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Ascites or pleural effusion? CT and ultrasound differentiation.

The differentiation of fluid immediately above the diaphragm, i.e., pleural effusion, from subdiaphragmatic fluid, i.e., ascites, can be difficult. Freely mobile pleural effusions are easily proven with decubitus chest films, but loculated subpulmonic effusions can mimic intraabdominal fluid. The simultaneous presence of both ascites and pleural effusion is difficult to identify with plain radiographs. Both computed tomography (CT) and ultrasound (US) can be used to differentiate ascites from pleural effusion. Four criteria have been described to differentiate ascites from pleural effusion by CT. These four signs (the diaphragm sign, the displaced crus sign, the interface sign, and the bare area sign) are reliable when only one abnormal fluid collection is present. When both a pleural effusion and ascites are present, none of these criteria can reliably identify both fluid collections. The combined use of the four criteria, however, leads to a correct identification of abnormal fluid collections in the region of the diaphragm. US examination can differentiate ascites from pleural effusion using three of the above-mentioned signs (the diaphragm sign, the displaced crus sign, and the bare area sign). We will review the four signs and discuss the limitation of these signs in clinical practice. A thorough understanding of these CT and US criteria will allow for accurate identification of all juxtadiaphragmatic fluid collections.

Ascites↗

Ultrafiltration by hemofilter--a new therapeutic measure in intractable ascites.

The clinical efficacy of ultrafiltration (UF) of ascitic fluid with hemofilter in the treatment of intractable ascites associated with chronic liver disease or intraabdominal malignancy was studied in fifteen patients. The ascitic fluid was reinfused into the peritoneal cavity after ultrafiltration. An average of 6.2 liters of fluid was removed during 4.4 hours of ultrafiltration with no significant change in blood pressure, central venous pressure, hemoglobin, platelets or plasma creatinine. Ascitic fluid albumin rose significantly immediately after the procedure (from 5.2 +/- 4.3 gm/L to 31.9 +/- 30.0 gm/L, P less than 0.01). The plasma albumin concentration increased significantly at the end of UF (P less than 0.001). Also there was a significant increase in urine output (P less than 0.001), urinary sodium excretion (P less than 0.001), and endogenous creatinine clearance (P less than 0.01) during the 48 hours following UF. There was no evidence of hemodynamic, renal or hematological dysfunction, and other complications, including encephalopathy, peritonitis and variceal bleeding were not experienced. Ultrafiltration of ascitic fluid with hemofilter may be safely used in the temporary relief of refractory ascites due to cirrhosis or intra-abdominal malignancy.

Adolescent↗

Factors that determine refractoriness of ascites to conventional therapy.

We compared the charts of 33 patients who had refractory ascites with those of 33 patients who had responsive ascites to identify factors responsible for resistance to conventional therapy. The results of biochemical tests of liver function were more abnormal in the responsive group than in the refractory group on admission to hospital, whereas the results of kidney function tests were worse in the refractory group. The transhepatic portal pressure was similar in the 7 patients with refractory ascites and the 11 patients with responsive ascites in whom it was measured. The portal vein pressure as calculated from the difference in albumin content between the serum and the ascitic fluid was similar in the two groups, as were the findings at histologic examination of the liver. We conclude that neither the severity of the liver disease nor the portal pressure is a critical factor in the development of refractory ascites. Kidney dysfunction, however, is important, but its mechanism remains unclear.

Adult↗

Successful use of the Denver peritoneovenous shunt in patients with nephrogenic ascites.

Tense ascites in patients who require hemodialysis for renal failure (nephrogenic ascites) is a rare but ominous complication. Its appearance is often followed by a rapid physical deterioration. Nonsurgical attempts to control the ascites are often unsuccessful. Four patients with refractory ascites were treated with Denver peritoneovenous shunts (DPVS). These patients suffered from ventilatory failure, anorexia with malnutrition, and hypotension during hemodialysis. Patients were followed for as long as 18 months after DPVS, and all experienced clinical resolution of the ascites. Ventilatory failure, malnutrition, and hypotension either improved or resolved after shunting. Shunt-related morbidity occurred in all patients and consisted of mechanical complications in four patients and bacteremia in one patient. These problems were resolved by either revision or removal of the DPVS. No deaths were directly related to shunting. Peritoneovenous shunting successfully treats nephrogenic ascites and reverses the morbid sequelae usually associated with this syndrome.

Adult↗

Concentration of fibronectin in plasma of tumor-bearing mice and synthesis by Ehrlich ascites tumor cells.

In the present paper we have studied: (a) the concentration of fibronectin (FN) in plasma and in ascitic fluid of mice at different times after inoculation of Ehrlich ascites tumor cells; (b) the ability of Ehrlich ascites cells to synthesize and release FN; and (c) the localization of FN in Ehrlich ascites cells by immunofluorescence microscopy. It was found that (a) 4 to 5 days after inoculation of the tumor, the plasma concentration of FN was significantly higher [1.7 +/- 0.07% (S.E.) of total plasma protein] than that in the normal control mice (0.8 +/- 0.035); (b) FN is present in the ascitic fluid in all phases of tumor growth; (c) Ehrlich ascites cells cultured in vitro synthesize and release large amounts of FN in the culture medium; and (d) only about 1 to 2% of the tumor cells show a very small amount of FN, and this is mostly in the area of cell-cell contact.

Animals↗

[3H-thymidine incorporation into the DNA of the nucleic factor in the ascitic fluid of Ehrlich cancer].

After intraperitoneal administration of 1.85 MBq 3H-thymidine to mice with Ehrlich ascites tumours the maximal radioactivity of nucleic factor DNA of ascitic fluid was observed when the isotope had been injected 5-6 days before extraction of ascitic fluid (4-5.10(5) cpm/mg). The maximal radioactivity of DNA of tumour cells themselves was registered when 3H-thymidine was administered 2 days prior to tumour ascites extraction (5.2.10(5) cpm/mg). The administration of even 37 MBq 3H-thymidine 1.5 h before the ascitic fluid extraction from the Ehrlich ascites tumours did not result in the incorporation of this radioactive precursor into nucleic factor DNA. The results obtained show that there is an interval (several days) between the nucleic factor DNA synthesis and its secretion.

Animals↗

Splanchnic hemodynamic factors in cirrhosis with refractory ascites.

Splanchnic and systemic hemodynamic observations in eight patients with cirrhosis and refractory ascites were compared to those of 25 patients with cirrhosis and responsive ascites. The refractory ascitic group was characterized by less portasystemic shunting from both the superior mesenteric and splenic vascular beds, a lower cardiac output, a higher systemic vascular resistance, a wider arterial-hepatic venous oxygen difference, and a tendency for a lower HBF and higher postsinusoidal resistance. Portal pressures assessed from hepatic vein catheterization were similar in the two groups. The absence of a well-developed portasystemic collateral bed in patients with refractory ascites could in part be caused by the tense ascites but could also be an important factor in the mechanism of refractory ascites.

Adult↗

[The effect of ischemia on ascites secretion in the perfused rat liver].

The ascites fluid secreted by the isolated perfused liver was studied in rats. The quantity of fluid appearing on the surface of the isolated perfused liver was independent of the pressure in the portal vein and could be raised by the amount of fluid flowing through the liver. Irrespective of the flow conditions, the ischaemic liver will produce more ascites than the intact liver und similar conditions. A rise of hepatic oncotic pressure will not reduce ascites production by the ischaemic liver. With respect to osmolarity there is no difference between the perfusing fluid and ascites. As regards the quantity of bilirubin secreted with ascites no significant difference was found between the control and the ischaemic group. The pertaining literature and the theories of ascites formation are discussed.

Animals↗

[Medulloblastoma with intractable ascites treated by carboquone--a complication of a ventriculoperitoneal shunt (author's transl)].

Although complication occasionally occur in the use of ventriculoperitoneal shunts (VP-shunt), the occurrence of intractable ascites and extracranial metastasis through the shunt are uncommon. Recently intractable ascites occurred in a two years old girl in whom a left VP-shunt had been placed before four month for obstructive hydrocephalus secondary to medulloblastoma. Paracentesis was performed with recovery of clear, straw-colored fluid with a specific gravity of 1012, a protein content of 0.3 gm/L and many of mononuclear cell on microscopic examination. Liver-scan and enzyme profile gave normal results. During 3 weeks, 6 times paracentesis were performed and total volumes of ascites were 3850 ml. At 5 and 6 times paracentesis, Carboquone 1 mg was injected into peritoneal cavity and 0.1 mg into ventricle cavity through flashing device. After these injection, intractable ascites were cured, no metastasis can be seen in peritoneal cavity when died 4 month later. No precise explanation can be offered for occurrence of this intractable ascites. It is said that chronic irritation of the visceral and parietal peritoneum or sub-clinical peritonitis may cause peritoneal malabsorption. In our case, antitumor agent was very effective, so this treatment will be recommended to try for intractable ascites.

Ascites↗

Further experience in testing the sensitivity of human ovarian carcinoma cells to interferon in an in vitro semisolid agar culture system: comparison of solid and ascitic forms of the tumor.

We studied the in vitro growth characteristics of 10 solid-tumor samples of patients with ovarian carcinoma using a semisolid agar culture technique. Tumor cell colonies were observed in 8 of 10 samples, but sufficient number of tumor colonies to evaluate the effects of interferon and other antitumor agents were obtained in only four samples. As compared with cell suspensions prepared from ascitic fluid samples, solid-tumor samples had markedly lower viability, 39% vs 89%, and had more tumor cells, 81% vs 28%. Also, whereas the maximum increase in tumor-colony number occurred during the first week of growth in both solid- and ascitic-fluid-derived samples grown concurrently from the same donors, increase in tumor colony number was sustained for longer periods in ascitic-fluid-derived cultures. The ascitic-fluid-derived tumor colonies were more sensitive to the antiproliferative effects of interferon than colonies derived from solid-tumors. At a concentration of 300 units/ml incorporated into the agar for the duration of the culture, three of four ascitic fluid samples showed a reduction in tumor colony number by greater than or equal to 25%, whereas none of the solid-tumor samples were affected by the interferon to that degree. In contrast, solid-tumor samples showed greater response to cis platinum and Adriamycin than did ascitic-fluid-derived cultures. Such studies and observations are critical in designing clinical trials for the use of interferon in the treatment of malignancy and the judicious selection of patients and route of administration most likely to provide optimal results, especially in view of present critical shortages in availability of interferon.

Adult↗

The significance of bloody ascites in patients with cirrhosis.

Five percent of cirrhotic patients with ascites in our unit have grossly bloody fluid. Eleven of 32 randomly selected retrospective patients had hepatocellular carcinoma, one tuberculous peritonitis, seven prior trauma, and in 13 the bloody ascites was apparently spontaneous. Five prospectively encountered patients brought the number of cases of spontaneous bloody ascites available for review to 18. Three of these had sudden large intraperitoneal hemorrhages, and bloody ascites in the remaining 15 was incidentally noted at routine diagnostic paracentesis. Bleeding in the former three patients was from a retroperitoneal vein, spontaneous splenic rupture, and an unknown site, respectively. All patients required laparotomy and two died. Ascites red cells in the latter 15 patients may have been from a slowly leaking collateral vein or a hepatic lymphatic and required no treatment. However, the prognosis of these patients was significantly poorer than that of a control group of patients with similar liver tests and clear ascites.

Adult↗

Comparison of six treatments of ascites in patients with liver cirrhosis. A clinical trial.

UNLABELLED: A national multicenter study (34 centers) compared six treatments in 328 patients with cirrhotic ascites. Excluded were patients with g.i. bleeding within the last six months, chronic encephalopathy, cancer, tuberculosis or the following complications persisting after three weeks: acute encephalopythy, fever greater than 38 degrees C, infected ascites or biochemical abnormalities: blood urea greater than 8 mmol/l, natremia less than 130 mmol/l, kaliemia less than 2.5 or greater than 5.5 mmol/l, WBC greater than 12000 mm3, total bilirubin greater than 85.5 mumol/l. In each center patients were randomized into two treatment groups, each center using 2 of 6 proposed treatments: (1) Spironolactone and 500 mg Na p.d (77 patients), (2) Spironolactone + furosemide or Moduretic (amiloride + hydrochlorothiazide) and 500 mg Na p.d (80 patients), (3) Spironolactone + Furosemide or Moduretic and unrestricted sodium diet (86 patients), (4) Concentrated ascites reinfusion and 500 mg Na p.d. (36 patients), (5) Unmodified ascites reinfusion and 500 mg Na p.d. (23 patients), (6) Slow ascites drainage and 500 mg Na p.d. (31 patients). Statistical analysis methods were X2, variance analysis and Spotvoll-Stoline and Dunn-Sidak tests. Before treatment, there was no significant difference between the 6 groups. RESULTS: After one month of treatment, no difference was found in the frequency of total or partial regression of ascites, complications of cirrhosis, mortality, acceptability of treatment. Mechanical treatments induced more rapid weight loss but more frequent recurrence; comparison of groups 2 and 3 did not confirm any benefit associated with unrestricted Na diet. Duration of treatment and hospitalization were shorter in group 4 than in groups 3 and 6.

Amiloride↗

[Chemotherapy of peritonitis with particular reference to concentrations of sulbenicillin in human ascites (author's transl)].

Twenty-seven patients with peritonitis to whom a drain was applied were given sulbenicillin (SBPC), a broad-spectrum antibiotic, which has so little hepatic and renal toxicity that massive doses may be feasible, and examination was made as to its therapeutic effects and concentrations of the antibiotic in the ascites. Daily dosage of SBPC was 10g in two divided doses in most cases given by the intravenous infusion. Medication was continued for 3 approximately 15 days. The highest daily dosage was 20g and the largest total dosage reached 190g, but there was no adverse reaction except for one case of a slight anemia. Peritonitis complicated appendicitis, adnexitis, duodenal ulcer perforation, intestinal obstruction or trauma as its primary disease. No difference in the therapeutic effect existed among the primary diseases. The response to SBPC treatment was excellent in 8 of the 27 patients and good in 17. Two patients failed to respond to the therapy. When SBPC was given just before operation, the SBPC concentration in ascites obtained at operation was 112 microgram/ml in 2 cases. The SBPC concentrations in ascites were examined following intravenous infusion of 5g over an hour, and a peak concentration of 94.7 microgram/ml was obtained at the completion of infusion (an hour after the start of infusion), which gradually decreased thereafter. In the ascites excreted from the drain after operation, a high concentration of 12.7 approximately 90.2 microgram/ml (mean: 51.7 +/- 7.7 microgram/ml) was obtained on the day after the operation day, but the concentration was lower thereafter. The SBPC concentrations in ascites were compared as regards the sites of drainage (Winslow's foramen, ileocecum and Douglas' fold), but no particular difference was observed. The SBPC concentrations in ascites after operation were in inverse proportion to the alleviation of peritonitis. They were higher when the inflammation was severer.

Adolescent↗

Ip cisplatin in patients with malignant ascites: pharmacokinetic evaluation and comparison with the iv route.

Ip chemotherapy may be useful in managing patients with malignant ascites. This approach should result in a high concentration of drug at the site of disease, while the plasma concentration and therefore systemic toxicity remain low. Six patients with malignant ascites were treated with cisplatin at a dose of 60 mg/m2. Three patients received the drug iv; one of these patients and three other patients were treated with ip cisplatin. Platinum concentrations in plasma, ascites, protein-free ultrafiltrates of plasma and ascites, and urine were assayed by flameless atomic absorption spectrophotometry. The area under the concentration x time curve for ultrafilterable platinum in ascites was 30 times greater after ip administration of cisplatin than after iv cisplatin. Ip cisplatin can be administered safely to patients with malignant ascites and may be useful in patients with minimal residual intraperitoneal disease, particularly ovarian carcinoma.

Adenocarcinoma↗

Outcome after peritoneo-jugular shunting of pancreatic ascites.

Three patients with pancreatic ascites documented by ascitic fluid protein greater than 2.5 g/dl and elevated amylase in their peritoneal fluid were treated by peritoneo-jugular shunting (PJS). Patient 1 was so treated inadvertently; Patient 2 had resolving amylase levels but increasing amounts of ascites; Patient 3 had clear, active pancreatic ascites. None incurred untoward effects from this procedure. Ventilatory compromise from reduced diaphragmatic excursion was ameliorated in all patients. Two patients required no further therapy. The third patient was greatly improved in preparation for definitive surgical therapy for a leaking pancreatic pseudocyst. The infusion of enzyme-rich fluids into the circulation may be responsible for certain systemic effects of pancreatitis. Coagulation defects are a known complication of PJS for the ascites of Laennec's cirrhosis. There was no evidence of histamine-mediated cardiovascular collapse, exacerbation of respiratory failure, or coagulation defects in these patients. We conclude that these complications are not the inevitable results of PJS of pancreatic ascites.

Adult↗

Carcinoembryonic antigen gradients between plasma and malignant ascites: use in detecting peritoneal and liver metastases.

In the study of 19 patients with malignant ascites and elevated plasma carcinoembryonic antigen (CEA) (greater than 2.5 ng/ml) and/or ascites CEA (greater than 10 ng/ml), two patients emerged: 1) The 10 patients with higher ascitic fluid than plasma CEA levels (medians: 230 and 10.6 ng/ml, respectively) had exudates and intraperitoneal cancer but usually had no hepatic metastases. 2) The 9 patients with lower ascitic fluid than plasma CEA levels (medians: 29 and 140 ng/ml, respectively) had transudates and negative cytology examinations but did have demonstrable liver metastases. Determination of ascitic fluid and plasma CEA gradients in patients with malignant ascites may help localize, with potentially therapeutic importance, the site of metastases.

Ascites↗

Rescue of thymidine cytotoxicity in L1210 ascites by elevated endogenous levels of deoxycytidine.

Although the biochemical and cytokinetic effects of thymidine (TdR) have been extensively studied in vitro, other parameters may be encountered in vivo that could alter its therapeutic efficacy. L1210 cells in culture are sensitive to the growth inhibitory effects of TdR, while TdR infusions in mice bearing L1210 ascites fail to prolong survival. Our results demonstrate that the TdR levels achieved in the serum and ascites fluid during sc and iv infusions range between 10(-4) and 10(-3) M. These levels are sufficient to inhibit the growth of bone marrow and intestinal mucosa cells, as evidenced by 32P incorporation studies. However, these TdR levels fail to exhibit the growth of L1210 ascites, despite the fact that these cells are sensitive to similar concentrations in vitro. The absence of growth inhibition in the L1210 ascites is shown to be due to increased endogenous CdR levels (approximately 2 X 10(-5) M) in the ascites fluid. The concomitant serum CdR levels were at least ten times lower than those achieved in the ascites. This factor probably accounts for the differential effect of TdR on normal cells as compared in vivo with agents such as TdR or even antimetabolites, such as cytarabine, may be modulated by increased CdR levels in the local tumor milieu. These studies are relevant in that TdR is currently being used in a variety of clinical protocols using the nucleoside alone at high doses or in combination with methotrexate, 5-FU, or cytarabine.

Animals↗

Inhibition of human lymphoblastoid cell line proliferation by ascites fluids from ovarian cancer patients.

Ascitic fluids from ovarian cancer patients which contained a component (lymphocyte-inhibitory activity) that inhibited the blastogenic responses of normal lymphocytes were tested for their effect on established lymphoblastoid cell lines. These ascites fluids inhibited proliferation as measured by [3H]thymidine uptake and cell growth in vitro of two different B- (SB and IM-1) and two different T- (HSB and CEM) lymphoblastoid cell lines but were not cytotoxic. No difference in the sensitivity of T- and B-lymphoblastoid cell lines to the active component in the ascites fluids could be demonstrated. In contrast, established nonlymphoid cell lines (HEp-2, oligodendroglioma, and bladder tumor cell lines) were unaffected by the ascites fluids. Two different preparations of partially purified lymphocyte inhibitory activity from these ascites fluids also inhibited lymphoblastoid cell line proliferation. In addition, both B- and T-lymphoblastoid cell lines absorbed and/or metabolized the lymphocyte-inhibitory activity at 37 degrees but not at 4 degrees. These data suggest that the inhibition of lymphoblastoid cell line proliferation and the inhibition of the blastogenic responses of normal lymphocytes by the ascites fluids are attributable to the same or similar factors.

Ascites↗