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PubMed1997

A novel approach to the treatment of ascites associated with ovarian hyperstimulation syndrome.

Ascites is a clinical manifestation of severe ovarian hyperstimulation syndrome (OHSS) which may complicate the induction of ovulation using exogenous gonadotrophins. In severe OHSS severe ascites may occur and can lead to dyspnoea, abdominal discomfort and oliguria. To relieve ascites paracentesis is performed two to three times weekly as needed. We report three cases where an indwelling peritoneal catheter was used to decrease the need for repeated paracentesis. Under ultrasound guidance a closed system Dawson-Mueller catheter with 'simp-loc' locking design was inserted to allow continuous drainage of the ascitic fluid. A total of 23 l of the ascitic fluid were drained from the first, 20 l from the second and 28 l from the third patient with significant decrease in abdominal discomfort and improvement in the urine output. No complications or adverse reactions were noted. Continuous drainage of the ascitic fluid is efficient. It quickly decreases the abdominal discomfort, improves the urine output and prevents the need for multiple abdominal paracenteses which some patients may require.

Adult↗

PubMed1976

Ascites form of a human cancer serially transplantable in nude mice.

Human adenocarcinoma cells injected into the peritoneal cavities of BALB/c nude mice (nu/nu) induced ascites carcinoma. The inoculant was obtained from subcutaneous tumors produced in nude mice by an injection of ascites cells from a patient with carcinomatous peritonitis caused by mucinous adenocarcinoma of the stomach. An ascitic fluid began to accumulate 45 days after inoculation and reached the maximum volume within 120 days. Dispersed stomach cancer cells in the ascites could be serially transplanted in nude mice in an ascites form. The morphology of these cells was similar to that of the original cells in the ascitic fluid of a patient with carcinomatous peritonitis.

Adenocarcinoma, Mucinous↗

PubMed2002

Strict volume control in the treatment of nephrogenic ascites.

BACKGROUND: Nephrogenic ascites refers to the condition of refractory ascites of unknown aetiology and occurs mainly in patients with end-stage renal disease who are undergoing haemodialysis. Despite many treatment modalities, nephrogenic ascites remains difficult to control and has a poor prognosis. METHODS: We investigated six such patients who had developed severe, apparently refractory ascites during haemodialysis. They all had seriously disturbed cardiac dimensions and function. They were treated with repeated isolated ultrafiltration and severe salt restriction, while their cardiac functions were monitored with echocardiography. RESULTS: After a mean of 18+/-4 l of fluid per patient was removed in 27+/-8 days, ascites disappeared in all patients. Blood pressure and cardiothoracic indices were decreased from 130+/-20/83+/-10 to 95+/-11/60+/-6 mmHg (P<0.02) and from 0.61+/-7 to 0.47+/-5 (P<0.02), respectively. At the end of treatment, heart rates had decreased from 102+/-10 to 85+/-6 beats/min. Previously increased left atrial diameters, end-systolic and end-diastolic dimensions of the left ventricles, and right ventricular diameters reached normal values. Ejection fractions initially decreased in all patients, and then increased slightly to markedly after treatment. CONCLUSION: Nephrogenic ascites is a component of right-sided cardiac congestion mediated by volume overload, and it should be treated with severe salt restriction and frequent ultrafiltration with haemodialysis and, if that fails, with daily isolated ultrafiltration.

Adult↗

PubMed1984

Glycolipid composition of ascitic fluids from patients with cancer.

The glycolipid composition of ascitic fluids from nine patients with cancer and one pleural effusion from a hepatoma patient was studied. Glucosylceramide, lactosylceramide, globotriaosylceramide, and globotetraosylceramide were found in all samples and also in normal human serum. These glycolipids accounted for more than 90% of the neutral glycolipid fraction and the composition in ascitic fluids was similar to that in normal human serum. From ascitic fluids, several minor glycolipids, which could not be detected in normal human serum, were isolated and characterized by exoglycosidase treatment. Lactoneotetraosylceramide was found in eight samples of ascitic fluids, and globopentaosylceramide was detected in two samples from hepatoma and one from pancreatic cancer. A fucolipid which was converted to lactoneotetraosylceramide by alpha-L-fucosidase treatment was recognized in two samples from hepatoma patients. In the ganglioside fraction, GM3 was the predominant component both in normal human serum and in ascitic fluid. The GM2 content in ascitic fluids was much higher than that in normal human serum. From these results, lactoneotetraosylceramide and GM2 are possible candidates as cancer markers, because they seemed to be derived from cancer tissues by shedding.

Ascites↗

PubMed1997

Chronic unilateral occlusion of an extrapulmonary primary bronchus induces pulmonary hypertension syndrome (ascites) in male and female broilers.

Previously, it was demonstrated that acute (4 min) and chronic (12 d) occlusion of an extrapulmonary primary bronchus triggers pulmonary hypertension but not pulmonary hypertension syndrome (PHS, ascites) in broilers. The present study was conducted to determine whether a more prolonged period of bronchus occlusion causes PHS similar to that induced by clamping one pulmonary artery. Male and female broiler chicks, 14 to 18 d old, were anesthetized, the thoracic inlet was opened, and a silver clip was positioned to fully obstruct the left extrapulmonary primary bronchus (BRONCHUS CLAMP group) or the left pulmonary artery (PA-CLAMP group). Sham-operated chicks were anesthetized and the thoracic inlet was opened; however, neither the pulmonary artery nor the bronchus was clamped (SHAM group). An electrocardiogram (ECG) was obtained whenever clinical ascites became apparent in individual broilers, or prior to the final necropsy for broilers surviving to the end (Day 36) of the experiment. The right:total ventricular weight ratio (RV:TV) was evaluated as an index of pulmonary arterial pressure. Early post-surgical mortality (up to 21 d of age) was higher in the PA-CLAMP group (27% for males and females combined) than in the BRONCHUS CLAMP (10%) and SHAM (2%) groups. Cumulative ascites mortality (Days 22 to 36) also was higher in the PA-CLAMP group (86% for males, 77% for females) than in the BRONCHUS CLAMP (69% for males, 41% for females) and SHAM (23% for males, 0% for females) groups. Ascitic birds in all treatment groups had higher RV:TV ratios and more negative ECG Lead II S-wave amplitudes than nonascitic birds, reflecting the right ventricular hypertrophy and generalized ventricular dilation typically associated with PHS. These results demonstrate that unilateral bronchus occlusion is an effective experimental model for triggering ascites at a lower incidence than that obtained by occluding one pulmonary artery. Following the onset of pulmonary hypertension, the pathophysiological progression leading to ascites appears to be similar for broilers with either unilateral bronchus or pulmonary artery occlusion.

Animals↗

PubMed2006

Pulmonary hypertension triggered by lipopolysaccharide in ascites-susceptible and -resistant broilers is not amplified by aminoguanidine, a specific inhibitor of inducible nitric oxide synthase.

Nitric oxide (NO) is a potent pulmonary vasodilator that modulates the pulmonary vasoconstriction and pulmonary hypertension (PH) triggered by bacterial lipopolysaccharide (LPS) in broilers. The amplitude and duration of the LPS-induced PH are markedly enhanced following pretreatment with N(omega)-nitro-L-arginine methyl ester (L-NAME), which inhibits NO synthesis by both the constitutive (endothelial) and inducible (inflammatory) forms of nitric oxide synthase (eNOS and iNOS, respectively). In the present study L-NAME and the selective iNOS inhibitor aminoguanidine (AG) were administered to differentiate between iNOS and eNOS as the primary source of NO that attenuates the pulmonary vascular response to LPS. Clinically healthy male progeny from ascites-susceptible and ascites-resistant lines were anesthetized, and their pulmonary artery was cannulated. The initial pulmonary arterial pressure (PAP) was recorded, then the broilers either remained untreated (control group) or were injected i.v. with AG. Ten minutes later all birds received an i.v. injection of LPS, followed 40 min later by an i.v. injection of L-NAME. When compared with untreated controls, AG neither increased the baseline PAP nor did it increase or prolong the PH response to LPS. The ascites-susceptible broilers maintained a higher PAP than the ascites-resistant broilers throughout the experiment, and the ascites-resistant broilers exhibited greater relative increases in PAP in response to LPS than did the ascites-susceptible broilers. Within 40 min after the LPS injection, PAP subsided to a level that did not differ from the respective preinjection value for each line. Injecting L-NAME reversed the decline in PAP, and within 5 min PAP returned to hypertensive levels approaching the maximum peak PH response to LPS. The absence of any impact of AG coupled with the profound response to L-NAME indicates that NO synthesized by eNOS rather than iNOS likely modulated the acute (within 1 h) PH elicited by LPS. Evidently eNOS is activated by the increased shear stress exerted on the endothelium during the PH response to LPS, whereas LPS-mediated up-regulation of iNOS expression may take longer than 1 h before biologically effective quantities of NO are produced.

Animals↗

PubMed1999

Massive ascites caused by peritoneal extramedullary hematopoiesis as the initial manifestation of myelofibrosis.

An 83-year-old man presented with massive ascites. Cytological examination of the ascites revealed primitive hematopoietic cells. The specimen of bone marrow biopsy disclosed diffuse fibrosis, which suggested myelofibrosis with extramedullary hematopoiesis as the cause of ascites. His symptoms resolved dramatically after administration of hydroxyurea. Ascites formation in myelofibrosis is often attributed to presinusoidal portal hypertension and occurs in the context of well-established disease. This case demonstrates that myelofibrosis may manifest as massive ascites caused by peritoneal implants of myeloid tissues. Extramedullary hematopoiesis should be included in the differential diagnosis of ascites.

Aged↗

PubMed1985

The LeVeen shunt in the elective treatment of intractable ascites in cirrhosis. A prospective study on 140 patients.

One hundred and forty patients with an intractable ascites complicating a chronic liver disease received a peritoneovenous shunt (PVS) using the LeVeen valve. Operative mortality was ten per cent but was 25% in patients with severe liver failure. Intraoperative drainage of ascites sharply decreased postoperative complications and mortality. One-year actuarial survival rate was 81.4%, respectively 77.7%, 61.3%, and 24.7% in patients with good liver function and moderate or severe liver failure. Variceal hemorrhage occurred in 11 patients and late infection in another 11 patients. Thirty-eight patients (30.5%) had recurrence of ascites. This was mostly due to an obstruction on the venous side of the shunt. An elective portacaval shunt had to be done in 23 patients for recurrence of ascites or variceal bleeding. Among the 57 patients still alive at time of writing, 51 were free of ascites. These results suggest that PVS is an efficient operation. This procedure may be largely indicated in the selected and small group of cirrhotic patients with true intractable ascites and moderate or no liver insufficiency.

Adult↗

PubMed1979

Use of an AR-1 resin column to reduce bilirubin-level in modified ascitic fluid.

Intractable ascites has been accompanied by significant jaundice in some patients. In such cases, a newly developed synthetic resin, AR-1, has been successfully employed to reduce excess bilirubin from the ascitic fluid. This resin has proved to be excellent compared with XAD-2, XAD-7 and activated charcoal, for removal of bilirubin from the plasma and ascitic fluid in our experiments. A column containing 100 ml of AR-1 is inserted in the drip infusion line between the modified ascitic fluid reservoir in the Autoascit device and the patient. This method has been used in 7 cases of intractable ascites associated with advanced gastric, pancreatic, hepatic, rectal and ovarian cancers. The column has sufficient capacity to adsorb excess bilirubin from the modified ascitic fluid. Other biochemical parameters were eseentially unchanged from pre-column values.

Acrylic Resins↗

PubMed1985

Postsurgical chylous ascites in sarcoidosis with portal hypertension.

A patient with extensive thromboses of portal and mesenteric veins and sarcoid of the liver developed recurrent pulmonary emboli, which necessitated the insertion of an umbrella into the inferior vena cava. Chylous ascites appeared shortly thereafter; the ascitic fluid fat content was strikingly reduced after reduction of dietary long chain triglycerides, but the ascitic fluid volume was reduced only after insertion of a peritoneovenous shunt (LeVeen). The shunt was found to be nonfunctioning 4 months later, but ascites did not recur. Seven years later, while eating a normal diet and still having a nonfunctioning shunt, he remains free of ascites. We postulate that iatrogenic obstruction of the inferior vena cava in the presence of mesenteric and portal vein thromboses, as well as obstruction of mesenteric lymphatics by sarcoid lymphadenopathy, led to the formation of chylous ascites and that establishment of adequate mesenteric and portal venous and/or lymphatic collateral circulation was responsible for his sustained improvement.

Biopsy↗

PubMedDate not supplied

Five days of ceftriaxone to treat culture negative neutrocytic ascites in cirrhotic patients.

The goal of this study is to establish whether 5 days of ceftriaxone treatment was sufficient to cure culture-negative neutrocytic ascites in cirrhotic patients. We studied 50 cirrhotic patients with culture-negative neutrocytic ascites. All were treated with ceftriaxone, 1.0 g IV, twice a day for 5 days. A control paracentesis was performed 48 hours after starting the therapy to assess response to the treatment. A total of 17 demographic, clinical, and laboratory variables were recorded in all cases on the day of diagnosis of CNNA. The mean age of the patients was 57.7 +/- 13.2 years. Thirty-two patients were males and 18 females. The etiology of cirrhosis was hepatitis C virus in 20 patients (40%), hepatitis B virus in 16 patients (32%), cryptogenic in 13 patients (26%), and alcohol abuse in 1 patient (2%). Eighty percent of the patients were in Child-Pugh Class C. Resolution rate of culture-negative neutrocytic ascites on day 5 of treatment was 78%. Hospital mortality in cirrhotic patients with culture negative neutrocytic ascites was 4%. Statistical analysis showed that none of the 13 selected variables as covariates significantly related with the resolution of culture-negative neutrocytic ascites. Five days of ceftriaxone treatment is an adequate therapy for culture-negative neutrocytic ascites.

Adult↗

PubMed1996

Ascites and the acquired immunodeficiency syndrome. Report of 54 cases.

We identified 54 patients with AIDS and ascites seen over a 4.5-year period at a university hospital. This retrospective study is the largest reported series of patients with AIDS and ascites. Patients with AIDS who are evaluated for ascites should be stratified by the CD4 + cell count and the presence or absence of portal hypertension based upon the serum-ascites albumin gradient and clinical presentation. Awareness of possible surgery-related causes of ascites is crucial, as these patients may not manifest the usual signs and symptoms of peritonitis or abdominal catastrophes seen in immunocompetent hosts. Patients with evidence of portal hypertension due to hepatic cirrhosis and an elevated ascitic neutrophil count should be suspected to be infected with common bacterial pathogens associated with peritonitis unless the CD4 + cell count is below 50 cells/mm3. When the CD4 + cell count declines below this threshold, infections due to Mycobacterium avium complex, cytomegalovirus, and other opportunistic infections should be considered.

Acquired Immunodeficiency Syndrome↗

PubMed1984

Secondary bacterial peritonitis in cirrhotic patients with ascites.

Bacterial peritonitis in patients with cirrhosis has a wide variety of clinical presentations. We report a group of 21 cirrhotic patients with secondary peritonitis from intra-abdominal sources. Seven had infected ascites. All of them had unrecognized secondary peritonitis which was diagnosed and treated as spontaneous (primary) bacterial peritonitis (SBP). Ascitic fluid analysis yielded a mean white blood cell count of 23,750 +/- 10,935/cu mm with 91.5% polymorphonuclear leukocytes, significantly higher than patients surveyed with SBP, 1,757 +/- 2,154/cu mm (P less than .001). Ascitic fluid protein levels were also higher than those typically seen in SBP: 4.4 +/- 1.5 gm/dl vs 0.8 +/- 0.4 gm/dl (P less than .001). The ascites: serum protein ratio was consistent with an exudate in those patients with secondary peritonitis (0.7 +/- 0.2) in contrast to typically infected transudate in patients with SBP (0.15 +/- 0.05) (P less than .001). Bacteriologic determination was similar: single organisms with Escherichia coli the most common. Often the clinical features and ascitic fluid analysis will not differentiate spontaneous from secondary peritonitis. It is, therefore, clinically prudent to consider secondary bacterial peritonitis in cirrhotic patients, especially with ascitic fluid WBC counts in excess of 5,000/cu mm and protein levels of greater than or equal to 2.5 gm/dl. Noninvasive diagnostic procedures should be included to search for sources of intra-abdominal infection.

Anti-Bacterial Agents↗

PubMed1996

Ascites associated with antibiotic-associated pseudomembranous colitis.

We report the case of an elderly patient who had ascites due to pseudomembranous colitis and associated hypoalbuminemia. Computed tomography showed diffuse colonic wall thickening. An indium-111 scan to localize the site of infection showed abnormal localization of 111In throughout the colon. Despite treatment, the patient died. Autopsy disclosed no other cause for the ascites, except for possible sepsis. To study the cause of ascites in patients with pseudomembranous colitis, we reviewed our institutions' experience with ascites in association with Clostridium difficile colitis, identifying 16 cases over a 1-year period (which included our case). In most of the other cases, the ascites could be attributed primarily to another mechanism, including portal hypertension, congestive heart failure, and sepsis (intra-abdominal and systemic). We also reviewed the literature regarding the association of ascites with C difficile colitis.

Aged↗

PubMed1997

Molecular cloning of a defective hepatitis C virus genome from the ascitic fluid of a patient with hepatocellular carcinoma.

A defective hepatitis C virus (HCV) genome in the ascitic fluid of a patient with hepatocellular carcinoma was cloned and sequenced up to the 3' poly(U) stretch. When compared with the published Taiwanese HCV sequence, this defective genome contained deletions of single nucleotides at eight sites, double nucleotides at two sites, triple nucleotides at four sites, quadruple nucleotides at one site and replacement of a short stretch of sequence at one site. For comparison, the corresponding regions containing these mutations were also cloned from a serum sample from this patient. Except for deletions of two triple nucleotides in the hypervariable region, the reading frames of all serum-derived clones were intact. The defective HCV genome encoded a truncated core protein with 90 amino acid residues (the last 20 amino acid residues came from a different reading frame), whereas the serum-derived genome encoded a full-length core protein. When expressed in Huh-7 cells, these two proteins were localized to the nucleus and cytoplasm, respectively. Using specific primer-sets, ascites- and serum-derived genomes were each detected alone in ascitic fluid and serum samples, respectively, whereas both sequences were present in ascitic mononuclear cells. The defective sequence thus constituted the major virus population in the ascitic fluid whereas a putative helper genome coexisted with it inside the ascitic mononuclear cells. This sequence is possibly a defective and interfering genome.

Amino Acid Sequence↗

PubMed1995

New strategies for the management of malignant ascites.

Intractable malignant ascites accounts for 6% of all hospice admissions. The onset of malignant ascites indicates a poor prognosis, hence minimal supportive therapy is indicated. This paper examines the method of control for malignant ascites presently available to patients, examines their limitations and proposes new strategies for managing intractable malignant ascites. Ascites is discussed in terms of its pathology--that is, as a form of lymphoedema. With this in mind treatment is proposed based upon principles incorporated into lymphoedema management. Nurses have taken a dominant role in the care of patients with lymphoedema and there appears no reason why ascites management cannot become the remit of nurses offering appropriate, but predominantly palliative therapy.

Ascites↗

PubMed1986

Renin, aldosterone and arginine vasopressin in patients with liver cirrhosis: the influence of ascites retransfusion.

Plasma renin activity (PRA), and concentrations of aldosterone (PAL) and arginine vasopressin (AVP) in plasma were determined in 15 patients with ascites due to cirrhosis. The concentrations in ascites were analyzed simultaneously. Six patients were studied during extracorporeal ascites retransfusion. All but one patient with ascites showed elevated PAL (642 +/- 255 pg ml-1) and PRA (43 +/- 26 ng ml-1 h-1); all had increased AVP (7.3 +/- 5.1 pg ml-1). A low ascites to plasma ratio was found for aldosterone (0.023 +/- 0.023), but not for AVP (0.71 +/- 0.82). Retransfusion resulted in a normalization of central venous pressure (CVP), urinary volume, sodium/potassium ratio in urine, PAL and PRA, but not of AVP, serum sodium concentration and urinary sodium excretion. PRA and PAL increased again after cessation of treatment, while urinary output, CVP and sodium/potassium ratio in urine decreased. The results support the 'underfilling' concept, but give evidence that, in addition, other factors must be involved in the impaired natriuresis in cirrhotic patients. They further support the concept of volume expansion and increased renal perfusion as reason for the therapeutic efficacy of ascites retransfusion. Previous diuretic treatment seems not to be of importance for altered hormone metabolism in liver cirrhosis. Storage in a third compartment may be a factor in the persistently elevated AVP levels.

Adult↗

PubMed1991

Plasma noradrenaline in cirrhosis: a study of kinetics and temporal relationship to ascites formation.

The kinetics of plasma noradrenaline (NA) were studied in 14 patients with cirrhosis and ascites and 13 normal subjects. [3H]noradrenaline ([3H] NA) was infused intravenously to steady state and the spillover of NA into plasma and its clearance from plasma calculated. The increase in plasma NA in the cirrhotic patients was due to an increase in NA spillover (14.5 vs 3.9 nmol min-1m-2; P less than 0.001). NA plasma clearance was also increased in the cirrhotic patients (3.5 vs 2.11 min-1m-2; P less than 0.01). Plasma NA and dihydroxyphenylglycol (DHPG), a metabolite of NA of which a portion is formed after re-uptake of NA into sympathetic nerve endings, were then measured in 23 patients with cirrhosis and ascites, 17 patients with cirrhosis who had never had ascites, and 34 normal subjects. Both plasma NA and DHPG were significantly increased in the patients with ascites (NA 4.7, DHPG 14.7 nmol l-1 and in the patients with cirrhosis but no ascites (NA 3.8, DHPG 12.0 nmol l-1) compared with normal subjects (NA 1.9, DHPG 8.8 nmol 1-1). Therefore, the increase in plasma NA in cirrhosis is due to increased activity of the sympathetic nervous system rather than interference with the metabolism of NA or impaired neuronal uptake of NA. This increase appears to precede the development of ascites.

Adult↗