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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gram-negative septicemia is an old disease with dramatic changes in the arena of modern medicine. Whereas it was most often the domain of the infectious disease specialist and the abdominal surgeon 25 years ago, it is now managed in most medical practice specialties. It requires thorough understanding by all practitioners. Its physiology is increasingly well understood. The relationships between sepsis and host underlying diseases are important. Nonspecific therapies are important for early management of septicemia and impending shock, but specific application of immunotherapy in the form of antibody or vaccines, antibiotics selected for the most likely organism, and perhaps even pharmacotherapy directed at recognized intrinsic mediators of host responses to bacteremia, hold the greatest promise for a successful outcome.
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PMID:Gram-negative septicemia and shock. 706 84

The present investigation was undertaken to standardize the early diagnosis of Gram-negative septicemia in burned children. Data were collected by means of a matrix which encompassed eight clinical variables routinely monitored by nursing personnel. These variables were evaluated according to their severity using a numerical scale of 0 to 3. A sepsis score was thus calculated for each of 243 burned patients, three times a day throughout their entire hospitalization. Eighty patients with suspiciously high scores (controls) were subjected to a battery of ten laboratory tests aimed at confirming the presence or absence of septicemia. During the 26 months of the study 16 patients (22 episodes) had clinical and laboratory evidence of Gram-negative septicemia. Multiple regression and discriminant analysis techniques were then used to develop statistical models for early diagnosis of septicemia. The two most practical and reliable of these are reported herein. Model I and II would have predicted the diagnosis of sepsis, 83% and 86% of the time, respectively, 1 day before the diagnosis was made using conventional methods. The false positive rates of Models I and II were 7% and 3%, respectively. On the basis of this information it seems possible and rewarding to utilize decision-making charts for monitoring and diagnosis of septicemia.
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PMID:An objective method for early diagnosis of gram-negative septicemia in burned children. 721 84

Human monoclonal IgM antibody HA-1A, which recognizes the lipid A component of bacterial lipopolysaccharide (LPS), has been shown to reduce mortality in Gram negative septicemia. The vascular endothelial lining of blood vessels, which controls leucocyte traffic and activation, as well as haemostatic balance, may be one of the primary targets of LPS action during sepsis. In earlier studies we have described HA-1A-induced immune adherence of LPS to complement receptors on erythrocytes, and showed that pre-incubation with HA-1A, in the presence of complement and red blood cells, markedly reduced LPS-induced cytokine production from peripheral blood mononuclear cells. In the present study, we measured the effect of immune adherence of LPS in the presence of HA-1A on the responses of cultured endothelial cells, and found that subsequent expression of adhesion molecules such as E-selectin, ICAM-1 and VCAM-1, and secretion of the cytokines interleukin-6 and granulocyte-macrophage colony stimulating factor were markedly reduced. Moreover, the ability of LPS to increase levels of tissue factor procoagulant activity on endothelial cells was markedly diminished by LPS immune adherence to HA-1A. This decrease in endothelial activation in response to LPS following immune adherence to HA-1A may play a significant role in the protective effect of HA-1A in vivo during the course of Gram negative sepsis.
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PMID:Antilipid A monoclonal antibody HA-1A decreases the capacity of bacterial lipopolysaccharide to activate human vascular endothelial cells by an immune adherence mechanism. 751 52

Gram negative sepsis causes changes in oxygen supply-demand relationships. We have used a primate model of hyperdynamic gram negative sepsis produced by intravenous infusion of Escherichia coli (E. coli) to evaluate sepsis-induced alterations in mitochondrial oxidation-reduction (redox) state in muscle in vivo. The redox state of cytochrome a,a3, the terminal member of the intramitochondrial respiratory chain, was assessed in the intact forearm by near-infrared (NIR) spectroscopy. The muscle NIR data were compared to routine measures of oxygen delivery (DO2) and oxygen consumption (VO2). After E. coli infusion and fluid resuscitation, DO2 and VO2 showed minimal changes through 24 hr of sepsis. In contrast, changes in cytochrome a,a3 redox state evaluated by NIR occurred within a few hours and were progressive. Mitochondrial functional responses were correlated with structural changes observed on serial muscle biopsies. Gross morphological changes in muscle mitochondria were present in some animals as early as 12 hr, and, in most animals, by 24 hr. The morphologic changes were consistent with decreases in oxidative capacity as suggested by NIR spectroscopy. The NIR data also suggest that two mechanisms are operating to explain abnormalities in oxygen metabolism and mitochondrial function in lethal sepsis. These mechanisms include an early defect in oxygen provision to mitochondria that is followed by a progressive loss in functional cytochrome a,a3 in the muscle.
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PMID:Altered mitochondrial redox responses in gram negative septic shock in primates. 798 71

The in-vitro susceptibility pattern to newer beta lactams namely Ticer/Clav, Azlocillin, Piperacillin and Imipenem was determined with 50 clinical strains isolated from neutropenic patients with strains isolated from neutropenic patients with sepsis, with an objective of evolving a strategy for empirical antibiotic therapy for febrile neutropenic patients. The MIC90 value for Imipenem for the Gram negative bacilli tested, other than Pseudomonas was < 0.25 mcg/ml therapy revealing a high degree of susceptibility, while for Ps. aeruginosa and related species MIC50 and MIV90 values were 2.0 and 64.0 micrograms/ml respectively. A comparatively lower degree of susceptibility was found among Gram negative bacilli included in the study to ticar/clavu, azlocillin and piperacillin indicating a moderate degree of resistance to these antibiotics. The data from this study suggests that (i) Ureidopenicillins with an aminoglycoside should be effective therapy for proven Pseudomonas and other Gram negative sepsis in febrile neutropenic patients. (ii) Imipenem would be the antibiotic of choice in Gram negative bacterial sepsis in febrile neutropenic patients where the organism is resistant to cephalosporins and ureidopenicillins.
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PMID:In vitro evaluation of newer beta-lactam antibiotics against gram negative bacilli isolated from neutropenic patients. 806 32

During sepsis, the systemic inflammatory response is characterized by the release of numerous mediators supporting and dispersing inflammation. In Gram negative sepsis, the endotoxins play a starting role, while in other sepsis, the triggering mediators or mechanisms are unknown but lead to a similar inflammatory reaction. Coagulation and complement cascades are activated, with the release of chemoattractive substances, mediators and proteases and the activation of phagocytic cells. Macrophages/monocytes and polymorphonuclear leucocytes produce then active oxygen species and cytokines; they degranulate (releasing active enzymes such as myeloperoxidase), they express an increasing number of membrane receptors able to interact with endothelial cells and release a supplementary lot of inflammatory mediators (prostanoids, platelet activating factor, leukotrienes ... ). Platelets, also activated, produce the same mediators (TXA2, PAF ...) or specific ones such as serotonine, platelet factor 4, growth factors. Last, but not least, the endothelial cells are stimulated, directly (by endotoxins) or undirectly (by cytokines, C5a, PAF ...). These cells play then a main role by their own phagocytic activity, by alteration of their antithrombotic and fibrinolytic potential, by their secretion of inflammatory mediators and by an increased expression of receptors of adhesivity for the activated phagocytes or platelets, what leads to endothelium injury with membrane permeability alterations. These cascades of activation, these extensions of the inflammatory reaction by the mediators and by the phagocytes and platelets can explain the frequency of multiple organ failure during sepsis as well as the difficulty of an adequate pharmacological therapy.
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PMID:[Other mediators of inflammation and sepsis]. 846 93

The present study outlines the relationship between cerebral and systemic hemodynamics in patients with septic shock. Sepsis is an immune mediated systemic disease in which the systemic vascular resistance (SVR) often decreases as a result of a Gram negative sepsis. The result is a hyperdynamic systemic circulation with redistribution phenomena in different organ systems. In order to study the effect of sepsis on cerebral vessels 20 patients with septic shock (12 men, 8 women, mean age 57.9 years) were subjected to both pulmonary artery catheter and transcranial Doppler (TCD) monitoring. The data were correlated to the APACHE II score and outcome. The study showed that cerebral mean and end-diastolic blood flow velocities (BFV) in the middle cerebral arteries significantly enhanced if the SVR-index decreases. In some patients a severely reduced SVRI (below 500 dynes.s/cm5.m2) was observed in combination with a downstroke latent steal phenomenon. TCD abnormalities were strongly related to disease severity and outcome. The increased BFV are explained by a mild vasospasm of the basal cerebral arteries. TCD appears to be a valuable tool to monitor the cerebral hemodynamics in these patients. They are particularly at risk for ischemic brain damage if they are subjected to therapeutic or spontaneous hyperventilation, which can potentially be detected by TCD.
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PMID:Transcranial Doppler and systemic hemodynamic studies in septic shock. 887 47

Acute acalculous cholecystitis (AAC) is marked by a very high mortality rate but its relative rarity makes its features obscure to many physicians. This often contributes to a delayed diagnosis. In this study, we review one center's experience, examine the clinical features of the disorder, and describe the progression of pathological events that culminate in AAC. We performed a 10-year retrospective review of cases of AAC reported at our institution between 1988 and 1998. Fifteen cases of AAC were identified from this period, during which 5804 cardiovascular operations were performed. The mortality rate was 46.6%. Multiple organ failure was present in 12 of the 15 cases, and 9 of the patients were over 60 years of age. Prolonged hypotension occurred in 13 patients, and fever in all 15. Nine cases of gangrenous gallbladder occurred. Gram-negative septicemia was present in 12. Visceral arterial hypoperfusion was frequently evident at operation or necropsy. Thirteen patients showed clinical jaundice, a disproportionate elevation of the alkaline phosphatase, or both. Heart failure was found in 9 patients. Open cholecystectomy was most often the definitive intervention. Arterial hypoperfusion of the gut and or sepsis appear central to the pathogenesis of AAC in our series. Gallbladder inflammation and cholestasis result and bacterial invasion of the organ ensues, culminating in AAC, frequently with gangrene. A model of the pathogenesis of AAC is discussed.
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PMID:Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology. 1462 41

Lipopolysaccharide (LPS) endotoxin is the bacterial product responsible for the clinical syndrome of Gram-negative septicemia and endotoxic shock. During sepsis, microbial antigens, such as LPS, activate monocytes and macrophages to produce several pro-inflammatory cytokines, among which tumor necrosis factor-alpha (TNF-alpha) appears to be very important for the development of endotoxic shock. The endotoxic properties of LPS principally reside in the lipid A (LIP A) component, which is the primary immunostimulatory center of Gram-negative bacteria. In recent years there has been a continuous effort to identify molecules able to antagonize the deleterious effects of endotoxic shock. In this study we show that a novel LIP A fraction from the LPS of Halomonas magadiensis (Hm), a Gram-negative extremophilic and alkaliphilic bacterium, significantly inhibits the synthesis of TNF-alpha by human monocytes activated by Escherichia coli LPS. LIP A from Hm exerts these effects by interfering with E. coli LPS for activation of Toll-like receptor 4 expressed in human cells. This result defines Hm LIP A as a novel class of LPS antagonist whose structural features could be utilized for the design of compounds for the treatment of Gram-negative sepsis.
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PMID:A novel lipid A from Halomonas magadiensis inhibits enteric LPS-induced human monocyte activation. 1636 14

Urinary tract infections can occur in all age groups and produce an exceptionally broad range of clinical syndromes ranging from asymptomatic bacteriuria to acute pyelonephritis with Gram negative sepsis to septic shock. In approximately one-quarter of all patients with sepsis, the focus of infection is localized to the urogenital tract. This may lead to substantial morbidity and significant economic implications. We present a review of the current approaches to managing urospesis.
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PMID:Approach to a patient with urosepsis. 2030 Mar 89


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