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

In the critically ill surgical patient a variety of therapeutic maneuvers is required to maintain a "healthy gut." Provision of adequate amounts of glutamine to the gastrointestinal mucosa appears to be just one of these maneuvers. Other methods utilized to protect the gut from becoming a wound include: (a) minimizing additional systemic insults (such as hypotension, sepsis, multiple operative procedures); (b) aggressive pulmonary care; (c) the judicious use of antibiotics; and (d) aggressive enteral or parenteral feedings. The concept that the gut is an organ of quiescence following surgical stress merits reconsideration. The intestinal tract plays a central role in interorgan glutamine metabolism and is a key regulator of nitrogen handling following surgical stress. Critically ill patients are susceptible to developing gut-origin sepsis, the incidence of which will be diminished by instituting measures and providing treatments which support intestinal structure, function, and metabolism. Provision of glutamine-enriched diets to such patients may be one of these therapies.
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PMID:The role of glutamine in maintaining a healthy gut and supporting the metabolic response to injury and infection. 218 15

There is accumulating evidence that multiple organ failure is not always the result of an established septic focus. Increasing attention has centred on the gut as a reservoir of bacteria (and bacterial endotoxins) that can traverse the intestinal mucosal barrier (a process called 'bacterial translocation') and initiate the septic state. Although the link between haemorrhagic shock and sepsis was recognized decades ago, the full experimental demonstration of this phenomenon is more recent. It was shown to occur in three main settings: physical disruption of the gut mucosa, impaired defence mechanisms and altered gut microbial ecology. Conditions such as haemorrhagic shock, burns, protein malnutrition and sepsis are seen in the severely ill surgical patient or the multiply injured, and are known to cause various combinations of circumstances favourable to bacterial translocation and endotoxin absorption. These may play an important role in the mortality of the critically ill.
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PMID:Gut barrier function and the surgeon. 219 47

Tumor necrosis factor (TNF), a polypeptide produced predominantly by activated macrophages, is an important mediator of sepsis. We analyzed the specific metabolic changes that occur in the gut following TNF administration. Following general anesthesia, hemodynamic and metabolic indices were measured serially in control dogs (n = 7) and animals receiving a continuous sublethal intravenous infusion of TNF (0.57.10(5) IU/kg/6 hours, n = 7). During TNF infusion mean arterial pressure gradually decreased despite fluid administration, which maintained wedge pressure and cardiac index, which were similar to control animals. While TNF significantly reduced intestinal blood flow to 12 +/- 3 mL/min/kg compared to 28 +/- 3 mL/min/kg (p less than 0.01) in controls, intestinal oxygen consumption was maintained due to an increased extraction rate. Despite hypoperfusion the intestinal exchange of metabolic substrate (glucose, lactate, pyruvate, alanine, glutamine, glutamate, and ammonia) was comparable between the control and TNF-infused animals. However, when substrate carbon balance across the intestinal tract was calculated, it appeared that there was a limitation in fuel availability in the TNF animals. This may be due to competition for fuel between the gut and other major organs. Fuel limitation may jeopardize rapid cell proliferation and mucosal repair and with regional hypoperfusion these processes may account for the mucosal ulcerations observed at the termination of the study.
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PMID:The effects of tumor necrosis factor on intestinal structure and metabolism. 225 57

Eight neutropenic patients with acute lymphocytic or nonlymphocytic leukemia had septicemia due to different strains of Streptococcus mitis (St. mitis), a microorganism not commonly recognized as a special pathogen in leukemic patients. Four of the patients had been treated with high-dose cytosine arabinoside as part of the cytostatic regimen, six had a central venous line and four patients had oral lesions prior to the infection. Selective gut decontamination consisted of co-trimoxazole/colistin in five patients and quinolones in three patients. The first three patients died, either due to interstitial pneumonia with the adult respiratory distress syndrome (ARDS), or due to infection-triggered disseminated intravascular coagulation despite prompt empiric antibiotic therapy including vancomycin. The other patients improved after empiric supplementation of penicillin G (30 Mega/day) to the antibiotic regimen. Beginning ARDS in two of these patients dramatically responded to high-dose steroids. We conclude that St. mitis is a major pathogen in neutropenic leukemic patients. Infection appears to occur independently of acute leukemic cell type, regimen of selective gut decontamination, venous access, visible oral lesions or treatment with high-dose cytosine arabinoside. The clinical course of our patients raises questions about the value of commonly recommended empiric antibiotic regimens, which were clearly ineffective to control infections with St. mitis in this patient group. Our data indicate that immediate antibiotic therapy with penicillin G is indicated and may be life-saving for suspected St. mitis infections in neutropenic leukemic patients.
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PMID:Septicemia due to Streptococcus mitis in neutropenic patients with acute leukemia. 229 85

Epidemiologic data suggest that elderly adults are more susceptible to invasive bacterial infection by indigenous gut flora than are younger adults. The purpose of this investigation was to characterize a murine model of clinically encountered peritonitis in the aged. We subjected three different age groups (young, 16 weeks; mature, 12 months; senescent, 24 months) of C57BL/6NNia mice to surgically induced peritonitis by the cecal ligation and puncture procedure. Senescent mice died in a significantly shorter time following surgery than mature mice (median time to death, 24.4 versus 38.5 h, respectively; P less than or equal to 0.001). Blood, liver, spleen and occasionally, ceca were obtained at 2 and 12 h after the cecal ligation and puncture procedure and immediately following death, to characterize the bacterial kinetics of the model. Qualitative and quantitative aerobic, anaerobic, and coliform cultures were performed. No age-related differences were found in the types of bacteria isolated throughout the time course of progressive sepsis. In mice in the mature and senescent age groups, at 2 and 12 h postsurgery, gram-negative anaerobes and gram-positive aerobes predominated in all tissues that were cultured. At the time of death, however, blood and tissue isolates consisted predominantly of coliform bacteria. The shift from mixed infection during sepsis to predominantly gram-negative bacterial infection reflected a similar progressive shift in bacterial types found in the cecum. At death, senescent mice had 100-fold fewer coliform bacteria in the bloodstream than those found in mature mice (2.5 x 10(9) versus 4.6 x 10(11), respectively). The increased sensitivity of aged mice to invasive bacterial infection documented in this series of experiments accords well with human epidemiologic experience and demonstrates the appropriateness of the model for continued investigations of sepsis in the aged.
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PMID:Mortality and bacteriology of sepsis following cecal ligation and puncture in aged mice. 230 15

Mesenteric venous thrombosis is a clinical entity, which is rarely recognized on admission. The patients are admitted with vague abdominal complaints and, eventually, abdominal sepsis might occur requiring laparotomy. Nowadays, underlying hypercoagulable states such as antithrombin-III, protein-C and protein-S deficiencies are recognized more frequently as a distinct cause of mesenteric venous thrombosis. In this paper, a case of mesenteric venous thrombosis due to protein-C deficiency is presented. The patients generally have a history of thromboembolism of the deep veins of the legs at young age. The combination of vague abdominal complaints and a history of thrombosis of the deep veins of the legs should arouse the suspicion of mesenteric venous thrombosis. In these cases, contrast-enhanced computerized tomography is a non-invasive diagnostic means which may provide the diagnosis. If infarction of the gut is present, resection is mandatory and a second-look operation should be performed. After surgery, heparinization is essential. This must be followed by administration of oral anticoagulants for an indefinite period in case of an underlying antithrombin III, protein-C or protein-S deficiency.
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PMID:Mesenteric venous thrombosis caused by deficiency of physiologic anti-coagulants: report of a case. 232 Feb 74

Previous studies describing the histologic elements of multi-system organ failure caused by bacterial sepsis may have been complicated by a significant interaction on tissue injury from either a preterminal low-flow state or the effects of therapy immediately before death. Therefore we evaluated the nonpulmonary histologic findings of sepsis during a 3-day period that followed cecal ligation and perforation. In this septic model, mean arterial perfusion pressures remained unchanged from baseline, systemic flows rose by 54%, and laboratory evidence of organ dysfunction including an elevation of the serum bilirubin levels and a depression of the serum total protein values was considered mild. Concurrently, development of the hyperdynamic central circulatory septic state was associated with widespread histologic changes in myocardium, striated muscle, liver, gut, and pancreas. Lesions common to these organs included high-protein interstitial and intracellular edema, mitochondrial destruction, and patchy cell necrosis. Lesions within the pancreas were exaggerated over those noted in other organs. Of all organs examined, only the liver demonstrated microvascular neutrophil accumulation. Unlike models of shock caused by sepsis, fibrin thrombi were not seen in the microvasculature of any organ. We conclude that tissue injury characterized by the accumulation of protein-rich extravascular fluid and the development of reversible and irreversible cell injury antedated significant multiple-system organ failure in this animal model of normotensive sepsis.
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PMID:Histologic and ultrastructural changes in nonpulmonary organs during early hyperdynamic sepsis. 232 Nov 37

The effects of sepsis on gut glutamine (GLN) metabolism were studied to gain further insight into the regulation of the altered glutamine metabolism that characterizes critical illnesses. Studies were done in laboratory rats and in hospitalized patients. The human studies were done in seven healthy surgical patients (controls) and six septic patients who underwent laparotomy. Radial artery and portal vein samples were obtained during operation and were analyzed for GLN and oxygen content. Despite no reduction in arterial glutamine concentration in the septic patients, gut glutamine extraction was diminished by 75% (12.0% +/- 1.6% in controls vs. 2.8% +/- 0.8% in septic patients, p less than 0.01). Similarly gut oxygen extraction was diminished by nearly 50% in the septic patients (p less than 0.05). To further investigate these abnormalities, endotoxin (10 mg/kg intraperitoneally) or saline (controls) was administered to adult rats 12 hours before cannulation of the carotid artery and portal vein. The arterial GLN concentration was increased by 13% in the endotoxin-treated animals (p less than 0.05) but gut glutamine uptake was diminished by 46% (526 +/- 82 nmol/100 g BW/minute in controls vs. 282 +/- 45 in endotoxin, p less than 0.01). Simultaneously gut glutaminase activity was diminished by 30% (p less than 0.01) and intestinal glutamate release fell by two thirds. Blood cultures were negative in control animals (0 of 20), but were positive in 25% of endotoxemic animals (6 of 24) for gram-negative rods (p = 0.019). Sepsis and endotoxemia impair gut glutamine metabolism. This impairment may be etiologic in the breakdown of the gut mucosal barrier and in the development of bacterial translocation.
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PMID:The effects of sepsis and endotoxemia on gut glutamine metabolism. 185 26

Yeasts may gain entry into the blood via routes such as intubation, intravenous catheterization or by direct persorption from the gut. The latter route becomes important when the numbers of commensal yeasts in the gut exceeds a threshold which may vary between animal species. In a prospective study utilizing serial, twice weekly quantitative stool cultures during the first 6 weeks of life of 40 very low birth weight infants, we found a threshold of 8 x 10(6) Candida colony-forming units/gram of stool. Beyond this threshold 50% of the infants developed gastrointestinal symptoms and 28.5% developed systemic sepsis within 1 to 3 weeks of heavy colonization. The gastrointestinal colonization rate was 62.5% (25/40) with 66% having Candida colony-forming units greater than 8 x 10(6)/g stool.
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PMID:Gastrointestinal colonization with yeast species and Candida septicemia in very low birth weight infants. 234 16

Solid organ transplant recipients can experience serious disease and death from infection due to the parasitic roundworm Strongyloides stercoralis. This parasite lives in soil contaminated with human feces. Domestic dogs and cats may be another reservoir. Larvae can penetrate the skin, are carried hematogenously to the lungs, migrate up the bronchial tree, and then can be passed to the upper small intestine. Autoinfection occurs in the setting of immunosuppression when invasive larvae penetrate the gut wall and cause disseminated infection. Polymicrobial sepsis is sometimes seen due to enteric organisms adhering to the parasite. Transplant recipients are at highest risk during the first 3 months posttransplant. Many organ systems may be affected. Pulmonary symptoms include cough, wheezing, sputum production, dyspnea, hemoptysis, tachypneas, and pleuritic pain. Hyperinfection, an augmentation of the normal skin-lung-intestine life cycle, occurs in roughly two-thirds of infected transplant recipients, with dissemination in the remainder. Diagnosis is made primarily by examination of the stool or intestinal secretions for ova and parasites. Occasionally, parasites are noted in the sputum. New serologic tests show promise. The parasite may remain in the host for over 25 years before immunosuppression causes either dissemination or hyperinfection. Thiabendazole given for 3 to 7 days is the treatment of choice for organ transplant recipients. Repeat courses may be needed to eradicate infection.
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PMID:Strongyloides infections in transplant recipients. 234 6


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