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

Previously asymptomatic aneurysms in ten patients ruptured within 36 days (mean, ten days) of a prior laparotomy. The laparotomy and associated intra-abdominal disease may have precipitated rupture of the unresected abdominal aneurysms by reduction of the collagen content of the aneurysm wall, thus making the wall weaker. The scar-like collagen fibers of an aneurysm wall provide the strength that permits the wall to resist rupture. There is a dynamic equilibrium between synthesis and lysis of this collagen. Lysis of collagen is enhanced by injury, such as laparotomy, and by nutritional depletion and local inflammation. Collagen lysis is greatest in the area adjacent to the injury, but also occurs at remote sites as well. Lysis is greatest during the first postoperative week, after which, in the absence of sepsis or starvation, synthesis exceeds lysis and the equilibrium is restored. A thin aneurysm wall may be weakened enough during this period of negative collagen balance to allow rupture.
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PMID:Laparotomy as a precipitating factor in the rupture of intra-abdominal aneurysms. 735 84

Critical illness is characterized by the presence of several factors that can cause marked alterations in the structure and function of multiple organ systems (1-2). These factors include injury, ischemia, sepsis, and starvation (Fig. 1). It is common for more than one of these problems to be present in the individual patient. Our current understanding of the effect of these various factors on intestinal structure and function has increased markedly during the past decade (3). Furthermore, the patterns of intestinal dysfunction that occur in response to these conditions have also been better characterized. Although malabsorption and motility disorders have long been recognized as clinical problems, more recently loss of intestinal barrier function and immune dysfunction have gained attention. This improved understanding of the response of the intestine to critical illness may lead to prevention of intestinal failure or permit more specific therapy when it occurs. The goals of this manuscript are to describe the response of the small intestine to critical illness and to identify potential therapeutic strategies for preventing and treating intestinal failure in this setting.
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PMID:The intestinal response to critical illness. 784 84

Sepsis, shock, multiple trauma, and burns are often associated with altered metabolism characterized by severe catabolism, wasting of the lean body mass, immune dysfunction, and compromised wound healing. Nutrition support is one of the mainstays in the management of these critically ill patients and is aimed at minimizing these complications. The purpose of this article is to compare stress hypermetabolism and starvation metabolism, to review current recommendations for the provision of energy and substrate to the critically ill patient, and to review pertinent literature regarding enteral vs parenteral nutrition. Finally, this article will provide a brief overview of new and future therapies with emphasis on specific substrates and growth factors and the potential for their use in the critically ill patient.
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PMID:Nutrition support in critical illness. 807 50

Dichloroacetate has been shown to have therapeutic effects on sepsis and endotoxin shock and to reduce liver damage in rats intoxicated with ethanol or carbon tetrachloride. In this study, the effect of dichloroacetate on endotoxin hepatitis was investigated. Endotoxin hepatitis was induced by an intraperitoneal coadministration of 50 micrograms/kg lipopolysaccharide from Escherichia coli, and 200 mg/kg D-galactosamine in starved, male Wistar rats. This treatment induced the following changes within 24 hr: an increase in the serum aminotransferase activity, histological alterations of the liver including focal necrosis of liver cells and inflammatory infiltrates, an increase in blood pyruvate and alanine concentrations, and inhibition of starvation ketosis. The intraperitoneal administration of 250 mg/kg dichloroacetate 30 min after the administration of the toxins partially counteracted all of these changes. The administration of dichloroacetate might be useful in coping with hepatic damage as well as lacticemia and cardiovascular depression induced by endotoxins.
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PMID:The limiting effect of dichloroacetate on endotoxin-induced liver damage in starved rats. 814 37

Patients with advanced cancer and cachexia typically demonstrate modestly increased rates of energy expenditure in the presence of diminished food intake due to anorexia and to gastrointestinal disturbances. Rates of glucose production by the liver, gluconeogenesis and glycolysis to lactate (Cori cycle) are increased, fat mobilisation and oxidation are accelerated. There is a redistribution of body proteins away from muscle towards visceral proteins, resulting in marked muscle protein loss. Cancer cachexia differs from simple starvation and demonstrates metabolic similarities to sepsis or polytrauma. The metabolic response in the patient with cancer is largely due to mediators released by the tumour or by the host; recently the role of cytokines such as tumour necrosis factor alpha (TNF alpha), interleukin-1 (IL-1) and -6 (IL-6) and interferon gamma (INF gamma) has been emphasized. Catabolic hormones such as glucocorticoids and adrenaline have also been implicated. Cytokines have the potential to reproduce experimentally the clinical syndrome of cancer cachexia. There is evidence of increased production of several of them in certain types of cancer. There are overlapping activities of the cytokines TNF alpha, IL-1, IFN gamma and IL-6. The contribution of each of them to cancer cachexia remains unclear. Inhibition of cytokine activity using specific antibodies in cancer-bearing experimental animals demonstrated partial prevention of cachexia. A positive feedback between macrophage-derived IL-1 and tumour-derived IL-6 has been demonstrated recently in experimental cancer cachexia. Cytokines may support tumour growth by acting as growth factors.
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PMID:Pathophysiology of cancer cachexia. 815 43

Three hundred patients undergoing major general surgical procedures were randomized by means of a computer-assisted algorithm to receive either total parenteral nutrition (TPN) from the first postoperative day or only prolonged glucose administration (250-300 g/day) up to 15 days after operation. All patients receiving TPN were treated individually based on daily measurements of energy and nitrogen balances. The treatment goal was to keep the patients in positive energy balance (+20%) and close to nitrogen balance. The effects of the two "nutrition regimens" on outcome such as mortality rate, complications, the need of additional medical support and patient-related functional disabilities were investigated. No selection of patients was made, that is, malnourished patients were also randomized. There were no differences among TPN versus glucose treatment when results were analyzed according to intent to treat. Approximately 60% of all patients were able to start eating within 8 to 9 days after operation. No differences were observed between such patients regardless of being treated with TPN or glucose only. Patients on glucose treatment during 14 days had a significantly higher mortality rate (p < 0.05) than patients on either continuous and uncomplicated TPN treatment or short-term glucose treatment. Similar results for mortality rates also were seen with regard to severe complications (cardiopulmonary problems, sepsis, and wound-healing insufficiencies), functional disturbances, the need of additional medical support, and abnormalities in nutritional state. Twenty per cent of the patients randomized to TPN treatment showed a statistical trend (p < 0.10) toward a higher mortality rate (36%) compared with patients randomized to prolonged glucose treatment (21% mortality rate). These patients could not be identified by evaluation of preoperative factors. Thus, the overall evaluation of the results makes it likely that a fraction of high-risk patients (approximately 20%) were not doing well on immediate postoperative intravenous feeding, and it is possible that TPN to such patients accentuated their morbidity rate. Although patients (20%) on prolonged semi-starvation (14 days glucose treatment) had increased mortality rate and severe complications, it was possible that undernutrition induced a slightly different complication scenario than induced by TPN in the high-risk patients. The results demonstrate that in most surgical patients (60%), postoperative semi-starvation is not a limiting factor for outcome. In remaining 40%, inadequate nutrition was associated with both increased morbidity and mortality rates. In this sense, inadequate nutrition represents both too much and too little, whereas overfeeding seemed to be a larger problem than underfeeding.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of postoperative intravenous feeding (TPN) on outcome following major surgery evaluated in a randomized study. 843 16

The learning curve of nutritional support in the critically ill began with the amelioration of the effects of starvation in patients with a disabled intestine. Next, there was an appreciation that feeding formulas could be tailored to support patients with specific organ insufficiencies. Then it was realized that feeding enterally has distinct advantages over feeding parenterally. In addition to a decrease in catheter-related sepsis, there was noted a distinct decrease in "remote site" sepsis. In fact, good scientific reasons have been identified to explain why this occurs, such as maintaining the competency of the intestine against a translocation of endotoxin and bacteria and "turn-on" of the stress response. Further, we now know that specific nutrients can produce desirable pharmacologic effects. In the future, feeding formulae will be devised that continue to modify the patient's response to illness favorably. Another important consideration is to begin nutritional support as soon as possible--i.e., on the day of admission, if appropriate. The critical care specialist should be expert in these techniques, with the goal of eliminating malnutrition as a confounding variable in the clinical course of the intensive care unit patient.
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PMID:Metabolic and nutritional support of the intensive care patient. Ascending the learning curve. 849 Jul 67

The relation between weight loss and the risks of major surgery have been investigated for more than 50 years. It can now be said, with some confidence, that the underweight patient has an increased risk of complications following major surgery. This understanding, however, is based on methods of nutritional assessment that are of limited relevance to hospitalized patients whose malnutrition might be due to sepsis, neoplasia, trauma, or starvation. A consequence is the widespread belief that protein-energy malnutrition (PEM) has been overemphasized as a surgical risk factor, and that the many nonnutritional risk factors ought to be implicated more often. An argument is made for a fresh approach to nutritional assessment in order to better identify the individual patient who, by virtue of PEM, stands an increased risk of a complicated postoperative course. It is suggested that an evaluation of the impact PEM has on vital physiologic function provides a clinically relevant defect to identify and treat and a means of monitoring response to nutritional intervention.
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PMID:Underweight patients and the risks of major surgery. 851 9

"Septic autocannabalism" been coined to describe the metabolic response that follows severe sepsis in humans. The normal protein- and energy-conserving mechanisms evoked during simple starvation are not observed following the onset of sepsis. The metabolic response to sepsis entails rapid breakdown of the body's reserves of protein, carbohydrate, and fat. Hyperglycemia with insulin resistance, profound negative nitrogen balance, and diversion of protein from skeletal muscle to splanchnic tissues are prominent features. These responses are believed to be mediated in large part by inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha), interleukin 1beta (IL-1beta), and IL-6. Secondary induction of catecholamines, cortisol, and glucagon by cytokines is likely to be another important effector mechanism. Infection and inflammation elicit a complex network of interwoven responses, and no single mediator alone accounts for the responses observed. Sepsis also commonly involves alterations in cardiovascular function with altered flow to key metabolic sites, hypoxia, damage to the gut's mucosal barrier, secondary organ failure, and alterations in capillary permeability. These structural and functional alterations also strongly influence the metabolic profile during infection. If these catabolic responses persist for more than a few days, severe malnutrition results and is likely to be an important risk factor for mortality in these patients. The altered metabolic milieu during sepsis prevents effective use of exogeneously delivered glucose and protein; at best, administration of these agents ameliorates but does not prevent the persistence of catabolism. Delivery of agents that antagonize cytokines and other moieties such as glutamine and growth hormone may, in the future, help to restore nitrogen balance during sepsis.
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PMID:Metabolism of sepsis and multiple organ failure. 866 35

The medical records of 74 neonates dependent on parenteral nutrition for at least 21 days after emergency abdominal surgery (performed between 1988 and 1992) were reviewed respectively. The role of enteral starvation, prematurity, composition and duration of parenteral nutrition, and sepsis in the evolution of parenteral nutrition-related cholestasis was evaluated by multiple regression analysis. The most important factors for cholestasis were low gestational age (median, 34 weeks), early exposure to parenteral nutrition, and sepsis. Episodes of sepsis were associated with a 30% increase in the bilirubin level. Enteral starvation and composition and the duration of parenteral nutrition solutions did not correlate significantly with the development of cholestasis. Prevention of sepsis should be the priority in minimising cholestasis in postsurgical neonates who are dependent on parenteral nutrition.
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PMID:Parenteral nutrition-related cholestasis in postsurgical neonates: multivariate analysis of risk factors. 880 24


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