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

Repeated large-volume paracentesis (4-6 L/day) is an effective and safe therapy of ascites in patients with cirrhosis provided albumin is infused intravenously. To investigate whether ascites can be safely mobilized in only one paracentesis session ("total paracentesis"), 38 cirrhotic patients with tense ascites were treated with total paracentesis plus intravenous albumin (6-8 g/L ascites removed). Standard liver tests and renal function tests, glomerular filtration rate, free water clearance, plasma volume, plasma renin activity, and plasma aldosterone and norepinephrine concentrations were measured before and after treatment. Total paracentesis was effective in mobilizing ascites in all but 1 patient and did not impair any of the parameters studied. The volume of ascitic fluid removed and the duration of the procedure were 10.7 +/- 0.5 L (mean +/- SEM) and 60 +/- 3 min, respectively. Five of the 38 patients (13%) developed complications during the first hospital stay (hepatic encephalopathy and gastrointestinal hemorrhage in 2 patients each and culture-negative bacterial peritonitis in 1). No patient developed renal impairment. This complication rate, as well as the clinical course of the disease during follow-up, estimated by the probability of readmission to hospital, causes of readmission, and survival probability after treatment, was similar to that reported in patients treated with repeated large-volume paracentesis. These results indicate that total paracentesis associated with intravenous albumin can be safely performed in cirrhotic patients with tense ascites and suggest that these patients could be treated in a single-day hospitalization regime.
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PMID:Total paracentesis associated with intravenous albumin management of patients with cirrhosis and ascites. 229 73

Primary bacterial peritonitis and catheter-associated infections compose the large majority of abdominal events in continuous ambulatory peritoneal dialysis (CAPD) patients. Yet occasionally primary pathology involving the abdominal viscera develops, and surgery is frequently considered. The early manifestations of intraabdominal inflammation or bleeding in patients undergoing CAPD depend on the pathological process, its access to the peritoneal cavity, and whether generalized bacterial peritonitis supervenes to obscure helpful physical findings. Clear dialysate is not a reliable sign that major pathology is absent, nor does initial stabilization of the clinical course with antibiotic therapy uniformly indicate that surgery will not be necessary. Polymicrobial peritonitis may develop in cholecystitis, pancreatitis, or from a colonic source, the latter featuring more bacterial species and more gram-negative and anaerobic organisms. A history directed at progression of symptoms and sites of abdominal discomfort and an examination for deep local tenderness and bowel incarcerated in an abdominal wall hernia are essential. Measurement of dialysate amylase and Gram stain of dialysate for food fibers may be helpful. Imaging techniques such as abdominal radiographs for dilated bowel or free subdiaphragmatic air, ultrasonography of the gallbladder or pancreas, computed tomographic (CT) scanning of the lower abdomen, and water-soluble contrast colonic studies may help identify the pathologic process. Special studies such as these should be considered early in the course of suspected unusual abdominal events in patients on CAPD.
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PMID:Abdominal catastrophes and other unusual events in continuous ambulatory peritoneal dialysis patients. 236 12

A single ip injection of distilled water osmotically disrupts almost the entire population of peritoneal mast cells in rats. The metachromatic granules released from disrupted mast cells are phagocytosed by peritoneal macrophages increasing their chemotactic and spreading activities. On this basis a study was carried out to determine whether an ip injection of distilled water, by releasing an abundance of these granules for peritoneal macrophage stimulation, protects rats subsequently exposed to peritonitis. We found that a single ip injection of distilled water lowers the mortality in rats exposed to bacterial peritonitis 2-3 weeks later from 80 to 33%.
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PMID:Resistance to peritonitis following disruption of peritoneal mast cells. 318 30

A cirrhotic patient with ascites was apparently well managed with diuretics and salt and water restriction for 9 months. A spontaneous bacterial peritonitis (SBP) developed and the patient finally died following septic shock. There were enough findings indicating that SBP in this case had been existing silently for some time. During this period the only apparent manifestation of this complication was a cutaneous pigmentation on the abdomen. It is suggested that pigmentation may be incuded among other presentations of this frequently silent process.
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PMID:Cutaneous pigmentation: a probable sign of spontaneous bacterial peritonitis. 699 87

The disulphate ester of ursodeoxycholyl-p-aminobenzoic acid (PABA-UCDA) was synthesised and compared with PABA-UDCA for its use in detection of intestinal bacteria. This compound, PABA-UDCA disulphate, had characters in common with PABA-UDCA in that it was deconjugated by cholylglycine hydrolase to release free PABA and bacteria that split glycocholic acid deconjugated PABA-UDCA disulphate. Further, in rat experiments urinary excretions of PABA were measured for six hours after oral administration of 15 mg PABA-UDCA disulphate. Ten control rats excreted (mean (SE) 188.2 (13.6) micrograms of PABA; 10 rats with an intestinal stagnant loop excreted more (530.1 (30.1) micrograms; p < 0.001): whereas 10 rats in each of three groups pretreated by oral administration of various antibiotics excreted less (polymixin B+tinidazole, 4.9 (1.6) micrograms; kanamycin, 31.0 (4.7) micrograms; clindamycin 40.9 (5.5) micrograms; p < 0.001). By contrast with PABA-UDCA, PABA-UDCA disulphate was not actively absorbed from any part of the small intestine in everted gut sac experiments, and showed poor recovery from bile after its intraileal instillation in rats. This indicated that PABA-UDCA disulphate is a single pass type substance in the gut and its oral administration test reflects the sum of the activities of bacteria in the small intestine and colon. The disulphate was easily soluble in water and this allowed its application in an in vitro test involving PABA-UDCA disulphate incubation with intraperitoneal pus (PABA-UDCA disulphate incubation test) from patients with peritonitis. This test was carried out on six patients with peritonitis, and the severity of bacterial peritonitis was expressed quantitatively. From the results obtained PABA-UDCA disulphate was considered a good material to detect intestinal bacteria.
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PMID:Use of the conjugate of disulphated ursodeoxycholic acid with p-aminobenzoic acid for the detection of intestinal bacteria. 831 17

Cirrhosis is a chronic disease of the liver in which dense bands of fibrosis enclose regenerative hepatocellular nodules. Clinical and radiologic features of advanced liver disease provide presumptive evidence for the presence of cirrhosis. Major complications are related to the increased hepatic resistance, increased sodium and water retention, and hyperdynamic changes of the circulatory system. Patient management should consist of appropriate prophylaxis for the life-threatening complications of variceal bleeding and spontaneous bacterial peritonitis and treatment of other complications as signs and symptoms develop.
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PMID:Complications of cirrhosis. Why they occur and what to do about them. 947 17

Selective intestinal decontamination with norfloxacin is useful in preventing spontaneous bacterial peritonitis in cirrhotic patients and also in cirrhotic rats. The emergence of norfloxacin-resistant infections in these patients warrants a search for alternative therapies. The aim of this study was to evaluate the effect of long-term trimethoprim-sulfamethoxazole administration on carbon tetrachloride (CCl4) -induced cirrhosis in rats with specific attention to intestinal flora, bacterial translocation, spontaneous bacterial peritonitis (SBP), and survival. Male Sprague-Dawley rats received CCl4 administered weekly by gavage. After eight weeks of CCl4 administration rats were randomly allocated into two groups. Group I received daily overnight trimethoprim-sulfamethoxazole diluted in phenobarbital water during follow-up and group II did not. The rats were killed when gravely ill, and a laparotomy was performed to culture samples of cecal stool, mesenteric lymph nodes, and portal and inferior vena caval blood. There was a trend toward a reduction in the incidence of bacterial translocation (8/17 vs 11/14, respectively) and SBP (5/17 vs 7/14, respectively) in treated rats that were killed just before death compared to untreated rats. A decrease in the incidence of bacterial translocation caused by gram-negative bacilli was observed in group I (17.6% vs 78.6%, P < 0.01). The development of ascites was delayed in group I (P < 0.05) and survival was prolonged in group I (P < 0.05), despite a higher CCl4 dose in this group (P < 0.05). In conclusion, long-term prophylactic trimethoprim-sulfamethoxazole administration in CCl4-induced cirrhosis in rats delayed the development of ascites, prolonged survival, and reduced the incidence of gram-negative bacterial translocation but not of SBP, without increasing gram-positive episodes. These data suggest that trimethoprim-sulfamethoxazole might be a good alternative to norfloxacin for preventing gram-negative bacterial translocation.
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PMID:Effect of long-term trimethoprim-sulfamethoxazole prophylaxis on ascites formation, bacterial translocation, spontaneous bacterial peritonitis, and survival in cirrhotic rats. 1054 43

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

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensin-aldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as transjugular intrahepatic portosystemic shunt or vasopressin analogues may serve as a bridge to transplantation. Another complication of decompensated cirrhosis is spontaneous bacterial peritonitis, the incidence of which can be reduced by primary or secondary antibiotic prophylaxis by using orally active antibiotics.
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PMID:Update on peripheral arterial vasodilation, ascites and hepatorenal syndrome in cirrhosis. 1111 Jun 23

Hepatic cirrhosis is the most common cause of ascites. It is caused by liver failure leading to complex interrelated circulatory and renal changes resulting in retention of sodium and water and portal hypertension localising that sodium and water in the peritoneum. Ascites is an important development in cirrhosis as it implies a generally poor long term prognosis. Investigation is important as ascites is not always dueto cirrhosis, may bethe consequence of complications of cirrhosis such as hepatocellular carcinoma, and may be associated with infection which is fatal if untreated. Most patients respond to treatment with sodium restriction and diuretic drugs. This treatment takes time, and increasingly doctors use therapeutic paracentesis with sodium restriction and diuretics to prevent recurrence of ascites. Paracentesis, however, is not without complications, and it is particularly important to give colloid replacement to prevent hypovolaemia which can lead to renal failure. Patients who do not respond to this treatment may be helped by a TIPSS procedure or a peritoneovenous shunt. However, these patients usually have very poor liverfunction and the possibility of fiver transplantation should be considered. Infection is a very serious complication of ascites (spontaneous bacterial peritonitis) and carries a generally poor prognosis.Antibiotic prophylaxis is important to prevent recurrence and liver transpiantation shoulcl be considered.
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PMID:[ASCITES IN HEPATIC CIRRHOSIS: RECOGNITION INVESTIGATIONAND TREATMENT] 1221 41


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