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

At physiologic pH, S. epidermidis moves along an electrical potential gradient. We measured the epidermo-peritoneal electrical potential (EPP) in 23 end-stage renal failure patients treated with CAPD. There was a negative correlation between the mean EPP and the patient's age (r = 0.47, p = 0.016), but no correlation between the mean EPP and the duration of treatment (r = 0.003, p = 0.5). The EPP was greater in those patients with a history of recurrent bacterial peritonitis due to S. epidermidis [median EPP 23 mv (95% confidence limits 16-51)] compared to those with only one or no episodes of bacterial peritonitis due to S. epidermidis infection [11 mv (9-17), p < 0.05]. Thus electrical gradients caused by the presence of the CAPD catheter could contribute to colonisation and subsequent infection by skin commensals, by aiding bacterial migration.
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PMID:The epidermo-peritoneal potential in patients treated with continuous ambulatory peritoneal dialysis. 848 15

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

An increased plasma lactate concentration (PLC) is a recognized danger signal often found in cases of shock, septicaemia, hepatic and renal failure, and diabetic ketoacidosis. In 120 patients with abdominal complaints, we found the PLC to be above normal limits in 96 per cent (24/25) of the mesenteric ischaemia subgroup, in all 20 of the general bacterial peritonitis subgroup, in 30 per cent (6/20) of the acute pancreatitis subgroup, and in about half of the 25 cases of intestinal obstruction. In all other abdominal conditions represented (n = 30), comprising various inflammatory or infectious abdominal diseases, the PLC was within the normal range. In patients with abdominal complaints, an increased PLC usually indicates the needs of emergency surgery. In the present series, the PLC manifested a sensitivity of 96 per cent and a specificity of 38 per cent as a marker of mesenteric ischaemia, and was also found to be a useful aid in the diagnosis of bowel obstruction and general bacterial peritonitis.
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PMID:[Warning signals in acute abdominal disorders. Lactate is the best marker of mesenteric ischemia]. 919 Apr 79

Twenty two patients of subacute hepatic failure (SAHF), diagnosed when jaundice progressed for more than 8 weeks with appearance of ascites, with or without encephalopathy, along with biochemical evidence of hepatocellular damage, were studied. The male and female ratio was 4.5:1 and majority (45.4%) of cases were between the age group of 41-50. The mean biochemical values were: S.bilirubin; 9.2 +/- 3.8 mg/dl SGOT; 94.4 +/- 25.0 I.U./lit., SGPT; 107.8 +/- 32.7 I.U./lit., S.Protein; 5.2 +/- 3.5 secs. Ascitic fluid analysis showed transudate in 16 (72.7%) and exudate in 6 (27.2%) patients. Bacterial peritonitis was found in 5 (22.7%) patients. Liver biopsy showed bridging and submassive necrosis. The complications developed in the hospital were: renal failure (36.3%), infection (27.2%), G.I. bleeding (18.1%) and encephalopathy (13.6%). The mortality was (86.3%). Out of 3 (13.6%) patients who survived, only two recovered completely and one had biochemical evidence of hepatocellular necrosis after 6 months of follow up.
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PMID:Clinicopathological profile of subacute hepatic failure. 928 51

Spontaneous bacterial peritonitis (SBP) is associated with an important production of inflammatory mediators. However, it is unknown whether there is a relationship between the abdominal production of these mediators and the development of renal impairment, one of the most important prognostic parameters in spontaneous bacterial peritonitis. We studied 52 cirrhotic patients at diagnosis and resolution of the infection, by measuring endotoxin, tumor necrosis factor (TNF), and interleukin-6 (IL-6) levels in plasma and ascitic fluid. Thirteen patients (25%) developed renal impairment. Patients developing renal impairment showed significantly higher plasma and ascitic fluid cytokine levels at diagnosis of infection than patients who did not (plasma TNF-alpha: 96.0+/-38.7 vs. 39.1+/-3.6 pg/mL, P=.0209; ascitic fluid TNF-alpha: 474.5+/-118.1 vs. 160.8+/-42.7 pg/mL, P=.0173; plasma IL-6: 6,635+/-2,897 vs. 458+/-109 pg/mL, P=.0004; ascitic fluid IL-6: 182,559+/-47,328 vs. 39,250+/-10,803 pg/mL, P=.0001). Independent predictors of development of renal impairment at diagnosis were: renal failure (blood urea nitrogen > 30 mg/dL or serum creatinine > 1.5 mg/dL) (P < .001), IL-6 levels in ascitic fluid (P < .001), and mean arterial pressure (P < .05). Ten of the 13 (77%) patients who developed renal impairment died during hospitalization, but only 2 of the 39 (5%) patients who did not (P=.0001). In addition, renal failure at diagnosis of the infection was the only independent predictor of hospital mortality (P < .001). In conclusion, the inflammatory response to the infection may be an important mechanism of renal impairment and the associated mortality in SBP.
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PMID:Tumor necrosis factor and interleukin-6 in spontaneous bacterial peritonitis in cirrhosis: relationship with the development of renal impairment and mortality. 958 75

Forty patients with spontaneous bacterial peritonitis, three of whom had complicating acute hepatitis syndrome, eight late-onset hepatic failure, and 29 with cirrhosis, were treated with ceftriaxone 2 g intravenously once daily for 5 days. Ascitic fluid culture was positive in 28 patients, with Escherichia coli and Klebsiella as common isolates. All the bacteria isolated were sensitive to ceftriaxone except Enterococcus faecalis, which was isolated in a cirrhotic patient. All culture-positive patients sensitive to ceftriaxone showed bacteriological cure and 26 (65%) patients showed cytological cure after 48 hours of treatment. A total of 95% were cured of their infection after 5 days of treatment. Twelve (30%) patients died during hospitalisation after documented cure of their spontaneous bacterial peritonitis (renal failure, gastrointestinal bleed and cerebral oedema were the primary causes of death). Infection-related mortality due to Pseudomonas septicaemia was seen in one cirrhotic patient.
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PMID:Short-course ceftriaxone therapy in spontaneous bacterial peritonitis. 1021 51

An ad hoc Committee appointed by the Italian Association for the Study of the Liver prepared these Clinical Practice Guidelines for the Management of Cirrhotic Patients with Ascites. The initial evaluation of a patient with ascites should include a history, physical evaluation, paracentesis with ascitic fluid analysis, abdominal ultrasonography and biochemistry to assess the severity of liver disease and renal functionality. To improve the efficiency of the choice between the different opportunities available in the treatment of ascites, patients can be classified into two subgroups: patients with uncomplicated ascites and patients with complicated ascites, including refractory ascites, bacterial peritonitis, hyponatraemia and renal failure. Based upon evidence emerging from controlled clinical trials or case-control studies, satisfactory treatment for uncomplicated ascites is represented by paracentesis, sodium-restricted diet and diuretics, whereas the treatment of patients with complicated ascites requires other specific approaches. As the prognosis for most patients with ascites is poor, the last part of the paper offers simple criteria in the selection of patients candidates for liver transplantation. The aim of these guidelines is to reduce inappropriate practice and to improve efficiency in the management of patients with ascites. The Committee holds that a periodic update will be necessary to conform to future scientific developments.
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PMID:Clinical practice guidelines for the management of cirrhotic patients with ascites. Committee on Ascites of the Italian Association for the Study of the Liver. 1060 7

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

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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