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PubMed1978

Diagnostic value of ascitic fluid lactic dehydrogenase, protein, and WBC levels.

Three characteristics of an exudate, ie, an ascitic fluid lactic dehydrogenase (LDH) level of greater than 400 Sigma units (SU), an ascitic fluid-serum LDH ratio of greater than 0.6, and an ascitic fluid-serum protein ratio of greater than 0.5, were studied in a prospective fashion to determine their usefulness in the differential diagnosis of ascites. The ascitic fluid LDH level did not exceed 400 SU in any patient with uncomplicated chronic liver disease, whereas in patients with malignant, tuberculous, or pancreatic ascites it exceeded 500 SU in 12/19 patients. The finding of two of the three characteristics indicated a nonhepatic cause for the ascites whereas the absence of all three strongly suggested uncomplicated liver disease as the sole cause. The ascitic fluid WBC count was also useful in that values exceeded 500/cu mm in bacterial and tuberculous peritonitis whereas it was low (297 +/- 49/cu mm) in chronic liver disease.

Ascites↗
PubMed1995

[Sero-ascitic gradient of albumin: usefulness and diagnostic limitations].

The serum-ascites albumin (SAA) gradient has been defined as the serum albumin concentration minus the ascitic fluid albumin concentration. The SAA gradient is superior to the exudate-transudate concept to classify ascites, being a exact portal hypertension (PH) marker. An elevated SAA gradient (1.1 g/L or greater) correlates with PH, whereas a low gradient indicates no PH. The SAA gradient correlates well with PH in cirrhotic patients. It is also of particular utility to differentiate between congestive heart failure and malignant ascites without liver metastases (both of them with elevated ascites fluid proteins -AFP-). However, a low SAA gradient do not differentiate between tuberculous and malignant ascites. Consequently, there are still need for tests a cytology, culture for mycobacteria or ascites fluid polymorphonuclear cell count in some cases. The level of AFP, apart from the exudate-transudate concept, has some value for certain cases (a low level of AFP implicates a high risk of spontaneous bacterial peritonitis). The SAA gradient should replace the AFP concentration as the initial test to classify ascites.

Albumins↗
PubMed2003

Mechanism of acute ascites formation after trauma resuscitation.

BACKGROUND: Severely injured patients have been observed to acutely develop ascites; however, the pathogenesis of this rare phenomenon is poorly understood. OBJECTIVES: To report the factors common among severely injured patients developing ascites and to formulate a hypothesis regarding its origin. METHODS: Retrospective review of case series. RESULTS: We identified 9 injured patients between January 1, 1993, and December 31, 1998, who acutely developed significant amounts of ascites. The mean +/- SD estimated ascites volume was 2.0 +/- 0.8 L. All 9 patients had severe shock and were mechanically ventilated before abdominal decompression for the abdominal compartment syndrome. The mean +/- SD peak inspiratory pressure was 39.0 +/- 5.8 cm H2O. The mean +/- SD volumes of crystalloid and blood product infusion before decompression were 16.1 +/- 10.2 L and 5.2 +/- 4.8 L, respectively, in a mean +/- SD of 17 +/- 15 hours. In comparison, the mean +/- SD volumes of crystalloid and blood product transfusion among 100 contemporary, randomly selected patients undergoing trauma laparotomy were 5.1 +/- 5.5 L and 1.1 +/- 2.5 L, respectively (P<.001). Eight patients had only extra-abdominal injuries, while 1 patient had a combination of extra- and intra-abdominal injuries. Two patients were found to be cirrhotic by liver biopsy, but the other 7 patients had no known preexisting hepatic disease. Eight patients had absorbable mesh temporary abdominal closure, and 1 patient had primary fascial closure. There was persistent ascitic drainage in 5 patients; however, in all but 1 patient with cirrhosis, the drainage did not persist beyond 3 days. Two patients died, 1 of sepsis and the other of a closed head injury. CONCLUSIONS: Common denominators of posttraumatic ascites include shock, massive fluid resuscitation, and elevated intrathoracic pressure. The rapid onset of ascites in the setting of elevated intrathoracic pressure suggests that the patient's ability to clear ascitic fluid is overwhelmed.

Abdominal Injuries↗
PubMed1996

Ascitic fluid adenosine deaminase insensitivity in detecting tuberculous peritonitis in the United States.

Tuberculous peritonitis, although common in Third World countries, remains an uncommon cause of ascites in the United States. Ascitic fluid adenosine deaminase (ADA) activity has been proposed as a useful diagnostic test. The aim of this retrospective study was to determine the clinical utility of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population. A total of 368 ascitic fluid specimens from a well-characterized ascitic fluid bank, including tuberculous peritonitis (n = 7), tuberculous peritonitis in the setting of cirrhosis (n = 10), and consecutive specimens of widely varied etiologies (n = 351) were analyzed for ADA activity by ultraviolet spectrophotometry at 265 nm. The overall sensitivity of the ADA determination in diagnosing tuberculous peritonitis was only 58.8%, and the specificity was 95.4%. The accuracy of ADA determination (93.8%) compared favorably with that of the common ascitic fluid tests of white blood cell (WBC) count (>500/mm3), total protein (>2.5 g/dL), and combined WBC count and total protein (45.8%, 74.4%, and 81.3%, respectively). However, ADA was only 30% sensitive in detecting tuberculous peritonitis in the setting of cirrhosis, and cirrhosis was present in 59% of the tuberculous peritonitis patients in our population. In addition, malignancy-related ascites (13%) and bacterial peritonitis specimens (5.8%) occasionally yielded false-positive results. In conclusion, our results indicate that the ascitic fluid ADA activity has good accuracy but poor sensitivity and imperfect specificity in a U.S. patient population in which the prevalence of tuberculosis is low and underlying cirrhosis is common.

Adenosine Deaminase↗
PubMed1997

Evidence of functional and structural cardiac abnormalities in cirrhotic patients with and without ascites.

Cirrhosis is associated with cardiovascular abnormalities. Scanty information is available as to whether these include left ventricle diastolic dysfunction and wall thickness increase. To this aim in 27 cirrhotic patients with tense ascites, 17 cirrhotic patients with previous episodes of ascites (not actual), and 11 controls we investigated by echocardiography and echocolor Doppler left ventricle diastolic function (E wave, A wave, E/A ratio, deceleration time of E wave), systolic function (ejection fraction), and wall thickness (left ventricle posterior wall thickness + interventricular septum thickness) along with neurohumoral variables. All measurements (supine position) were repeated after total paracentesis (10.7 +/- 0.6 L of ascites) in ascitic patients. Both in patients with and without ascites E/A ratio was reduced as compared with controls (0.93 +/- 0.07 and 0.97 +/- 0.06 vs. 1.18 +/- 0.08, P < .05) while left ventricle wall thickness was increased (18.6 +/- 0.6 and 20.1 +/- 0.8 vs. 17.2 +/- 0.7, P < .05 and P < .01, respectively), irrespective of the postviral or alcoholic cause of liver disease. In all cirrhotics both right and left atrial and right ventricle diameters were significantly greater. Ejection fraction was slightly but significantly (P < .01) reduced in ascitic patients. Paracentesis induced a reduction of the highly increased basal plasma renin activity, aldosterone, norepinephrine (P < .01), and epinephrine (P < .05) and improved diastolic function (E/A, P < .05). Systolic function was unaffected. Thus, irrespective of ascites and cause, advanced cirrhosis is associated with left ventricle diastolic dysfunction and wall thickness increase. We can speculate that neurohumoral overactivity, known to stimulate cardiac tissue growth, may challenge the heart, promoting fibrosis and exerting a further hindrance to ventricular relaxation in patients with cirrhosis experiencing episodes of ascites.

Aged↗
PubMed1977

Resistance of guinea-pig hepatoma cells to complement-mediated lysis induced by ascites fluid or serum from tumor-bearing animals.

The mechanisms of tumor cell susceptibility and resistance to cytotoxic antibodies were investigated in the guinea-pig ascites hepatoma (line-1 and line-10) system. Treatment of line-specific rabbit antibody-coated tumor cells by ascitic fluid, by serum of tumor bearers or by tumor extract inhibited subsequent complement-mediated lysis. Inhibition by ascitic fluid and serum was not line-specific, but inhibition by tumor extract was line-specific. Treatment of tumor cells with ascitic fluid or tumor extract prior to exposure to specific cytotoxic antibody and complement did not inhibit lysis. Incubation of cytotoxic rabbit antisera with ascitic fluid, tumor-bearer serum or tumor extract neutralized their complement-dependent cytotoxic activity on tumor cells. Tumor-immune guinea-pigs exhibited line-specific delayed cutaneous reactions after injection with ascitic fluid or tumor extract. Studies with indrect immunofluorescence revealed that exposure to ascites fluid or tumor extract caused a rapid shedding of rabbit antibodies from the tumor cell surface. Evidence is presented indicating that the active fraction of ascites fluid was associated with immune complexes consisting of IgG and tumor antigen in excess. The relevance of these findings to tumor escape from immune destruction in vivo is discussed.

Animals↗
PubMed1994

Differential expression of the cell-cell adhesion molecule E-cadherin in ascites and solid human ovarian tumor cells.

Advanced ovarian cancers contain 2 distinct phenotypic populations: (a) free-floating tumor cells in the ascitic fluid and (b) solid tumors. Ascites cells are derived from the solid tumors and spread throughout the peritoneum. Changes in cell-cell and cell-extracellular matrix interactions are thought to be responsible for the origin of ascites cells. Since E-cadherin molecules play a crucial role in the cell-cell interactions in epithelial cells, we investigated the expression of E-cadherin in these 2 phenotypic populations. Paired samples of ascites and solid tumors were obtained from patients. Both primary tumors and tumor cells isolated from an experimental model showed a marked decrease in E-cadherin expression in the ascites cells compared to the respective solid tumors. Semi-quantitative, reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the steady-state levels of E-cadherin-specific mRNA. Results indicate that the primary tumors had significantly lower levels of E-cadherin transcript in ascites cells when compared to their solid tumor counterparts. Changes in E-cadherin expression were also reflected in the invasion capacity of tumor cells in vitro. Ascites cells were 4-fold more invasive then solid tumor cells, suggesting that ascites cells are a highly malignant phenotype.

Animals↗
PubMed1977

Ascites following renal transplantation.

Idiopathic ascites has been described in patients on maintenance peritoneal dialysis and hemodialysis. The mechanism responsible for ascites formation in these patients is unknown, and therapy has been generaly unsuccessful. However, renal transplantation has been associated with resolution of this form of ascites. We describe a patient who was free of ascites during maintenance dialysis, in whom ascites developed following renal transplantation associated with transient impairment of renal function. No specific cause of the ascites was found. Resolution of ascited occurred as renal function improved. This experience extends the spectrum of idiopathic ascites in uremic patients to the transplant recipient.

Ascites↗
PubMed1992

Analysis of clinical course and prognosis of culture-positive spontaneous bacterial peritonitis and neutrocytic ascites. Evidence of the same disease.

The clinical significance and prognosis of culture-negative neutrocytic ascites in cirrhotic patients is a controversial topic. In the present study, the clinical and humoral presentation and the short- and long-term prognosis were analyzed in 36 patients with cirrhosis and culture-positive spontaneous bacterial peritonitis and in 28 patients with cirrhosis and ascitic fluid polymorphonuclear count greater than 250/mm3, a negative ascitic fluid culture, and without previous antibiotic therapy. On admission there were no significant differences between groups related to age, sex, alcoholism, fever, abdominal pain, serum albumin, serum urea, serum creatinine, Child-Pugh score, polymorphonuclear count, and total protein concentration in ascitic fluid. A greater frequency of positive blood culture was found in patients with spontaneous bacterial peritonitis (15/21 vs 2/18) (P < 0.001). Mortality during the first episode was 36% in patients with spontaneous bacterial peritonitis and 46% in patients with culture-negative neutrocytic ascites (NS). Mortality during follow-up was high and survival probability at 12 months was 32% in spontaneous bacterial peritonitis and 31% in culture-negative neutrocytic ascites. The probability of recurrence at 12 months was 33% in spontaneous bacterial peritonitis and 34% in culture-negative neutrocytic ascites. Our results show that spontaneous bacterial peritonitis and culture-negative neutrocytic ascites are variants of the same disease with a high mortality and poor prognosis.

Aged↗
PubMed1991

Ascitic fluid and serum cefotaxime and desacetyl cefotaxime levels in patients treated for bacterial peritonitis.

Forty-one episodes of ascitic fluid infection were treated with cefotaxime 2 g intravenously every 8 hr, and ascitic fluid and serum were sampled 6, 12, 24, 48, and 96 hr after the first dose of antibiotic. Concentrations of cefotaxime and desacetyl cefotaxime were measured in ascitic fluid and serum by high-performance liquid chromatography. There was essentially 100% penetration of cefotaxime and metabolite from serum into ascitic fluid at all time points. Ascitic fluid was sterilized in 94% of episodes after the first dose of antibiotic. The ascitic fluid concentration of cefotaxime 6 hr after the first dose of antibiotic was greater than 20 times the minimal inhibitory concentration of the drug for 90% of the isolated flora. This rapid ascitic fluid penetration of cefotaxime in high concentration explains the rapid sterilization of ascitic fluid by the drug in the setting of bacterial peritonitis and obviates the need to give a loading dose or intraperitoneal injection.

Adult↗
PubMed1981

Intracellular and exchangeable potassium in cirrhosis. Evidence against the occurrence of potassium depletion in cirrhosis with ascites.

The intracellular potassium content of leukocytes, the extracellular fluid volume (82Br space), and exchangeable potassium were determined in 28 patients with cirrhosis of the liver (18 with ascites) and in 15 hospitalized controls. No intracellular potassium depletion could be identified in these patients. Leukocyte potassium was similar in cirrhotic patients with and without ascites (355.9 +/- 25.3 and 348.1 +/- 31.9 mEq/kg of dry solids, respectively) and in hospitalized controls (359.7 +/- 27.4) (mean +/- SD). The extracellular fluid volume was similar in controls and cirrhotics without ascites, but markedly increased in cirrhotics with ascites. The exchangeable potassium (mEq/kg of body weight) was similar in nonascitic cirrhotics and in hospitalized controls, but significantly lower in patients with cirrhosis and ascites. However, when the estimated weight of the extracellular fluid volume was substrated from the total body weight, thus obviating the influence of the increased extracellular fluid volume of ascitic patients in the body weight, the exchangeable potassium (mEq/kg of "corrected" body weight) was similar in cirrhosis with ascites (52.9 +/- 6.7 mEq/kg), nonascitic cirrhotics (55.8 +/- 6.1 mEq/kg) and hospitalized controls (55.0 +/- 8.3 mEq/kg), and a significant correlation was obtained between the exchangeable potassium and the leukocyte potassium content. In five patients, the measurements were repeated after relieving ascites with diuretics. No change was observed in the leukocyte potassium, but exchangeable potassium (mEq/kg of body weight) increased, reaching values not significantly different from controls or nonascitic cirrhotics. The exchangeable potassium (mEq/kg of "correct" body weight) did not change. Our results strongly suggest that potassium depletion was not present in the series of cirrhotic patients studied.

Aged↗
PubMed1990

Degradation pathway of kinins in tumor ascites and inhibition by kininase inhibitors: analysis by HPLC.

We have recently found presence of a high concentration of a novel type of kinin, hydroxyprolyl3-bradykinin (Hyp3-BK) in human tumor ascites in addition to conventional bradykinin (BK). Because of their potential physiological activity, it is of interest to know how these bradykinins can be degraded in ascites. Degradation of two synthetic kinins, BK and Hyp3-BK, added to the ascitic fluid from patients with ovarian carcinoma and hepatoma, were analyzed by reversed phase HPLC. Both kinins were degraded into their desArg9-BK or -Hyp3-BK and desPhe8-Arg-9-BK or -Hyp3-BK products following incubation with the ascitic fluid. The rate of the degradation of BK and Hyp3-BK was the same. The formation of desArg9-BK was completely inhibited by kininase I inhibitor, while the formation of desPhe8-Arg9-BK was not completely inhibited by a kininase II inhibitor. The degradation of both kinins was inhibited completely by EDTA. The results indicate the presence of other metalloprotease(s) which cleaves kinins in the ascitic fluid, in addition to kininase I and kininase II. The carboxypeptidase A and carboxypeptidase B inhibitor, benzyl malic acid, failed to block degradation of both kinins. A rapid cleave of Phe-Arg into Phe and Arg was also found in the ascitic fluid. Thus, the major degradation products of kinins in the ascitic fluid were demonstrated to be either desArg9-BK or Hyp3-BK, desPhe8-Arg9-BK or -Hyp3-BK, phenylalanine and arginine. Lysyl-BK and lysylhydroxyprolyl3-BK were rapidly converted into BK and hydroxyprolyl3-BK by the ascitic fluid.

Amino Acid Sequence↗
PubMedDate not supplied

Quantitating bedside diagnosis: clinical evaluation of ascites.

The authors prospectively evaluated the operating characteristics of the history and physical examination for ascites in a broad spectrum of hospitalized patients. The overall clinical evaluation produced a positive likelihood ratio = 37.7-83.3 when suggestive of ascites, a likelihood ratio = 2.23-3.42 when intermediate, and a negative likelihood ratio = 0.77-0.90 when not suggestive of ascites. Patients' perceptions of increased abdominal girth (positive likelihood ratio = 4.16) or recent weight gain (positive likelihood ratio = 3.20) increased the likelihood of ascites. The absence of subjective ankle swelling (negative likelihood ratio = 0.10) or increased abdominal girth (negative likelihood ratio = 0.17) decreased the likelihood of ascites. The positive likelihood ratios for a fluid wave = 9.6 and shifting dullness = 5.76 favored ascites, while the absence of bulging flanks (negative likelihood ratio = 0.12) or peripheral edema (negative likelihood ratio = 0.17) favored ascites the least. Thus, a routine history and physical examination are quantitatively useful in the clinical evaluation of ascites.

Ascites↗
PubMed1996

Effects of granulocyte-colony-stimulating factor and interleukin-2 on ascites formation and the survival time of nude mice bearing human ovarian cancer cells.

The aim of this study was to elucidate the effect of intraperitoneal (i.p.) instillations of granulocyte-colony-stimulating factor (G-CSF) and/or interleukin-2 (IL-2) on ascites formation and the survival time of nude mice with malignant ascites, produced by i.p. inoculation of human ovarian cancer cells. When the nude mice were treated with medium alone, ascites was observed in all mice 28 days after tumor inoculation. When the mice were treated with cis-diamminedichloroplatinum(II) (cisplatin) alone, G-CSF alone or IL-2 alone, it took 35 days for the ascites to form in all mice. When cisplatin was combined with G-CSF or IL-2, one of ten mice did not form ascites during the observation period. Surprisingly, when G-CSF and IL-2 were simultaneously administered, ascites formation was not observed in any mice. Although i.p. treatment with cisplatin alone significantly prolonged the survival time, compared to medium alone, the lytic activity of spleen cells against HRA cells was significantly suppressed. When G-CSF or IL-2 was combined with cisplatin, the suppression by cisplatin was eliminated and subsequently resulted in a prolongation of the survival time. When G-CSF was combined with IL-2, both the peritoneal and splenic macrophages/ monocytes were stimulated and the splenic lytic activity was about double that following treatment with G-CSF alone on IL-2 alone, suggesting that complete inhibition of ascites formation results not only from a significant increase of the peritoneal macrophages but also from enhancement of the lytic activity. Two mice, died from dissemination of tumor in the abdominal cavity, but eight mice survived without tumor for more than 90 days. As confirmed by monitoring body weight and hematocrit, G-CSF and IL-2 seemed to have no adverse effect. From these results, we conclude that a combination therapy with G-CSF and IL-2 might be of clinical use for inhibiting large amounts of ascites, which may inhibit therapeutic effects for ovarian cancer patients.

Adjuvants, Immunologic↗
PubMed1999

Effects of "body compression" on parameters related to ascites formation: therapeutic trial in cirrhotic patients.

Decreased effective circulating blood volume is an important factor in ascites formation in liver cirrhosis. We designed a "body compression" apparatus as a means to restore effective blood volume and investigated its effectiveness in reducing ascites formation in cirrhotics in terms of its effect on parameters of ascites formation noted below. The subjects, eight cirrhotics with ascites and eight cirrhotics without ascites were given spironolactone (50-75 mg/day) and furosemide (40-80 mg/day) while they received a diet containing 85 mEq of sodium per day. All four limbs and the lower abdomen were compressed with constant pressure [height (cm) divided by 13.6 mmHg] once, for 3h, using stroke rehabilitation splints, while patients lay supine. In cirrhotics both with and without ascites, urine volume, urinary sodium excretion, and creatinine clearance during the body compression were greater than values during control (non-compression) periods (urine volume, means 285 vs 169 ml/3h; P < 0.001, urinary sodium excretion 15.8 vs 9.5 mEq/3h; p < 0.001, creatinine clearance 74 vs 59 ml/min, P < 0.001, respectively). The increased basal plasma renin activity, angiotensin II, aldosterone, and norepinephrine levels in all cirrhotics were significantly decreased by the body compression. In another group of six cirrhotics who received no diuretics or albumin, repeat body compression alleviated ascites in three with well preserved renal function, but was ineffective in three with markedly impaired renal function. These results suggest that the improvement in renal function brought about by the body compression is attributable to an increase in effective circulating blood volume. This maneuver may be a useful complementary therapy in patients with cirrhotic ascites with well preserved renal function.

Adult↗
PubMed1989

Peritoneovenous shunt for intractable ascites of hepatic, nephrogenic, and malignant causes.

A retrospective analysis of 54 patients with a peritoneovenous shunt inserted to control massive ascites refractory to conventional medical treatment is presented. The cause of ascites was hepatic in 29 patients (Group 1, 54 percent), malignant in 13 (Group 2, 24 percent), and nephrogenic in 12 (Group 3, 22 percent). The peritoneovenous shunt failed in 11 patients (20 percent): 6 in Group 1, 3 in Group 2, and 2 in Group 3. Shunt outflow obstruction (thrombosis) was the principal cause. Systemic sepsis in five patients and variceal hemorrhage in three were the factors responsible for most of the deaths (22 percent). Of the 42 patients who survived operation, the peritoneovenous shunt was effective in controlling the massive ascites in 37 (86 percent). Eight patients (15 percent), four with hepatic and four with nephrogenic ascites, survived 3 years or more without ascites. Removal of at least 50 to 70 percent of ascitic fluid at the time of shunt insertion was considered an important factor in decreasing morbidity and mortality. A peritoneovenous shunt can be effective for a long-term period in controlling massive ascites with an hepatic or nephrogenic cause in a selected group of patients; however, in patients with malignant ascites, although the benefit was substantial in half, the survival period did not exceed 6 months.

Adult↗
PubMed1995

Free fatty acid analysis in ascitic fluid improves diagnosis in malignant abdominal tumors.

The fasting concentration of free fatty acids (FFA) in the ascitic fluid was determined in 14 patients with malignant ascites and in 19 patients with liver cirrhosis. In malignant ascites FFA levels were increased more than three times when compared with the levels in cirrhotic ascites (5.241 +/- 0.493 vs. 1.558 +/- 0.170 mumol/ml; P < 0.0001). Palmitic acid was the most representative saturated FFA (which together accounted for 2.499 +/- 0.323 vs. 0.833 +/- 0.064 mumol/ml; P < 0.0001), while unsaturated FFA (2.741 +/- 0.298 vs. 0.725 +/- 0.111 mumol/ml; P < 0.001) were represented, in decreasing order, by oleic, linoleic and arachidonic acids. The ratio of unsaturated to saturated FFA was higher in neoplastic patients (1.35 +/- 0.29 vs. 0.826 +/- 0.065 P < 0.05). Albumin concentration in ascitic fluid of neoplastic patients was 22.44 +/- 1.35 g/l, while that of cirrhotic patients was 8.19 +/- 0.32 g/l, P < 0.0001. A close relationship (R2 = 95.14%) between albumin concentration in ascitic fluid and levels of total FFA was found. These data support the hypothesis that the elevation of FFA in ascitic fluid allows discrimination between malignant and non-malignant ascites.

Adult↗
PubMed1986

Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis.

To assess the risk of development of spontaneous bacterial peritonitis in relation to the ascitic fluid total protein concentration, routine admission abdominal paracentesis was performed on a group of 107 patients during 125 hospitalizations. The paracentesis was repeated if evidence of peritonitis developed during hospitalization. Twenty-one episodes of spontaneous peritonitis (or its culture-negative variant) were documented in 17 patients. The ascitic fluid protein concentration in the spontaneous peritonitis group (0.72 +/- 0.53 g/dl) was significantly lower (p less than 0.001) than that in the group of patients with sterile portal hypertension-related ascites (1.36 +/- 0.89 g/dl) and was significantly lower than that of patients with ascites due to miscellaneous causes. Of the patients whose initial sterile ascitic fluid protein concentration was less than or equal to 1.0 g/dl, 7 of 47 (15%) developed spontaneous peritonitis during their hospitalization; whereas only 1 of 65 (1.5%) patients who had an initial sterile ascitic fluid protein concentration greater than 1.0 g/dl developed spontaneous peritonitis. This difference in risk of development of peritonitis in relation to initial ascitic fluid protein concentration was also significant (p less than 0.01). Low-protein-concentration ascitic fluid predisposes to spontaneous bacterial peritonitis.

Ascitic Fluid↗