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

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of harmful substances (bacteria, toxins and antigens) present within the intestinal lumen. At birth, the newborn infant must be prepared to deal with bacterial colonization of the gut, with formation of toxic byproducts of bacteria and viruses (enterotoxins and endotoxins) and with the ingestion of antigens (milk proteins). These potentially noxious substances if allowed to penetrate the mucosal epithelial barrier under pathological conditions can cause inflammatory and allergic reactions which may result in gastrointestinal and systemic disease states. To combat the potential danger of invasion across the mucosal barrier the infant must develop an elaborate system of defence mechanisms within the lumen and on the luminal mucosal surface which act to control and maintain the epithelium as an impermeable barrier to uptake of macromolecular antigens. These defences include a unique immunological system adapted to function in the complicated milieu of the intestine as well as other non-immunological processes such as a gastric barrier, intestinal surface secretions, peristaltic movement and natural antibacterial substances (lysozyme, bile salts) which also help to provide maximum protection for the intestinal surface. Unfortunately, during the immediate postpartum period, particularly for premature and small-for-dates infants, this elaborate local defence system is incompletely developed. As a result of the delay in the maturation of the mucosal barrier newborn infants are particularly vulnerable to pathological penetration by harmful intraluminal substances. The consequences of altered defence are susceptibility to infection and the potential for hypersensitivity reactions and for formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis and hepatitis. Fortunately, 'nature' has provided a means for passively protecting the 'vulnerable' newborn against dangers of a deficient intestinal defence system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leucocytes but many other substances which can interfere with bacterial colonization and prevent antigen penetration.
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PMID:Gastrointestinal host defence: importance of gut closure in control of macromolecular transport. 26 21

We have studied cefuroxime, a new beta-lactamase resistant cephalosporin, and cefoxitin, the first cephamycin antibiotic, which is also resistant to many beta-lactamases. Both of these antibiotics have been shown to be microbiologically superior to the "first generation" cephalosporins, cefuroxime having notable activity against Haemophilus influenzae, and cefoxitin against Bacteroides fragilis. Neither antibiotic is absorbed from the gut but, following parenteral administration, serum, urine and bile concentrations are high. Clinical trials have been conducted on both cefoxitin and cefuroxime. The results of these have been satisfactory and untoward side-effects minimal. We suggest that cefoxitin will be particularly valuable in the management of abdominal sepsis and cefuroxime in infections caused by H. influenzae.
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PMID:Studies with cefuroxime and cefoxitin. 30 60

Sepsis is a frequent cause of morbidity following extensive bowel resection. It has been suggested that the lymphoid tissues of the gut may be essential to normal humoral immunity. This study evaluates: (1) the effect of endotoxin on mortality following selective massive bowel resection and jejunoileal bypass; (2) cellular immunity by skin allograft rejection and bypass, and (3) T and B cell lymphocyte subpopulations is mesenteric lymph nodes, intestine and appendix. Endotoxin increased mortality in rats with more distal bowel resection but not following bypass. Skin allograft rejection was similar in each group. Peyer's patches, mesenteric lymph nodes and appendices were evaluated for T & B cell subpopulations. These tissues had a greater percentage of B cells (53% lymph nodes, 63% appendix) with IgM the predominant immunoglobulin. Cellular immunity was not a factor. Lymphoid tissues of the distal bowel and mesentery contain abundant B cells and IgM that may contribute to humoral immunity. Massive bowel resection may increase the risk of morbidity from gram negative sepsis and/or endotoxin presumably due to decreased humoral immunity.
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PMID:Adverse effects of endotoxin following massive distal bowel resection. 31 29

The problem of fungus infections after liver transplantation was studied. In 100 consecutive recipients of orthotopic liver homografts there were 10 and 8 examples, respectively, of localized and disseminated infections caused by Candida species. Candidemia was demonstrated in 8 of these 18 patients. One patient who had a localized Candida infection also had disseminated cryptococcosis. An additional 31 patients were infested in that Candida could be cultured from sites where it is not normally found, such as the blood (8 examples), urine (8), ascitic fluid (8), and wounds (22). This exorbitant incidence of monilial infections and infestations was associated with a high frequency of complications involving the homograft as well as the hosts' gastrointestinal tract during the post-transplantation period. The yeasts found in blood, urine, ascitic fluid and elsewhere were thought to have originated from the gut. Ten of the 100 patients had aspergillosis which was localized in 7 instances and disseminated in 3. The lung was the most frequently affected organ. The fungus infections played a contributory role in the downhill course of our patients but in the event of death more fundamental and more frequent causes of failure were technical complications involving the homografts, difficulties in controlling rejection with reasonable immunosuppressive doses and bacterial sepsis. Suggestions have been made for the better control of fungal infections in liver recipients.
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PMID:Fungus infections after liver transplantation. 32 51

The plasma concentrations of substrates, together with transhepatic and transgut balances, have been studied in six control and eight septic awake fasted dogs. Four severely ill septic dogs (typically fluid in chest and/or abdomen, extensive peritonitis, respiratory difficulties) had high concentrations of threonine, glycine, tyrosine, lysine, histidine, tryptophan, and triglycerides (p less than or equal to 0.05). The other septic dogs (less severely ill) showed fewer and less pronounced alterations in the plasma substrates (aspartate and tryptophan were elevated, p less than or equal to 0.05). The infusion of glucose increased the concentration of glucose, lactate, and pyruvate and depressed the concentrations of most amino acids in both normal and septic dogs. Threonine, asparagine, glutamine, leucine, isoleucine, alpha-aminobutyrate, and tyrosine were significantly depressed in the severely ill septic dogs (p less than or equal to 0.05). In the normal dogs most amino acids were removed by the liver, with alanine accounting for approximately 40% of the total. Glutamine removal was negligible. In the septic dogs hepatic removal of amino acids was variable; livers of two severely ill septic dogs did not remove amino acids. In the control dogs glucose infusion (0.015--0.017 g/kg/min) tended to lower hepatic removal of amino acids. Hepatic dye removal in the septic dogs was always very poor. In the gut glutamine was removed and alanine, glutamate, glycine, and ammonia produced, but the overall sum of amino acid uptake was negligible in both the control and septic dogs. The ratio of tryptophan to the sum of valine, isoleucine, leucine, tyrosine, and phenylalanine concentrations was greatly elevated in all septic dogs in which it was measured. The free concentrations of amino acids in the liver, heart, and muscle tissues were grossly elevated in the low intravenous alimented septic state relative to the fasted normal state, whereas the tissue concentrative ability as measured by nonmetabolizable amino acids, alpha-aminoisobutyrate and cycloleucine, was not similarly increased. Sepsis clearly alters plasma and tissue concentrations, and in some instances hepatic uptake of amino acids.
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PMID:Plasma concentrations and tissue uptake of free amino acids in dogs in sepsis and starvation: effects of glucose infusion--some effects of low alimentation. 65 52

The Esch. coli harboured in the gut constitute a reservoir of potential pathogens in the infant and child. The conditions required for these intestinal inhabitants to cause infection are not well understood. The presence of virulence factors such as capsular antigens, especially K1, may be of significance for the ability of Esch. coli to cause neonatal meningitis. The capacity of certain Esch. coli to attach to epithelial cells of mucous membranes may be important for their infective powers in the urinary as well as the intestinal tract. Furthermore, the ability of certain Esch. coli to produce enterotoxins similar to that of V. cholerae is of importance for their capacity to provoke diarrhoea. The importance of the immune defence mechanisms for prevention of these Esch. coli infections is suggested, especially in the form of local immunity provided by secretory IgA antibodies. Such antibodies directed against Esch. coli O and K antigens as well as enterotoxins are present in large amounts in human milk and may be of considerable importance for protection against Esch. coli in the breast-fed baby. Breast feeding may be of special significance until the baby has built up its own local immune defence preventing the micro-organisms from attaching to and invading the intestinal mucous membranes. SIgA antibodies in urine may have a similar protective effect against urinary tract infections. The variable pictures of Esch. coli infections in childhood are striking, ranging from severe sepsis/meningitis or diarrhoea to "asymptomatic" bacteriuria. This variability is obviously closely connected with the presence of various virulence factors and the function of different components of the immune defence.
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PMID:Esch. coli infections in childhood. Significance of bacterial virulence and immune defence. 79 81

There was little dispute that endotoxin treatment of experimental animals could recreate the O2 extraction defect that had been observed in critically ill patients. The remaining question was whether or not this necessarily signified pervasive tissue hypoxia. Some limitation to O2 diffusion in the tissues had been postulated because of known effects of endotoxin that ultimately result in damage to endothelium. We were unable to alter the critical DO2 or 0(2)ER in endotoxic dogs by manipulating the arterial PO2. This tended to rule against there being a diffusion limitation created by the endotoxin as a result of endothelial disruption or microvascular dysfunction. The results of the DCA and dopexamine experiments served to remind us that arterial lactate measurements may or may not indicate widespread tissue hypoxia. Sepsis, as emulated by endotoxin infusions, is also a metabolic disease that can cause inactivation of PDH and thus cause lactacidosis without tissue hypoxia. Regional measurements of lactate flux indicated that gut was hypoxic in spite of DO2 above critical because of maldistribution of blood flow between muscularis and mucosa. The questions persist of how much tissue hypoxia is caused by sepsis or endotoxin when DO2 is supported at supposedly adequate levels and whether there are marked regional differences. Such questions still await answers. Newer technological advances that permit assessment of tissue oxygenation by noninvasive methods, such as near infrared spectrophotometry or nuclear magnetic resonance measurement of tissue energy potential, may soon be feasible in critically ill patients. This kind of information will be of vast importance in designing the most effective therapeutic regimen.
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PMID:Oxygen supply dependency in the critically ill--a continuing conundrum. 128 44

Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma. The metabolic response to injury in burn patients is biphasic wherein the initial ebb phase is followed by a hypermetabolic and catabolic flow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5-6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses. Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients.
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PMID:The metabolic effects of thermal injury. 129 Feb 69

This study examines the possible beneficial effect of Re-LPS (F515) antiserum on experimental multiple system organ failure (MSOF) in rabbits. The results showed that the plasma LPS level was significantly decreased, and it took a shorter period to clear up LPS in experimental than in control rabbits after receiving Re-LPS antiserum. Pretreatment with antiserum can markedly improve the function of the liver, lungs, kidneys, blood and gastrointestinal tract. The MSOF incidence in the group of rabbits receiving immune sera was only 11.2% and the survival rate was raised by about 40.0%. The results suggest that early passive immunotherapy may neutralize gut-derived endotoxin, inhibit endotoxin-induced mediators release and prevent development of severe complications due to sepsis. It is therefore postulated that LPS core antiserum may provide a prophylactic effect on the development of experimental MSOF.
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PMID:Protective effect of Re-LPS antiserum on experimental multiple system organ failure. 129 Dec 1

Gastric acid suppression by use of either antacids or histamine H2-receptor antagonist therapy is the mainstay of stress ulcer prophylaxis. Available evidence indicating an antimicrobial role for gastric acid calls for the reevaluation of gastric acid suppression. A pH of greater than 4.0 leads to bacterial overgrowth and colonization of the upper gastrointestinal tract which has been associated with nosocomial pneumonia, bacterial translocation from the gut, systemic sepsis, and multiple-organ failure. The availability of alternative therapy should discourage the routine use of acid-suppression therapy in the critically ill patient.
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PMID:A new perspective on stress ulcer prophylaxis. 135 68


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