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

In a search for clinical and laboratory factors that would aid in early diagnosis of spontaneous bacterial peritonitis, we identified two groups of patients with chronic liver disease and ascites: 1) 38 patients with 40 episodes of spontaneous bacterial peritonitis, and 2) 39 randomly selected patients with 40 sterile paracenteses who were matched for severity of liver dysfunction as a reference group. A variety of clinical and laboratory features were examined. The absolute lymphocyte count in peripheral blood was lower for the spontaneous bacterial peritonitis group (mean = 703/mm3 vs. 1,212/mm3, p less than 0.005). Four ascitic fluid variables, i.e., a white blood cell count of greater than or equal to 300/mm3, a polymorphonuclear leukocyte count of greater than or equal to 240/mm3, an ascitic fluid/serum LDH ratio of greater than or equal to 0.4, or an ascitic fluid/serum glucose ratio of less than or equal to 1.0, could separate the spontaneous bacterial peritonitis and reference groups with both sensitivity and specificity of greater than 70%. Although ascitic fluid total leucocyte and polymorphonuclear leucocyte counts are appropriate indicators for the early diagnosis of spontaneous bacterial peritonitis, the possibility of their false positivity should be warranted. The use of multiple tests including ascitic fluid/serum LDH and glucose ratios has better positive predictive value than a single test alone.
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PMID:Early diagnosis of spontaneous bacterial peritonitis: values of ascitic fluid variables. 366 66

Spontaneous bacterial peritonitis is an infection of the ascitic fluid of patients who, in general, have severe chronic liver disease. Several variants of this disease exist including bacterascites, culture-negative neutrocytic ascites, and secondary bacterial peritonitis. Spontaneous bacterial peritonitis is frequently manifested by signs and symptoms of peritonitis although the findings may be subtle; however, occasionally it may be completely without clinical manifestation. The clinician must have a high index of suspicion in order to make this diagnosis at a relatively earlier stage of infection. An abdominal paracentesis is required to make the diagnosis of spontaneous bacterial peritonitis. This paracentesis should be performed on all patients who are admitted to the hospital for ascites and should be repeated if there is any manifestation of bacterial infection during the hospitalization. Patients with severe intrahepatic shunting--as manifested by marked redistribution of activity from the liver to the spleen and to the bone marrow on liver-spleen scan as well as patients with an ascitic fluid total protein concentration of less than 1 g/dl--appear to be particularly susceptible to bacterial infection of their ascites. In order to optimize the yield of ascitic fluid culture, it is probably appropriate to inject blood culture bottles with ascites at the bedside immediately after the abdominal paracentesis. The mortality of spontaneous bacterial peritonitis continues to be very high. Perhaps routine admission paracentesis and prompt empiric antibiotic therapy with a third-generation cephalosporin will decrease the mortality of this infection if the Gram stain of the ascitic fluid demonstrates bacteria or the ascitic fluid neutrophil count is greater than 250 cells/cu mm. Repeating the paracentesis after 48 hours of treatment to reculture the fluid and reassess the ascitic fluid neutrophil count appears to be the best way to assess efficacy of treatment. After 48 hours of treatment the ascitic fluid neutrophil count should be less than 50% of the original value if the antimicrobial therapy is appropriate. The optimal duration of antibiotic treatment is unknown; however, until controlled trials provide data regarding duration of treatment it is appropriate to treat with parenteral antibiotics for 10 to 14 days. Research is also needed to determine if there are measures which can be taken to prevent the development of spontaneous peritonitis.
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PMID:Spontaneous bacterial peritonitis. 389 55

We describe the clinical and laboratory features of a case of spontaneous bacterial peritonitis caused by Neisseria gonorrhoeae in a sexually active woman with Laennec's cirrhosis, ascites, and asymptomatic cervical gonorrhea. Treatment of the infection with high-dose parenteral penicillin was associated with resolution of the infection. This first report of spontaneous gonococcal peritonitis provides highly suggestive evidence that the transfallopian route is a mechanism whereby bacteria may enter the peritoneal cavity. Appropriate cultures for this organism should be included when a woman with chronic liver disease, who is sexually active, presents with spontaneous peritonitis.
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PMID:Spontaneous bacterial peritonitis caused by Neisseria gonorrhoeae. Evidence for a transfallopian route of infection. 391 60

We analyzed the clinical and bacteriologic features of 12 episodes of spontaneous bacterial peritonitis (SBP) in 11 children (four boys, median age 5.5 years) with chronic liver disease. All patients had cirrhosis and ascites; four had hypersplenism, and one was asplenic. Symptoms included increasing abdominal distention, pyrexia, abdominal pain, gastrointestinal disturbance, and encephalopathy. Nine had rebound tenderness on abdominal palpation, and 12 had reduced bowel sounds. The most frequent organisms isolated from culture of ascitic fluid were Streptococcus pneumoniae (nine). Klebsiella (two), and Haemophilus influenzae (one); blood cultures grew identical organisms in nine. Seven patients died despite intensive antibiotic therapy. In the 3 months prior to onset of SBP, defective yeast opsonization and reduced serum concentration of C4 were found in all nine children tested; eight had reduced concentration of C3. Functional deficiency of all complement components was present in four tested within 1 to 5 months of the onset. In contrast, only eight of 59 cirrhotic children without SBP had low C3, and eight had defective yeast opsonization, although 35 had low C4 values. Four of the patients with SBP and low C3 and C4 concentrations had normal concentrations at the time of diagnosis of liver disease 2 to 5 years previously. Opsonization of type III pneumococci was reduced in sera from three patients who subsequently developed pneumococcal peritonitis. The incidence of SBP in children with chronic liver disease is similar to that in adults, as are the clinical features. Our observations suggest that complement deficiency induced by chronic liver disease may be important in the pathogenesis of SBP.
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PMID:Spontaneous bacterial peritonitis in children with chronic liver disease: clinical features and etiologic factors. 399 46

Several recent reports suggest that Chlamydia trachomatis causes peritonitis and perihepatitis in young women. We studied nine patients with chronic liver disease and ascites to determine a possible role for C. trachomatis in the bacterial peritonitis of cirrhotic patients. C. trachomatis was isolated and identified from the peritoneal fluid in three of these patients. In these patients, the peritoneal fluid was a transudate that contained fewer than 250 white blood cells/mm3, with fewer than 10% neutrophils, except when a bacterial organism other than C. trachomatis was also present. Two of these patients developed peritonitis that was associated with other bacterial organisms. Unless specific tests for C. trachomatis was performed, its presence will not be detected, and the peritoneal fluid cell count will not suggest bacterial infection.
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PMID:Chlamydia trachomatis in the ascitic fluid of patients with chronic liver disease. 684 7

Forty-three patients with spontaneous bacterial peritonitis (SBP) between 1973 and 1978 were identified. Criteria for SBP included a positive ascites culture and polymorphonuclear cell concentration greater than 250 cells per mm3. Chronic liver disease was documented by varices in 91%, severe histologic fibrosis or cirrhosis in 94%, splenomegaly in 91%, and past hospitalization for liver disease in 57% of the patients. SBP was detected within 7 days of admission in 17 patients (40%) and within 35 days in 38 patients. Single organisms were isolated from 38 patients and multiple organisms from 5 patients. Twenty-six of 43 patients survived the episode of SBP, but only 13 survived the hospitalization. Analysis of the survival curve from the onset of SBP revealed a rapid death rate and a slow death rate set of patients. Rapid death (less than or equal to 7 days from SBP onset) correlated with a lack of prior hospitalization for liver disease (p less than 0.001), hepatomegaly (p less than 0.001), increased serum bilirubin (p less than 0.005), serum creatinine (p less than 0.05), and peripheral white blood cell concentrations (p less than 0.05). Survival during hospitalization was associated with prior hospitalization with liver disease (p less than 0.001) and chills during the episode of SBP (p less than 0.001). The 43 patients were divided into Group 1 patients on the basis of a serum bilirubin greater than 8 mg% and/or serum creatinine greater than 2.1 mg%; Group 2 patients had lower values. Survival was greater in Group 2 patients with advanced, relatively quiescent liver disease compared to Group 1 patients for both the episode of SBP (91 vs. 29%; p less than 0.001) and for hospitalization (50 vs. 9%; p less than 0.05). Death in Group 2 patients was related to inadequate antibiotic therapy (p less than 0.05), nonhepatic factors, and new onset of renal failure. Although SBP in the setting of severe acute liver injury has a dismal prognosis, SBP with minimal acute liver injury has a relatively good prognosis for hospital survival even with advanced chronic liver disease. Long-term survival is also possible since 4 of 9 patients with prolonged follow-up have survived 3 years.
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PMID:Spontaneous bacterial peritonitis. 709 41

The prevalence of hepatitis C virus (HCV) infection in patients with chronic liver disease (CLD) in Israel has not yet been reported. A retrospective analysis was performed on the first 92 consecutive patients referred to our Liver Unit with serologically confirmed antibodies to hepatitis C virus (anti-HCV) who had evidence for chronic hepatitis, cirrhosis, and hepatocellular carcinoma. We compared 31 patients who were anti-HCV positive with 61 patients who had evidence for both previous or present infection with hepatitis B virus (HBV) as well as HCV. Dual infection was significantly more prevalent in Jewish patients of non-Ashkenazi origin, who were also characterized by higher rates of portal hypertension manifested by ascites, bleeding esophageal varices as well as hepatic encephalopathy and spontaneous bacterial peritonitis. We conclude that dual infection of HBV and HCV was found in 66% of patients with anti-HCV positive liver disease in Jerusalem, and that these patients develop more serious complications than CLD patients with anti-HCV alone.
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PMID:Chronic hepatitis C virus infection with exposure to hepatitis B virus. 817 25

We report the case of a patient with peritonitis caused by Brucella melitensis who also had chronic liver disease. At first the patient was treated for bacterial peritonitis but when a lymphocytic ascites was aspirated antituberculosis chemotherapy was given. However, the serological tests for brucellosis were strongly positive and subsequently B. melitensis was isolated from ascitic fluid.
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PMID:Brucella peritonitis. 822 98

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 prevalence of spontaneous bacterial peritonitis (SBP) or its variants, bacterascites (BA), and culture-negative neutrocytic ascites (CNNA), may vary depending on the underlying liver disease and protein content of ascites. In this study, we compared the frequency of peritonitis (SBP, BA, CNNA) upon admission in alcoholic (ALD), cholestatic (CLD), and hepatocellular liver disease (HLD); determined the relationship between Child's class and prevalence of peritonitis; and assessed ascitic total protein as a risk factor for peritonitis. Between January 1989 and April 1991, 113 consecutive patients were admitted with chronic liver disease and ascites (49, ALD; 22, CLD; and 42, HLD). All had admission paracentesis. SBP was defined as polymorphonuclear cell count (PMN) > or = 250 mm3 with a positive culture, BA as PMN < 250/mm3 and positive culture, and CNNA as PMN > or = 250/mm3 with negative culture. No patients with obvious intraabdominal source for infection (i.e., secondary peritonitis) were included in the analysis. The prevalence of peritonitis was 8/113 (7%); four patients had SBP, one BA, and three CNNA. The occurrence of peritonitis was independent of the type of liver disease (ALD, 8%; CLD, 9%; HDL, 5%). Neither ascitic fluid total protein nor the severity of liver disease (Child's class) predicted the occurrence of peritonitis. We conclude that the occurrence of peritonitis is unrelated to the type of liver disease, and severity of liver disease did not predict the presence of peritonitis. Also, ascitic fluid total protein < 1.0 g/dl may not be a sensitive predictor of risk of peritonitis.
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PMID:Prevalence of peritonitis and the ascitic fluid protein concentration among chronic liver disease patients. 839 75


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