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

The heat sensitivity of the murine jejunum from C3H/HeJ mice and its capacity to develop thermotolerance were measured. Exteriorized loops of murine jejunum were heated in water baths at temperatures of 43-46 degrees C for various times. Animal mortality was used to calculate the median lethal dose by day 7 (LD50/7) in minutes as a function of temperature. The LD50/7 value was independent of the length of the intestinal loop, the presence of serum in the heating medium, prior starvation of animals, and fluid replacement post heating. The time-temperature plot for the LD50/7 values had an exponential slope constant of -0.71 degrees C-1, similar to that for other normal tissues. A heat treatment of 5 minutes at 45 degrees C increased the LD50/7 (total time at 45 degrees C) from 5.9 minutes to 13.0 and 15.6 minutes for 1- and 3-day fractionation intervals, respectively. Death after intestinal heating was associated with septicemia and reached a peak on days 2 and 3 post hyperthermia. Gentamicin (0.1 mg/mouse/day) increased the LD50/7 at 45 degrees C from 5.9 to 9.6; however, septicemia was still noted in dying, gentamicin-treated mice. Additional antibiotics did not further increase the LD50/7. Heat fractionation with gentamicin increased the LD50/7 (total time at 45 degrees C) to 23.0 and 12.5 minutes at 45 degrees C for 1- and 3-day intervals, respectively. These data suggest that thermotolerance plays a significant role in the intestinal heat response, but that the heat damage to intestinal barriers against bacterial septicemia may be superimposed on the cellular damage to the crypt-villus system.
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PMID:Thermotolerance in the murine jejunum. 695 68

Amino acids and dextrose infusion were given for short periods of time to a young man whose basal state is characterized in the previous paper in this series, and their effects were documented in terms of plasma concentrations and splanchnic extraction. The basal state measurements show in the acute trauma state and its subsequent starvation state a largely balanced splanchnic extraction of amino acids but at a decreasing rate. Amino acid (FreAmine) infusion at low rates on this background produced a large increase in extraction of a largely balanced mixture of amino acids but a minimal change in glucose release. The septic state is characterized in both the basal and amino acid infusion state by splanchnic extraction of an unbalanced mixture of amino acids which is deficient in branched-chain amino acids and in relative excess of glucogenic amino acids with increased glucose release and increased utilization of amino acids for gluconeogenesis. In early sepsis this state can largely be repaired by exogenous amino acid infusion but in late sepsis can only be partially repaired. The data suggest that the patient in late sepsis should have a branched-chain rich amino acid mixture and that the hepatic failure of sepsis is strongly associated with peripheral release of an unbalanced mixture of amino acids secondary to enhanced branched-chain catabolism. Infused glucose produces a large increase in the plasma glucose but also improves the balance of the splanchnic amino acids extracted. The statistical validity of the preceding statements are examined in detail in the manuscript.
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PMID:Multiple systems organ failure: II. The effect of infusion of amino acids and glucose. 721 85

Hypoglycemia is but one of a number of causes of hypothermia, but is important to keep in mind as a possible precipitating or concurrent event even in those cases in which there are other obvious explanations for decreased body temperature (exposure, alcoholism, starvation, sepsis or hypothyroidism). Hypoglycemia may occur in as many as 40 percent of very cold patients, and be clinically unrecognized because symptoms are masked by the hypothermia itself. Although serum glucose levels are depressed, a cold-induced renal tubular glycosuria may occur. Glucose in the urine, therefore, cannot be used as assurance of hyperglycemia in a hypothermic patient. And, although cold protects against serious end organ damage from hypoglycemia by decreasing tissue metabolic need for glucose, a serum specimen should be drawn for glucose determination in all hypothermic patients and a 50 percent glucose solution immediately given intravenously. If this is not done, serum glucose levels may plummet as the patient is rewarmed and begins to shiver.
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PMID:Hypoglycemia and accidental hypothermia in an alcoholic population. 723 90

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

The peak time period for the average beef producer to experience the majority of calf losses has consistently been from the time of birth through the first seven days of life. Weakness is a principal clinical sign of diseases or conditions responsible for mortality including birth trauma, prematurity or dysmaturity, congenital malformations, metabolic defects, intrauterine infection, anoxia or hypoxia, hypothermia, starvation, extremes in birth weight, and post-natal infection. This article discusses anoxia/hypoxia and septicemia in greater detail because of their involvement as a common cause of weakness in the newborn calf.
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PMID:Weakness in the newborn calf. 819 20

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


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