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PubMedDate not supplied

Ascites in liver diseases.

The clinical course of patients with cirrhosis of the liver is frequently complicated by progressive impairment of renal sodium handling leading to the formation of ascites. The occurrence of ascites is generally accompanied by the activation of several hormones and intrarenal autacoids and a complex derangement of systemic, portal and renal hemodynamics. The earliest "underfilling" theory of sodium retention proposes that ascites formation leads to hypovolemia and secondary sodium retention. According to the "overflow" theory, ascites formation is a secondary event with respect to sodium retention, which occurs as a primary phenomenon in the absence of hypovolemia. A third recently developed theory suggests that peripheral arteriolar vasodilation is the primary event of intravascular underfilling. The major documented site involved in arteriolar vasodilation is the splanchnic circulation. Occurrence of underfilling is not related to a reduction of plasma volume but to the enlargement of the vascular compartment. Vascular underfilling triggers a series of hemodynamic and hormonal compensatory events such as an increase in cardiac output and plasma volume, activation of the renin-angiotensin-aldosterone and sympathetic nervous system and non-osmotic hypersecretion of antidiuretic hormone and sodium retention, all of which aim at refilling the vascular compartment. In patients with compensated cirrhosis, i.e. without ascites, compensatory events maintain blood volume despite vascular underfilling, and so these patients do not develop ascites. In patients with decompensated cirrhosis, vascular underfilling due to arterial vasodilation, together with a reduced oncotic pressure and a severe degree of portal hypertension, favours the development of ascites. Underfilling of the arterial circulation is at its maximum in functional renal failure and the hepatorenal syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗

PubMed1991

Ascites in patients undergoing intermittent haemodialysis at Kenyatta National Hospital.

In a two-year-period (August 1984 to August 1986), 77 patients were admitted into the maintenance haemodialysis programme at Kenyatta National Hospital. 24 (31.5%) of these had ascites during haemodialysis. Nine (37.5%) of the patients who had ascites had prior peritoneal dialysis, while 15 (62.5%) had congestive cardiac failure at the time of development of the ascites. In 21 (87.5%), the ascites responded to therapy with diuretics, salt and fluid restriction, antibiotics when indicated and to ultrafiltration during dialysis. In 3 (12.5%) of the patients, the ascites developed in the absence of any predisposing cause. The ascites progressively increased in amount and was associated with marked wasting. These patients were considered to have refractory ascites of haemodialysis.

Adolescent↗

PubMed1991

Peritoneoscopy in diagnosis of ascites.

Diagnostic peritoneoscopies were performed in 226 patients with ascites. Satisfactory examination was possible in 220 patients. Clinical diagnosis was confirmed at peritoneoscopy in 82.7% of patients. Peritoneoscopic examination corrected the clinical diagnosis in 13.7%, was inconclusive in 2.6% and was incorrect in 0.8% of cases. It was 100% diagnostic in malignant peritonitis and 89.5% in patients with tuberculous peritonitis. Pseudomyxoma peritoneai and mesothelioma were suspected in one patient each at peritoneoscopy and was confirmed histologically. The utility of routine ascitic fluid examination was reviewed in all patients. The ascitic fluid was transudative in 81.9%, exudative in 8.6% and indeterminate in 9.5% of patients with cirrhosis of liver. Patients with tuberculous pertitonitis had exudative, transudative and indeterminate ascites in 71.8%, 3.2% and 25% respectively. The ascites in patients with malignant peritonitis was either exudative (80%) or indeterminate (20%). There was considerable overlap in the nature of ascites present in the three groups of patients. We therefore conclude that peritoneoscopy is the most valuable investigation in the diagnosis of ascites, particularly in exudative and indeterminate types.

Ascites↗

PubMed1990

[Clinical analysis of ascitic fluid in patients with liver cirrhosis and hepatocellular carcinoma].

To investigate the clinical significance of ascitic fluid in patients with a malignancy, an abdominal paracentesis to evaluate the ascitic fluid was performed in 10 patients with a hepatocellular carcinoma (HCC) and in 7 patients with liver cirrhosis (LC). The AFP levels in the ascitic fluid and in the serum of the HCC patients was found be significantly higher than that of the LC patients. In addition, the ratio of albumin/total protein in ascitic fluid was also higher in the HCC patients. However, no significant findings were uncovered with regard to the concentration of lipid in ascitic fluid, in either type of patient although 2 HCC patients were found to have a very high concentration of total cholesterol. The cytological findings provided no reliable marker because of significant number of false negatives in the HCC patients. Also, there was no significant difference between the fibronectin levels in the ascitic fluid of either type of patients. This finding differs from previous studies, and suggests that the fibronectin levels in the ascitic fluid may not be a useful marker in determining a malignancy.

Aged↗

PubMed1990

Comparison of two ascitic fluid culture methods in cirrhotic patients with spontaneous bacterial peritonitis.

The conventional method of ascitic fluid culture detects bacteria in only 50% of cirrhotic patients with neutrocytic ascites and suspected spontaneous bacterial peritonitis (SBP). We have prospectively compared two ascites culture methods in cirrhotic patients with spontaneous bacterial peritonitis: 1) conventional (on chocolate agar, blood agar, Mac Conkay agar, and thioglycolate broth), and 2) modified [inoculation of 10 ml of ascites in a tryptic soy broth (TSB) blood culture bottle at the patient's bedside]. In a 21-month period, 70 episodes of SBP were diagnosed according to our criteria in 60 cirrhotic patients. Both culture methods were performed simultaneously. The conventional grew bacteria in 40 episodes (57%), whereas the modified grew bacteria in 54 episodes (77%), a significantly higher sensitivity (p = 0.0001). In 16 cases (23%), ascitic culture was negative by both methods. The mortality rate was higher among patients with culture-positive SBP than those with culture-negative SBP (46% vs 37%), but did not reach statistical significance. We conclude that ascitic fluid inoculated into a TSB blood culture bottle at the patient's bedside should be used routinely for ascites culture in cirrhotic patients.

Ascitic Fluid↗

PubMed1990

[Chylous ascites in adults: etiological, therapeutic and prognostic aspects. Apropos of 35 cases].

Chylous ascites is a rare disease which often poses difficult problems in diagnosis and management. We reported a series of 35 patients with chylous ascites, seen between 1976 and 1989. Diagnosis of chylous ascites was made on: (1) a milky appearance of ascites; (2) an ascitic concentration of triglycerides higher than in serum and higher than 1.5 mmol/l. Incidence was about 1/8 850 admissions. Cancers (mainly lymphomas and abdominal carcinomas), cirrhosis and retroperitoneal surgery accounted for more than 90 p. cent of cases. In all cases of cancer the tumor was extensive, and the prognosis was poor with a one year mortality rate of 80 p. cent. The two postoperative chylous ascites without cirrhosis were cured, after treatment with medium chain triglycerides in one case, and surgical repair in the other case. Chylous ascites in cirrhosis, spontaneous or after porto-systemic shunt, became refractory in 13 of 15 patients, and the one year mortality rate was high (69%).

Adult↗

PubMed1989

Short- and long-term effectiveness, morbidity, and mortality of peritoneovenous shunt inserted to treat massive refractory ascites of nephrogenic origin analysis of 14 cases.

The experience with 14 patients with end-stage renal disease (ESRD), 13 of them maintained on chronic hemodialysis (x 20.4 months +/- 2.9 SEM) and one following successful renal transplantation, underwent placement of a peritoneovenous shunt (PVS) for refractory ascites that had been present before insertion from two to 15 months (x 5.3 +/- 0.8 SEM). A "specific" cause for the ascites could not be identified in any of the 14 patients. The ascites was an exudate in every patient (protein content greater than 3.5 gm/dl). Twelve patients (86%) obtained significant relief of the discomfort and all effects of the ascites, and objective clinical improvement persisted for at least six months. Nine patients (75%) survived one year and six (50%) survived three or more years. Three patients (21%) had recurrence of ascites because of shunt malfunction; however, two of them were successfully treated with placement of a second shunt. Eight (57%) patients have died since the onset of their ascites (x 14.1 months +/- 3.5 SEM); one death was attributable to PVS placement, while the other seven deaths were due to complications of their ESRD. Insertion of a PVS is an effective therapeutic alternative to palliate the discomfort and ill effects of massive nephrogenic ascites that is often refractory to hemodialysis with ultrafiltration.

Adult↗

PubMedDate not supplied

[The Denver shunt in malignant ascites].

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.

Abdominal Neoplasms↗

PubMed1989

[Effects of lymphokine-activated killer cells and interleukin-2 on the ascites formation and the survival time of nude mice bearing human ovarian cancer cells].

Effect of intraperitoneal instillations of interleukin-2 (IL-2) and/or lymphokine-activated killer (LAK) cells on the ascites formation and the survival time was examined by using a nude mice model with malignant ascites by intraperitoneal inoculation of human ovarian cancer cells (HRA) derived from ascites of a patient with serous cystadenocarcinoma of the ovary. On 28 days after tumor inoculation, all nude mice in both untreated and spleen cells only treated groups formed ascites. Two of 10 nude mice treated with IL-2 only after tumor inoculation survived without forming ascites during the experimental period. On the other hand, all nude mice treated with LAK cells only formed ascites by 14 days after tumor inoculation. When LAK cells and IL-2 were combined 5 of 10 mice survived without forming ascites during the experimental period. The survival time of the IL-2 only treated group was significantly prolonged, compared to that of medium only, spleen cells only and LAK cells only treated groups. When administration of LAK cells was followed by IL-2, the survival time was further prolonged.

Animals↗

PubMed1989

Re-evaluation of the value of ascitic fluid pH lactate dehydrogenase and total proteins in the diagnosis of spontaneous bacterial peritonitis (SBP).

In view of high mortality, variable clinical presentation, and late results of bacterial culture, early diagnosis of SBP and treatment are based on indirect parameters of infection. Forty-two patients with ascites and liver cirrhosis were studied. Ascitic fluid (AF) was examined for total protein content, pH, lactate dehydrogenase, amylase, absolute polymorphonuclear cell count (PMN) and for presence of bacteria by examining a fresh smear of the deposit and culture of the fluid under aerobic and anaerobic conditions. AF/serum gradient of total proteins and LDH was calculated. One patient proved to have a malignant ascites and was excluded. The remaining 41 patients fell into two groups: Group I PMN less than 250 cell mm-3, culture negative, sterile ascites, 36 patients. Group II PMN greater than 250 cell mm-3. (a) Culture positive neutrophilic ascites (SBP), three patients. (b) Culture negative neutrophilic ascites (CNNA), two patients. In both CNNA and SBP:AF/serum total LDH gradient greater than 0.75 In the sterile group: AF/serum total LDH gradient less than 0.58 There was no correlation between presence of infection and ascitic fluid pH, protein content and AF/serum total protein gradient. Therefore AF PMN greater than 250 mm and AF/serum total LDH gradient greater than 0.6 should be considered reliable, indirect parameters of infection, and CNNA a variant of SBP with a small bacterial inoculum size.

Ascitic Fluid↗

PubMed1988

IgD antibodies to DNP are specifically induced in ascitic fluid after intraperitoneal immunization.

The induction characteristics of IgD in serum and other body fluids are poorly understood. Here we report that Freund's complete adjuvant (FCA), when used in intraperitoneal (i.p.) immunization, resulted in significantly higher levels of IgD and specific IgD antibodies in ascitic fluid than in the serum of the same animals. This was in sharp contrast to the distribution of IgM and kappa light chain-bearing immunoglobulins (kappa Ig) between these compartments. Female rats were immunized subcutaneously (s.c.) on Day 0 with 1:1 FCA mixed with either 2,4 dinitrophenyl group A streptococcal vaccine (DNP-GASV), 2,4 dinitrophenyl ovalbumin (DNP-OVA), or saline. A week later (and weekly thereafter) they were boosted i.p. with these antigens mixed with FCA 1:9. Eleven of sixteen rats produced some ascites by Day 21, and 15/16 by Day 28. Total immunoglobulin and specific antibodies for the heavy-chain isotypes IgD and IgM and for kappa Ig were measured by ELISA. Between immunization groups no significant differences were observed in total immunoglobulin levels. Subcutaneous immunization with 1:1 FCA caused a significant two- to six-fold increase in serum IgD by Day 7 (P less than 0.01), while no change occurred with serum IgM or kappa Ig. Ascitic fluid collected on Day 21 had significantly high levels of IgD than that of serum IgD (P less than 0.01), with a mean level nine times that of the serum. In contrast, levels of total IgM, kappa Ig and total protein were significantly lower in ascitic fluid than in serum (all P less than 0.05). The high levels of IgD in ascitic fluid disappeared in Day 28 ascitic fluid, while IgM and kappa Ig levels were relatively unchanged. The ratio of ascitic fluid to serum IgD anti-DNP was 9.8 for the DNP-GASV-immunized group on Day 21, and 23.9 for the DNP-OVA-immunized group on day 28. The same ratios for IgM anti-DNP and kappa Ig anti-DNP were much lower, ranging from 0.4 to 2.3 and 0.3 to 3.3, respectively.

Animals↗

PubMed1987

[Chemical and cytologic tests in the differential diagnosis of ascites].

The value of chemical (protein, LDH, glucose, total and differential cell count) and cytological examination of the ascitic fluid in the differential diagnosis of peritoneal ascites was assessed in a prospective study of 98 patients. The ascites caused by hepatic metastases and primary carcinoma were of the transudative type and could not be distinguished from the type caused by cirrhosis on the basis of the parameters examined. In contrast the ascites caused by peritoneal carcinosis was exudative presenting a highly significant (p less than 0.001 for all parameters) difference from the three preceding groups. However there was no clear-cut distinction between the groups: in fact cirrhosis patients may present exudative ascites (8% in the present series, 12-19% in the literature). There was a substantial decrease in ascitic fluid glucose (less than 60 mg/dl) only in peritonitis and its measurement is therefore of secondary importance. In contrast with reports by other authors the ratio between LDH and protein concentrations in the effusion and the serum was found to be insignificant. The cytological examination revealed a significantly higher total cell count in bacterial peritonitis with a prevalence of polymorphonuclear cells and in peritoneal carcinoma where mononuclear cells predominate. Finally cytology revealed malignant tumour cells in the ascitic fluid and neoplastic peritoneal effusions in 28% of the patients examined.

Adult↗

PubMed1985

Effect of prostaglandin blockers on ascites fluid in pancreatitis.

UNLABELLED: Prostacyclin (PGI2), a potent vasodilator with complex effects on the mesenteric circulation, has been found to be elevated in the hemorrhagic ascitic fluid of pigs with hemorrhagic pancreatitis. This investigation was designed to determine if blockage of PGI2 significantly reduces the volume and/or toxicity of hemorrhagic ascitic fluid associated with hemorrhagic pancreatitis in pigs. Fifteen pigs were studied: five received corticosteroids, five received ibuprofen, and five were untreated. The relative toxicity of the hemorrhagic ascitic fluid was assessed by intraperitoneal injections of the fluid from pigs into mice. RESULTS: (1) hemorrhagic pancreatitis was associated with high levels of PGI2 in blood 15 times and in hemorrhagic ascitic fluid 25 times that of baseline; (2) steroids and ibuprofen blocked PGI2 production (p less than 0.05); (3) neither steroids nor ibuprofen, even when administered as pretreatment, decreased ascites formation; and (4) the mortality rate in mice was significantly reduced (p less than 0.05) in the ibuprofen-treated group as compared with the untreated and steroid-treated groups. CONCLUSION: PGI2 does not play a significant role in the volume of ascites formation. There was an absence of toxicity in the hemorrhagic ascitic fluid of the ibuprofen-treated group.

6-Ketoprostaglandin F1 alpha↗

PubMed1985

[Diffusion of cefotiam into ascitic fluid].

The large apparent volume of distribution of cefotiam (reported by Fourtillan et al. [4]), prompted an investigation of cefotiam diffusion into ascitic fluid. Eight patients with non-infected ascites were each given a single intravenous bolus of 2 gr cefotiam. Samples of blood and ascitic fluid were collected 0.5, 1, 2, 3, 4, 6 and 8 hours after the injection. Plasma and ascitic fluid concentrations of unchanged cefotiam were determined using HPLC. Peak concentration in ascitic fluid averaged 18 micrograms/ml and was reached at two hours. Concentrations were still high (approximately 13 micrograms/ml) at 8 hours, leading to further assays 12 and 24 hours after the injection in three subjects. Cefotiam concentrations achieved in ascitic fluid seem adequate for the treatment of infected ascites, given the antibiotic's MICs for the organisms most commonly involved.

Ascitic Fluid↗

PubMed1981

Distribution of copper-64 in control mice and in mice bearing ascitic Krebs tumor cells.

Three to 20 hr after an i.p. injection of 64Cu (half-life, 12.8 hr) into mice bearing Krebs ascites cells, a high amount of the radioisotope was recovered in the ascites cells themselves. In the control group, the radioisotope was mainly present in the liver. Similar amounts of 64Cu were recovered in regenerating as well as in normal liver, whereas in the liver of mice bearing ascites cells, this amount was lower by 40 to 50% regardless of the ascitic volume. Thus, the copper metabolism seems to be disturbed at the hepatic level in mice bearing ascites cells. The distribution of 64Cu was 'analyzed in DNA, RNA, and proteins from cellular lysates fractionated by CsCl gradient. There was a uniform pattern of distribution in the macromolecules from ascites cells, while 64Cu' was preferentially associated with the protein fraction from liver. Further experiments indicated that, in vivo, 64Cu was bound to the DNA of ascites cells.

Animals↗

PubMed1981

Immunoreactive forms of cationic trypsin in plasma and ascitic fluid of dogs in experimental pancreatitis.

A canine model of bile-induced pancreatitis has been employed to investigate time-dependent changes in the molecular forms of trypsin in blood and ascitic fluid in this disease. The distribution of immunoreactive trypsin as trypsinogen and trypsin bound to plasma inhibitors in ascitic fluid and plasma during the course of the disease has been investigated by means of a radioimmunoassay for canine pancreatic cationic trypsin. In addition, trypsinlike amidase activity was determined in plasma and ascitic fluid using Z-Gly-Gly-Arg-beta-Nap as substrate. Early plasma and ascitic fluid samples in four dogs that died contained primarily trypsinogen, while extensive activation of trypsinogen to alpha 2-macroglobulin and alpha 1-protease inhibitor-bound trypsin occurred in the course of the disease. A fifth dog survived and showed little activation of trypsinogen. In the four dogs that died, the levels of trypsinlike amidase activity in the ascitic fluid were substantial throughout the course of the disease. The plasma levels of trypsinlike activity in these animals were much lower, but increased during the disease process. The dog that survived had lower concentrations of trypsinlike activity in ascitic fluid and plasma. These results suggest that activation of trypsinogen resulting in inhibitor-bound forms of trypsin in ascitic fluid and plasma is important in the pathogenesis of acute pancreatitis.

Amidohydrolases↗

PubMed1983

[Suppression of immunological response by ascitic fluid from gastrointestinal cancer patients].

Immunological analysis of ascitic fluids from 49 patients with gastrointestinal cancer was performed and compared to those from 13 patients with hepatic cirrhosis and 3 with congestive heart failure. The analysis of ascitic fluid was performed using natural killer (NK) activity, MLR, PHA-induced lymphoproliferation (LP) and PPD-LP. Immunologic suppression by malignant ascitic fluid was more remarkably observed in PHA-LP, PPD-LP, MLR and NK assay than that by cirrhotic ascites, and it was further proved to be dose dependent. Ascitic fluids from patients with congestive heart failure showed no suppressive effects. There was no correlation between these suppressions and AFP, CEA or immunosuppressive acidic protein (IAP) levels in ascitic fluids. The first fraction of sephadex G 200 Gel filtration, which has a molecular weight of more than 200,000, showed the immunosuppressive activity. It is concluded from these results that this immunosuppressive factor does not involve AFP, CEA and IAP. Thus, it is presumed that the prognosis of the patients with gastrointestinal cancer might correlate with the immunosuppressive factor in their ascitic fluid.

Ascitic Fluid↗

PubMed1980

SEM study of the attachment of mouse ascitic hepatoma cells to various substrata.

Attachment of the cells of mouse ascitic hepatoma to various substrata was examined with the aid of SEM. Ascitic cells did not attach themselves in vitro to the mesothelium-covered surface of peritoneum. However, these cells were attached to the surface of peritoneum from which mesothelial layer had been removed. In the course of growth of ascitic tumor in vivo attached ascitic cells on the peritoneal surface were seen only in the areas of stomata but not in the mesothelium-covered areas. Ascitic cells taken from the peritoneal fluid adhered poorly to the glass surface in culture. However, adhesiveness of these cells to the glass and their ability to spread on the glass surface increased considerably after cultivation in vitro. This alteration of adhesiveness was completely reversible: the cultured cells transplanted intraperitoneally restored their poor adhesive properties. It is suggested that non-adhesiveness of mesothelial surface is the main factor preserving suspended state of intraperitoneally growing ascitic cells. Depending on the environment, ascitic cells may undergo reversible changes of adhesiveness.

Animals↗