Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To prospectively assess the value of an algorithm in differentiating spontaneous from secondary bacterial peritonitis, we performed serial paracenteses in 43 episodes of ascitic fluid infection (28 spontaneous and 15 secondary) in 40 patients. The algorithm involved identification of (a) secondary peritonitis associated with gut perforation, based on previously proposed criteria in patients with neutrocytic ascites (ascitic fluid total protein greater than 1 g/dl, glucose less than 50 mg/dl, and lactate dehydrogenase greater than the upper limit of normal for serum) and (b) separation of spontaneous from secondary peritonitis (unassociated with perforation) based on the response of the ascitic fluid cell count to antibiotic therapy. The perforation criteria had 100% sensitivity in detecting episodes of actual gut perforation; their specificity, however, was low (45%). After 48 h of treatment the concentration of ascitic fluid neutrophils was below the baseline pretreatment value in all episodes of spontaneous peritonitis but in only two thirds of the patients with secondary peritonitis. This algorithm is useful in (a) identifying patients who have infected ascites associated with perforation of an intraabdominal viscus, and (b) differentiating spontaneous from nonperforation secondary peritonitis on the basis of the response of the ascitic fluid cell count to appropriate antibiotic therapy. The optimal time for repeat paracentesis in patients with infected ascites appears to be 48 h after initiation of treatment.
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PMID:Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. 240 29

Bacterial infection is a serious and often fatal complication of patients with liver disease and can prove fatal either directly or by precipitation of gastrointestinal bleeding, renal failure, or hepatic encephalopathy. At greatest risk are patients with alcoholic cirrhosis or decompensated chronic liver disease, or cases of acute liver disease who progress to fulminant hepatic failure or subacute hepatic necrosis. Infection appears to be unusual in patients with primary biliary cirrhosis. The site and type of infection is unrelated to the aetiology of the liver disease. Bacteraemia, pneumonia, urinary tract infection and spontaneous bacterial peritonitis are most common but infective endocarditis and meningitis, especially with pneumococci, are easily overlooked. Clinical suspicion of infection must be high as the only indication may be a general deterioration in the patients' clinical state, increasing encephalopathy or renal impairment. In the case of patients with fulminant hepatic failure, infection may precipitate the initial or recurrent encephalopathy and contributes to death in 10% of fatal cases. Spontaneous bacterial peritonitis is now recognized to occur in the absence of clinical features of peritonitis. The PMN content of the ascitic fluid may provide the only indication of infection and is the most readily available screening test. The most common types of organism responsible for all types of infection are Gram-negative enteric and streptococci, especially pneumococci, while infection with anaerobes is rare. Risk factors for infection include decompensated alcoholic liver disease, fulminant hepatic failure, gastrointestinal bleeding, invasive practical procedures and impaired host defence mechanisms against infection. Of the host defence mechanisms, impaired function of the reticuloendothelial system, complement, and PMNs represent the most common and serious defects. Defects of humoral immunity are present in ascitic fluid from patients with cirrhosis and are probably a major reason for development of spontaneous bacterial peritonitis. Diuresis improves these functions and reduces the risk of peritonitis. Treatment of infections even with the appropriate antibiotic is still associated with a high mortality but the use of adjuvant gut sterilization is promising, particularly in cases infected with Gram-negative enteric organisms. Infusions of fresh frozen plasma, blood and cryoprecipitate improve some systemic host defences and may be beneficial in the treatment and reduction of risk of infection.
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PMID:Bacterial infections complicating liver disease. 265 49

Selective bowel decontamination with the orally administered quinolone antibiotic, norfloxacin, has been shown to suppress gut gram-negative bacteria and help prevent gram-negative infections in cirrhotic patients who are at high risk of bacterial infection. Because this drug does not eradicate gram-positive organisms, it is conceivable that gram-positives could replace the suppressed gram-negatives in the gut and lead to subsequent infection. Also the effect of norfloxacin on translocation (as defined by culture positivity of mesenteric lymph nodes) has received little attention. In this study, the effect of oral norfloxacin on translocation, bacterial peritonitis, and survival was investigated in an animal model of carbon tetrachloride-induced cirrhosis and ascites. Treated rats received daily doses of orally administered norfloxacin from the onset of cirrhosis until they died or were killed. Controls received no antibiotic. Norfloxacin led to a reduction in bacterial peritonitis from 70% in untreated cirrhotic controls to 28% in treated cirrhotic rats; these data were statistically significant (P = .012). There was no effect on overall translocation rate (28% with norfloxacin vs. 50% without norfloxacin) (P > .1). Gram-positives were isolated in 100% of the bacterial peritonitis episodes and in 71.4% of culture-positive mesenteric lymph nodes in treated animals compared with only 25% of peritonitis episodes and 10% of culture-positive mesenteric lymph nodes of untreated cirrhotic controls (P < .01 for peritonitis and P < .05 for translocation). The survival rate was not different between groups (P > .1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of selective bowel decontamination with norfloxacin on spontaneous bacterial peritonitis, translocation, and survival in an animal model of cirrhosis. 776 17

Spontaneous bacterial peritonitis is a common infection of ascitic fluid that develops in cirrhosis. The offending organisms are predominantly of enteric origin. However, the mechanism and route by which bacteria exit from the gut and enter the fluid remain unclear. "Translocation" of bacteria from the gut to extraintestinal sites has been postulated in the pathogenesis of gram-negative sepsis in intensive care unit patients, burn-wound sepsis, and sepsis associated with chemotherapy. Translocation is defined by culture-positivity (with enteric flora) of mesenteric lymph nodes. In this study we assessed the frequency of translocation in a carbon tetrachloride-induced rat model of cirrhosis, ascites, and spontaneous bacterial peritonitis. We determined that translocation was more common in rats with cirrhosis (78.1%) than in normal controls (4.3%) (p < 0.001). Escherichia coli and other gram-negative enteric organisms were cultured. Translocation of enteric bacteria in rats with cirrhosis to extraintestinal sites may be an important early step in the pathogenesis of spontaneous bacterial peritonitis.
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PMID:Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis. 789 Aug 96

To assess the risk of bacterial peritonitis following endoscopic variceal sclerotherapy (EVS), we recorded the incidence of this complication within 2 wk of the procedure in all patients (n = 216) undergoing 1092 sclerotherapy sessions in our hospital during a 5-yr period (1987-1992). The sclerotherapy sessions were separated in prophylactic EVS (without a previous bleeding, n = 172 sessions), elective EVS (following a previous variceal bleeding, n = 720), and emergency EVS (within 24 h of a variceal bleeding, n = 200). During the study period, 60 patients with spontaneous bacterial peritonitis were recorded. In 10 patients, peritonitis was diagnosed within 14 days after EVS. Six patients received emergency EVS and four elective EVS. In seven patients, Gram-negative aerobic and anaerobic microorganisms were cultured from the ascitic fluid, and in three patients cultures were negative; however, an elevated ascitic fluid polymorphonuclear cell count of > 0.5 x 10(9) cells/L was present. The mean period between EVS and the diagnosis of peritonitis was 3.5 days. On average, the patients had been febrile during 2.1 days before the diagnosis was established. None of the patients who had received prophylactic EVS developed peritonitis. The calculated risk to develop peritonitis following elective EVS was 0.5% (4/742 sessions) and following emergency EVS 3% (6/200 sessions) (p = 0.019, Fisher's exact test). Gram-negative gut-derived microorganisms were the most common pathogenic bacteria cultured from the ascites, which is different from the microbial flora causing bacteremia after EVS. This suggests that the risk for bacterial peritonitis is determined primarily by factors associated with bleeding, such as shock with increased bowel wall translocation of bacteria. These results indicate that standard antibiotic prophylaxis before EVS is not indicated, but could be considered in patients with liver cirrhosis and ascites receiving emergency EVS.
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PMID:Post-sclerotherapy bacterial peritonitis: a complication of sclerotherapy or of variceal bleeding? 819 94

We describe a case of spontaneous bacterial peritonitis in a 53 year old man affected by cryptogenic micro-macronodular cirrhosis, portal hypertention, splenomegaly and hypersplenism, who was admitted with hepatic failure and septic shock and successfully treated with antibiotics (combination of clindamycin and netilmycin), surgical abdominal drainage and splenectomy. This case gave reason for a literature review and an update on the therapeutic options in these high risk patients, especially concerning the role of surgery. Spontaneous Bacterial Peritonitis (SBP) is defined as a bacterial infection of ascitic fluid in the absence of any septic focus. It is a typical life-threatening complication of hepatic cirrhosis with ascites. Mortality is very high and ranges from 75% to 97% of patients, due to septic shock and hepatic failure (hepatorenal syndrome, hepatic encephalopathy, gastrointestinal bleeding). Infection with a single organism is found in most cases. Gram negative bacilli are present in about 70% of cases and E. coli (less frequently Klebsiella, Serratia, Pseudomonas) is principally found. Gram positive cocchi comprise an additional 30% of cases. Anaerobic and microaerophilic organisms seem to be rare causes of SBP (2.7-6%); this finding is probably due to the intrinsic bacteriostatic activity of ascites, which contains high oxygen tension (70 mmHg) and is an inhospitable environment for bacteroides and Clostridia. The prevalent isolation of enteric organism suggest that the gut is the most frequent source of infection, even if the pathogenetic mechanism is not yet well known. The right treatment depends on differentiating primary (SBP) from secondary peritonitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the surgical treatment of spontaneous bacterial peritonitis still up-to-date?]. 824 98

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

The purposes of this paper is to review the specific role of peritoneal dialysis (PD) in patients with liver disorders. We will pay attention to the confluence of liver diseases and situations for which chronic dialysis treatment is required. Hemodialysis (HD) and peritoneal membranes are safe barriers against the passage of the hepatitis C virus; consequently, while peritoneal effluent or HD ultrafiltrate drained from hepatitis B patients/carriers is infective, that from hepatitis C patients does not appear to present this risk. An important issue is horizontal transmission, which appears to occur with both viruses in HD units, and which is absent in peritoneal dialysis units. The incidence of hepatitis C among continuous ambulatory peritoneal dialysis (CAPD) patients is quite low, while it may reach almost 50%-60% of HD patients in some units. While hepatitis C transmission mechanisms are not completely understood and a vaccine is not available, PD provides some degree of protection when compared with HD, for and-stage renal disease patients. In summary, our experience and that of others, with a total of 19 PD-treated chronic liver disease patients, supports CAPD as the treatment of choice for cirrhotic patients with ascites who require chronic dialysis. Data on peritoneal diffusion of low molecular weight substances revealed a marked increase in most patients. The ultrafiltration capacity was clearly augmented with respect to noncirrhotic patients, making the use of hypertonic bags unnecessary. Hemodynamic tolerance was excellent. Complications and death were mainly related to liver disease complications. Spontaneous bacterial peritonitis (SBP), caused by gram-negative germs, is the most important complication directly related to ascites and may have some points in common with PD-related peritonitis. However, and in contrast to most PD peritonitis, two pathogenetic mechanisms have been suggested for SBP: (1) translocation of bacteria from the gut to the mesenteric lymph nodes, and (2) bacteremia in these patients is secondary to the general abnormal host defense mechanisms. Local factors such as intrahepatic shunting and the impairment of bactericidal activity in ascitic fluid favor the bacteria ascites. The hypothesis of a direct transmural contamination from bowel to ascitic fluid has been relegated to secondary bacterial peritonitis. Would cirrhotic patients with temporal or permanent renal function compromise benefit from peritoneal catheter placement and other PD practices to perform repetitive small ascitic drainages at home? Perhaps the time has arrived when hepatologists and PD nephrologists begin to work shoulder to shoulder in this particular field, as we have a common problem, the peritoneal cavity filled with fluid.
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PMID:Peritoneal dialysis in liver disorders. 872 96

The outcome of untreated spontaneous bacterial peritonitis (SBP) is fatal. In the onset of SBP clinical manifestations may be subtle, therefore every patient with hepatogenic ascites has to be examined for SBP at admission. If polynuclear cell count in ascitic fluid exceeds 250/microliter, antibiotic therapy has to begin immediately, until irreversible complications develop. Aerobic gram-negative bacilli of the normal intestinal flora are responsible for most cases of SBP, followed by gram-positive organisms and anaerobes. Antibiotic agents with extended spectrum, such as third-generation cephalosporins are considered the drugs of choice for SBP. In severe cases combination with metronidazole is recommended. As soon as repeated paracenteses show polynuclear cells beyond 250/microliter, the antibiotic therapy can be stopped. Selective decontamination of the gut with norfloxacin is effective to prevent SBP in high-risk patients. Trimethoprim-sulfamethoxazole is superior due to its activity even against gram-positive organisms. Overall prognosis of patients with SBP, however, is determined mainly to complications specific for cirrhosis, e.g. variceal bleeding, coma etc.
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PMID:[Therapy of spontaneous bacterial peritonitis]. 906 27

Bacterial translocation appears to be an important mechanism in the pathogenesis of spontaneous infections in cirrhosis. Cirrhotic patients are commonly treated with beta-adrenoceptor blockers, but the impact of this treatment in the factors promoting bacterial translocation has not been investigated. This study was aimed at investigating in cirrhotic rats with ascites the effect of propranolol on intestinal bacterial load, transit, and permeability of the bowel and on the rate of bacterial translocation. Bacterial translocation to mesenteric lymph nodes and intestinal bacterial overgrowth, permeability (urinary excretion of (99m)Tc-diethylenetriaminepentaacetic acid [(99m)Tc-DTPA]), and transit (geometric center ratio of (51)Cr) were assessed in 29 rats with carbon tetrachloride (CCl(4)) cirrhosis and 20 controls. These variables were then measured in 12 placebo- and in 13 propranolol-treated ascitic cirrhotic rats. Bacterial translocation was present in 48% of the cirrhotic rats and in none of the controls. Cirrhotic rats with intestinal bacterial overgrowth had a significantly higher rate of translocation and slower intestinal transit than those without it. Among the 15 rats with overgrowth and a (99m)Tc-DTPA excretion greater than 10%, 15 had translocation and 2 had bacterial peritonitis. Only 1 of the 14 rats with either intestinal overgrowth or a (99m)Tc-DTPA excretion greater than 10% presented translocation. Compared with the placebo group, propranolol-treated animals had significantly lower portal pressure, faster intestinal transit, and lower rates of bacterial overgrowth and translocation. In ascitic cirrhotic rats, bacterial translocation results from intestinal overgrowth and severe damage to gut permeability. In this setting, intestinal overgrowth is associated with intestinal hypomotility. Propranolol accelerates the intestinal transit, decreasing the rates of bacterial overgrowth and translocation.
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PMID:Effect of propranolol on the factors promoting bacterial translocation in cirrhotic rats with ascites. 1061 26


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