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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wide albumin gradient (transudative) ascites is usually due to liver disease but may also result from many other disorders, including heart failure, hepatic infiltration by tumor, hepatic vein thrombosis, and veno-occlusive disease. It has not been linked with small bowel obstruction. Narrow albumin gradient (exudative) ascites, usually due to peritoneal carcinoma or inflammation, has been noted in cases of necrotic or perforated bowel, but simple small bowel obstruction has not previously been appreciated as a possible cause for ascites. We report a patient who developed wide albumin gradient ascites and secondary bacterial peritonitis in association with small bowel obstruction. The small bowel obstruction, ascites, and peritonitis resolved with lysis of a single abdominal adhesion.
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PMID:Ascites and secondary bacterial peritonitis associated with small bowel obstruction. 805 42

To define patients with an ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3 or > or = 500 cells/mm3 but without spontaneous bacterial peritonitis, 166 patients with sterile cirrhotic ascites, 46 patients with spontaneous bacterial peritonitis, 123 patients with hepatocellular carcinoma, 67 patients with peritoneal carcinomatosis or massive liver metastasis and 12 patients with other miscellaneous diseases were studied. The sensitivity, specificity and accuracy of the diagnosis of spontaneous bacterial peritonitis were 100, 86 and 88% with the cut-off value of an ascitic fluid polymorphonuclear cell count > or = 250 cells/mm3; and were 93, 91 and 92% with that value > or = 500 cells/mm3, respectively. With the cut-off value > or = 250 cells/mm3 or > or = 500 cells/mm3, the prevalence was 18% or 14% in hepatocellular carcinoma; and 30% or 19% in peritoneal carcinomatosis or massive liver metastasis. The ascitic fluid lactate concentration was insensitive and nonspecific. Among the patients with an ascitic fluid polymorphonuclear cell count greater than the cut-off values, an ascitic fluid erythrocyte count > or = 10,000 cells/mm3, a ratio of ascitic fluid erythrocyte to total leukocyte count > or = 100, and the ratio of ascitic fluid polymorphonuclear cell to total leukocyte count < or = 75% indicated hepatocellular carcinoma, while serum to ascites albumin gradient < or = 1.1 g/dl and a ratio of ascitic fluid polymorphonuclear cell to total leukocyte count < or = 75% indicated peritoneal carcinomatosis or massive liver metastasis.
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PMID:Malignancy-related ascites: a diagnostic pitfall of spontaneous bacterial peritonitis by ascitic fluid polymorphonuclear cell count. 820 Dec 26

Selective intestinal decontamination (SID) for 7 days with norfloxacin (NF) was performed in 15 patients with schistosomal hepatic fibrosis (SHF) and low-protein ascites. Changes in ascitic fluid (AF) opsonic activity and complement3 (C3), complement4 (C4), total protein (TP) and albumin concentrations after NF therapy were compared with those of a control group composed of 15 untreated patients with similar characteristics. After oral NF administration, the mean % changes of AF opsonic activity & AF C3 & TP concentrations showed significant increases and were significantly higher than those in the control group. There were direct correlations between mean % changes in AF opsonic activity and C3 concentrations (r = 0.62). AF opsonic activity and TP concentrations (r = 0.54) and AF C3 and TP concentrations (r = 0.57) in the NF group. On the other hand, the AF C4 and albumin concentrations were not significantly changed in any group at the end of the study. Based on the results of the present study, it can be concluded that short-term NF therapy in patients with SHF and low-protein ascites increased AF opsonic activity and AF C3 and TP concentrations and hence, AF bactericidal activity. Study of larger numbers of patients for longer periods will determine if these beneficial effects on NF translate into a decreased incidence of spontaneous bacterial peritonitis in patients with chronic liver disease and high-risk of infection.
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PMID:Selective intestinal decontamination in patients with schistosomal hepatic fibrosis and low-protein ascites. 830 39

The pathophysiology of ascites in patients with cirrhosis is complex and includes increases in hepatic sinusoidal pressure, the formation of hepatic and splanchnic lymph, renal sodium retention, and hypoalbuminemia. However, the role of hypoalbuminemia in ascites formation is controversial. Evaluating ascites in hypoalbuminemic patients with nephrotic syndrome could add to our understanding of the role of hypoalbuminemia in ascites development. We conducted a retrospective analysis of 52 adults and 21 children with nephrotic syndrome who were hospitalized in the Hadassah University Hospital on Mount Scopus during 1981-1994. There was a significant difference in the prevalence of ascites between pediatric (52%) and adult patients (23%) (p = 0.024). Pediatric patients had lower serum albumin levels than adults (1.70 +/- 0.08 g/dl vs. 2.10 +/- 0.07 g/dl, p = 0.001). Adult patients with ascites had lower serum albumin levels than adult patients without ascites (1.80 +/- 0.13 g/dl vs. 2.20 +/- 0.07 g/dl, p = 0.01). This difference was not found in pediatric patients. Temporary fluctuations in liver enzymes (up to four times the upper limit of normal for transaminases) were evident in five patients from the pediatric group with ascites, whereas all pediatric patients without ascites had completely normal liver enzymes (p = 0.035). Among the 12 adult patients with ascites, seven had liver disease (three with cirrhosis and four with amyloidosis), and two had right-sided congestive heart failure. Among the 40 adult patients without ascites, only four had liver disease (amyloidosis). The plasma albumin levels of the patients with amyloidosis without ascites were higher than patients with amyloidosis with ascites (1.90 +/- 0.10 g/dl vs. 1.50 +/- 0.07 g/dl, p = 0.03). Two patients with nephrotic syndrome and ascites (one without liver disease) had episodes of spontaneous bacterial peritonitis. Ascites in nephrotic syndrome is more common in children than in adults. Although in most pediatric patients ascites formation is probably a common manifestation of the general fluid retention, in most adult patients with nephrotic syndrome ascites can be attributed to both hypoalbuminemia and the presence of liver disease or congestive heart failure, with increased hepatic sinusoidal pressure.
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PMID:Ascites in Nephrotic syndrome. Incidence, patients' characteristics, and complications. 877 92

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.
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PMID:[Sero-ascitic gradient of albumin: usefulness and diagnostic limitations]. 892 34

Ultrasonography detects ascites easily even in trace amounts. 80% of the cases are caused by hepatic disease, in the remaining 20% cancer, inflammation, pancreatic, renal, or cardiac disease can be found. The underlying disease should be investigated by few inexpensive laboratory test from serum, urine and ascites and by abdominal sonography. Hepatic ascites is caused by portal hypertension and disturbances of humoral factors. Sodium retention, peripheral, vasodilation, hyperdynamic circulation and progressive renal vasoconstriction lead to a stepwise deterioration of patients condition. Treatment with diuretics (furosemide, torsemide, or xipamide and spironolactone) and sodium-restriction (< 60 mval per day) control 85-90% of the cases with hepatic ascites. If this regimen fails, non-compliance, spontaneous bacterial peritonitis, hyponatremia or additional complications such as renal failure, Budd-Chiari syndrome or tumor should be considered. Ten to 15% of the patients develop refractory ascites and finally hepatorenal syndrome and have a poor prognosis. Early liver transplantation should be considered. Large volume paracentesis with albumin substitution is a therapeutic option in these patients. The transjugular intrahepatic portosystemic stent-shunt (TIPS) may be superior for patients with concurrent esophageal varices or hepatorenal syndrome. If TIPS is considered the patient should be referred to an experienced center. The peritoneo-venous shunt is restricted to rare indications. In the future, new drugs such as antagonists of endothelins or of the antidiuretic hormone may offer new therapeutic options.
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PMID:[Current ascites therapy]. 906 26

Although fluid analysis usually is the first step toward identifying the cause of pleural effusion in patients with cirrhosis and ascites, there are no available data on the reliability of this approach, therefore, we retrospectively evaluated hematologic and biochemical parameters from pleural fluid analysis in 21 patients with hepatic hydrothorax (with proven peritoneal-pleural communication) and 6 patients with primary pleural disease (2 with tuberculosis, 3 with parapneumonic effusion, and 1 with empyema). The criteria developed by Light were diagnostic of pleural "exudate" in only one of six patients with primary pleural disease, concentrations of leukocytes, total protein (TP), albumin, and lactic dehydrogenase (LDH) in both fluids were measured and pleural fluid-to-ascites ratios of these measurements were calculated. Only ratio values for leukocytes and TP were higher in the group of patients with primary pleural disease compared with those with hepatic hydrothorax. Ratio values for leukocytes and TP overlapped between both groups during baseline conditions and during episodes of spontaneous bacterial peritonitis and pleuritis. We conclude that pleural fluid analysis has limited diagnostic efficacy in the patient with cirrhosis. Data collected by other methods--clinical and radiologic--should assist in arriving at the correct diagnosis.
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PMID:Evaluation of pleural fluid in patients with cirrhosis. 945 75

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.
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PMID:Complications of cirrhosis. II. Renal and circulatory dysfunction. Lights and shadows in an important clinical problem. 1072 2

Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis characterized not only by renal failure due to a marked vasoconstriction of the renal circulation but also by marked alterations in systemic haemodynamics and activity of endogenous vasoactive systems. The pathogenesis of HRS is not completely known but it is probably the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in the splanchnic circulation. Besides the renal circulation all other extrasplanchnic vascular beds appears to be vasoconstricted. The diagnosis of HRS is currently based on the exclusion of non-functional causes of renal failure. Prognosis of patients with HRS is very poor. Liver transplantation is the best option in selected patients, but is seldom applicable due to the short survival expectancy of most patients with HRS, particularly those with the progressive type (type I HRS). Therapies introduced during the last few years, such as transjugular intrahepatic portosystemic shunts or, particularly, vasoconstrictor drugs with preferential effect on the splanchnic circulation (V1 receptor agonists) are very effective in improving renal function and reverting HRS. However, the impact of the improvement of renal function on the natural course of HRS is unknown. Finally, the development of HRS after spontaneous bacterial peritonitis can be effectively prevented by the administration of albumin together with antibiotic therapy.
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PMID:Diagnosis and treatment of hepatorenal syndrome. 1113 48

Hepatorenal syndrome (HRS) is a unique form of acute renal failure occurring in patients with advanced liver disease. Despite the severe derangement of renal function and ominous prognosis, minimal pathologic abnormalities of the kidneys are found at autopsy. The kidneys, if transplanted, are capable of normal function, which supports the concept that renal failure is functional and potentially reversible. The pathogenesis of HRS is not completely known, but it is probably the result of an extreme underfilling of the arterial circulation secondary to an arterial vasodilation located in splanchnic circulation. Besides the renal circulation, all other extrasplanchnic vascular beds also appear to be vasoconstricted. The diagnosis of HRS is currently based on several widely accepted diagnostic criteria aimed at excluding nonfunctional causes of renal failure. Recently initiated therapeutic approaches lend a note of optimism to the future management of HRS. These include liver transplantation as definitive treatment for patients with end-stage liver disease, and introduction of new vasoconstrictor drugs with the preferential effect on the splanchnic circulation. The development of HRS after spontaneous bacterial peritonitis may be effectively prevented by the administration of albumin together with antibiotic therapy.
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PMID:Hepatorenal syndrome: new perspectives in pathophysiology and management. 1137 81


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