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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postoperative peritoneal adhesions are a major cause of morbidity. The purpose of this study was to investigate the potential contributions of suturing and sepsis to their formation in animals undergoing laparotomy. Suturing the peritoneum with plain catgut was associated with a high incidence of adhesions to the wound at 8 days (11/15), but this was significantly less at 25 days (5/15, P less than 0.04). Use of monofilament nylon, or non-suture, were each associated with a low incidence of adhesions. Wound strength was significantly greater at 25 days than at 8 days (P less than 0.0005), but did not differ between groups. In a separate experiment, bacterial infection, even in the absence of a particulate carrier, proved to be a potent cause of postoperative peritoneal adhesions (8/9, P = 0.02) compared with uninfected controls (3/10). Suturing the peritoneum in the presence of infection caused an especially high incidence of adhesions to the wound (8/9, P = 0.004 vs 2/10 unsutured). It is concluded that the lowest incidence of adhesions to the wound is likely to be obtained, both in uninfected and in infected cases, if the peritoneum is not sutured during closure of abdominal wounds, and that such an approach does not compromise wound strength.
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PMID:The influence of suturing and sepsis on the development of postoperative peritoneal adhesions. 156 33

Young infants with fever are at risk for serious bacterial infection, but no consensus exists on the optimal approach to diagnosis and treatment. Although the traditional recommendation is always to perform all sepsis tests, including lumbar puncture, and administer intravenous (IV) antibiotics until culture results are negative, recent studies suggest administering intramuscular (IM) ceftriaxone with outpatient follow-up or using laboratory and clinical data to exclude low-risk patients from hospitalization, further testing, and antibiotic treatment. A decision analysis model was used to evaluate six strategies for the diagnosis and treatment of infants aged 28 to 90 days with temperature greater than or equal to 38.0 degrees C. Data from the literature, data from a 1991 study of 503 febrile infants, and direct, short-term costs from the Children's Hospital of Philadelphia were used as model inputs. The model was run for a hypothetical cohort of 100,000 febrile infants who did not require admission for focal infection or for other reasons that clearly necessitated admission. The model included six strategies: (1) no intervention; (2) all sepsis tests (lumbar puncture, blood culture, urine culture, white blood cell count, and urinalysis) followed by hospitalization and IV antibiotics for all infants; (3) all sepsis tests followed by IM ceftriaxone and outpatient management for most infants; (4) blood and urine cultures with white blood cell count and urinalysis followed by either lumbar puncture and IV antibiotics for high-risk infants or outpatient management without antibiotics for low-risk infants; (5) white blood cell count and urinalysis followed by either lumbar puncture, blood and urine cultures, and IV antibiotics for high-risk infants or outpatient management without antibiotics for low risk infants; and (6) clinical judgment followed by either all sepsis tests and IV antibiotics for high-risk infants or outpatient management without antibiotics for low-risk infants. The two "all sepsis tests" strategies prevented the most cases of death or neurologic impairment, 78% (when IV antibiotics were used) and 76% (when IM ceftriaxone was used) of all potential cases. The most cost-effective strategy was to use all sepsis tests followed by IM ceftriaxone for all patients without meningitis, at an incremental cost of only $3900 per sequela prevented relative to no intervention. Strategies under which only those patients selected as high-risk by laboratory criteria received antibiotic treatment were less effective but incurred lower rates of antibiotic complications. Clinical judgment alone was the least clinically effective and the second least cost-effective strategy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical and cost-effectiveness of outpatient strategies for management of febrile infants. 844 84

The expression of surface tissue factor procoagulant activity and its shedding by blood monocytes can be induced by several stimuli. Few of these defined situations, other than the presence of bacteria and their toxins, are commonly present in the young human infant. In this study, measurements were made of the percentage of monocytes expressing surface tissue factor apoprotein (TFA) in blood taken from babies in the early weeks of life. Mononuclear cells were separated from blood in an environment free of detectable endotoxin. After exposure to a polyclonal rabbit antibody raised to purified brain TFA and subsequent exposure to a fluorescin-labeled murine anti-rabbit IgG, the cell fluorescent activity was analyzed by flow cytometry. The percentage of monocytes showing strong fluorescence was determined. In every instance when systemic bacterial infection was present, more than 60% of the monocytes examined showed fluorescence indicative of the presence of surface TFA. In a single case of fungal Candida septicemia, none of the monocytes was positive. More than 60% of cells were found to be positive in certain instances where infection was highly probable but not proven. Positive cells were found in three cases of isoimmune hemolytic disease of the newborn, as had been anticipated from previous studies, whereas less than 25% of monocytes derived from babies in the absence of discernible infection or isoimmune hemolytic disease expressed surface TFA (p less than 0.001). These findings provide insight into a possible mechanism of coagulation activation in sepsis and may prove to be a useful predictor of the presence of infection or endotoxemia in young infants.
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PMID:The expression of surface tissue factor apoprotein by blood monocytes in the course of infections in early infancy. 163 18

Tumor necrosis factors (TNF) alpha and beta are structurally related cytokines that mediate a wide range of immunological, inflammatory, and cytotoxic effects. During bacterial infection of the bloodstream (sepsis), TNF-alpha induction by bacterial endotoxin is thought to be a major factor contributing to the cardiovascular collapse and critical organ failure that can develop. Despite antibiotic therapy, these consequences of sepsis continue to have a high mortality rate in humans. Here we describe a potent TNF antagonist, a TNF receptor (TNFR) immunoadhesin, constructed by gene fusion of the extracellular portion of human type 1 TNFR with the constant domains of human IgG heavy chain (TNFR-IgG). When expressed in transfected human cells, TNFR-IgG is secreted as a disulfide-bonded homodimer. Purified TNFR-IgG binds to both TNF-alpha and TNF-beta and exhibits 6- to 8-fold higher affinity for TNF-alpha than cell surface or soluble TNF receptors. In vitro, TNFR-IgG blocks completely the cytolytic effect of TNF-alpha or TNF-beta on actinomycin D-treated cells and is markedly more efficient than soluble TNFR (24-fold) or monoclonal anti-TNF-alpha antibodies (4-fold) in inhibiting TNF-alpha. In vitro, TNFR-IgG prevents endotoxin-induced lethality in mice when given 0.5 hr prior to endotoxin and provides significant protection when given up to 1 hr after endotoxin challenge. These results confirm the importance of TNF-alpha in the pathogenesis of septic shock and suggest a clinical potential for TNFR-IgG as a preventive and therapeutic treatment in sepsis.
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PMID:Protection against endotoxic shock by a tumor necrosis factor receptor immunoadhesin. 166 Jan 40

Pathological changes and significance of intrahepatic peribiliary glands, hitherto poorly recognized intrahepatic elements, have been evaluated in our laboratory. In this report, we surveyed necroinflammatory and cystic changes of the peribiliary glands in 1,000 consecutive autopsy livers because these two changes coexisted frequently in the same liver. The necroinflammatory change was found in 228 livers (22.8%) and the cystic change in 202 livers (20.2%), and 103 cases showed both changes in the same liver. The necroinflammatory change was frequently found in intrahepatic cholangitis and extrahepatic biliary obstruction with bacterial infection, suggesting that biliary bacterial inflammation extends into these peribilary glands. This change was also frequent in systemic infection or septicemia without biliary bacterial infection, implying that the peribiliary glands were also damaged in such conditions without direct infection. The cystic change was frequent in livers with portal hypertension or obstruction, adult polycystic disease and necroinflammation of the glands, suggesting that the cystic change of the glands could occur as the result of the disturbance of intrahepatic circulation or as the result of inflammatory destruction of the glandular conduits. Some of peribiliary cysts may be of congenital origin. Dysfunction related to these pathological changes in the glands may diminish seromucous secretion and cause alterations in hepatic bile composition. The cystic change of the glands may retard bile flow by compressing bile duct lumina.
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PMID:Pathological observations of intrahepatic peribiliary glands in 1,000 consecutive autopsy livers. III. Survey of necroinflammation and cystic dilatation. 169 63

We measured serum interleukin-6 (IL-6) and acute-phase proteins, alpha 1-acid glycoprotein (AGP) and alpha 2-macroglobulin (alpha 2M), after a retrograde intrabiliary bacterial infection in rats with biliary obstruction. Maximum serum IL-6 was obtained at 6 h in rats following inoculation of bacteria (10(6) CFU/ml E. Coli) in the bile duct and it was higher than that observed in rats undergoing a bile duct ligation or a laparotomy. There was a strict relationship between the level of IL-6 at 6 h and the modified levels of AGP and alpha 2M at 48 h. AGP and alpha 2M levels were the highest in sera of rats with bile duct infection as compared with those found in sera of rats with bile duct ligation or laparotomy. After inoculation of E. Coli or E. Fecalis, blood IL-6 level was always higher at 6 h in inferior vena cava as compared with that found in the supra hepatic vein. These results indicate that IL-6 is synthesized after a biliary sepsis and that its blood level is higher in the systemic circulation than in the local circulation.
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PMID:Interleukin-6 (IL-6) and acute-phase proteins in rats with biliary sepsis. 171 93

The C-reactive protein (CRP) level was evaluated in 142 infants requiring investigation for suspected infection. After excluding two neonates because of incomplete data, there remained 140 neonates, of whom 16 had septicemia. Fifteen of 16 had increased CRP levels. The CRP value was not elevated in any baby (n = 5) who had positive blood cultures for Staphylococcus epidermidis, all of whom had an uneventful clinical course. The CRP level was elevated in all six babies with meconium-aspiration syndrome, but was normal in five infants whose viral cultures were positive. Ninety-nine percent of uninfected babies had normal CRP values. Overall, CRP was a valuable test for diagnostic confirmation of bacterial infection. Elevated CRP level was always accompanied by at least one abnormality in the other tests performed. Although the study was not intended to predict clinical onset of bacterial disease, our results suggest that the CRP level, because of a high negative predictive value, may be useful in ruling out bacterial infection.
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PMID:Acute phase reactants in neonatal bacterial infection. 172 16

The bacterial infection are responsive of severe sepsis and localizations in neonates, with a high mortality. The right choice of the first antibiotics is essential, and they must be well-fitted, early and bactericidal. The antibiotics of choice in the mother-linked infections are directed towards streptococcus group B and E. coli. Ampicillin must be replaced by a third generation cephalosporin because E. coli are resistant in more than 50% of cases. In tropical areas the first neonatal infections may be also the fact of multiresistant hospital acquired bacteria, which are transmitted during delivery by lack of hygiene. As in the nosocomial infections the causative pathogens are resistant Enterobacteriaceae, Pseudomonas and Staphylococcus. In all cases the neonatologist must use cephalosporin 3rd generation associated to aminoglycoside. The biological background and the cost of those antibiotics must be reevaluated in the high risk-areas (delivery rooms, nurseries, pediatrics departments).
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PMID:[Current orientation of antibiotic treatment in neonatal bacterial infection]. 181 21

Numerous abnormalities in neonatal host-defense mechanisms have been documented over the past decade. Profound disturbances in myeloid progenitor proliferation, bone marrow neutrophil storage pools, a tendency to peripheral neutropenia and significant in vitro abnormalities of mature neutrophil cell effector function all predispose the neonate to a high mortality rate during bacterial sepsis. The recent use of hematopoietic CSFs and other cytokines to enhance host defense mechanisms in the adult has suggested a role for this new form of immunotherapy in the newborn. Several studies over the past 2 years have indicated that a number of these cytokines may in fact enhance neonatal myeloid progenitor proliferation, modulate neonatal bone marrow neutrophil storage and proliferative pools, induce peripheral neutrophilia and protect against the high mortality rate associated with experimental bacterial sepsis to enhance neonatal host defense against overwhelming bacterial infection.
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PMID:Cytokines: a new immunotherapy. 187 12

Monoclonal antibodies (MAb) directed against bacterial lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF) provide partial protection in experimental models of septic shock. To determine if additional benefit accrues from a combination of anti-TNF and anti-LPS MAb in the treatment of septic shock, a neutropenic rat model was developed to study active infection with Pseudomonas aeruginosa 12.4.4. Animals were treated intravenously with an irrelevant MAb (group 1); anti-TNF MAb (group 2); MAb directed against P. aeruginosa 12.4.4 LPS (group 3); or a combination of anti-TNF and anti-LPS MAb (group 4). None of the control animals in group 1 survived the 7-d period of neutropenia (0/16). In contrast, the survival rate was 44% in group 2 (P less than 0.02); 37% in group 3 (P less than 0.05); and 75% in group 4 (P less than 0.0002). The combination of monoclonal antibodies provided greater protection than either MAb given alone (P less than 0.05). Serum TNF levels during infection were significantly greater in groups 1 and 3 (20.1 +/- 3.3 U, mean +/- SE) than in groups 2 and 4 (0.9 +/- 0.8 U, P less than 0.0001). These results indicate that a combination of monoclonal antibodies to LPS and TNF have additive benefit in experimental Pseudomonas aeruginosa sepsis. This immunotherapeutic approach may be of potential utility in the management of serious, gram-negative bacterial infection in neutropenic patients.
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PMID:Efficacy of antilipopolysaccharide and anti-tumor necrosis factor monoclonal antibodies in a neutropenic rat model of Pseudomonas sepsis. 188 75


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