but the specific substances involved are still under investigation. Tumor exudates have been described to contain lysophosphatidic acid (LPA), a known platelet-activating substance, and the concentration of mediators present in malignant ascites are constantly equilibrated with the concentration in plasma. We hypothesized that the ascites of cancer patients might activate platelets, and that this may be caused by LPA. Indeed, ascites samples from 15 different patients with cancer induced shape change and an increase of cytosolic Ca2+ of isolated platelets; both responses were cross-desensitized by lysophosphatidic acid (LPA), but not by other platelet stimuli. Moreover shape change, Ca2+ mobilization and aggregation induced by ascites could be completely blocked by pretreatment of platelets with specific LPA-receptor antagonists. Phospholipids were extracted from ascites, separated by thin layer chromatography, and individual fractions were tested for activity on platelets. The platelet activating substance co-migrated with LPA, whereas other fractions were inactive. Notably, ascites induced through LPA-receptor activation platelet aggregation in whole blood. Our results suggest that LPA plays an essential role in the pathological platelet activation in cancer patients. We propose that LPA receptor antagonists could be effective in blocking cancer-associated platelet activation and thus preventing thrombosis.

Ascites↗
PubMed1992

[Immunologic indicators in ascites].

The authors investigated specific and non-specific immunological parameters in malignant, cirrhotic, cardial and nephrogenic ascites. At the same time bacteriological and cytological examinations of ascites were made. In the submitted paper the authors compare, using statistical methods, immunological parameters of ascites in different patient groups and pay attention to their relationship with positive bacteriological and cytological findings in ascites. The authors recorded the largest number of positive bacteriological cultivation in cirrhotic and malignant ascites which correlates with lower values of some non-specific immunological parameters in ascites.

Antigen-Antibody Complex↗