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

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

The purpose of this study was to determine the incidence of neonatal mortality in a large, extensively managed mare herd and what risk factors were involved in foal mortality. For a 6 wk period between April 18, 1994, and May 31, 1994, 334 foals were born, of which 74 died before reaching 10 d of age, giving an overall mortality of 22% for this period. Seventy four percent of the foal deaths occurred within 48 h of parturition. The major causes of foal mortality included starvation/exposure 27%, septicemia 26%, and dystocia 20%. Weekly incidences varied significantly, ranging from 67% for week 1 to 14% for week 5 (P < 0.01). Other risk factors that were associated with foal death included failure of passive transfer (P < 0.0001), poor mothering ability (P < 0.0001), the presence of dystocia (P < 0.0001), low birth weight (p < 0.05), lack of rainfall (P < 0.01), and low temperatures (P < 0.1). The effect of sire, mare age, mare body condition, and foal sex were not significant risk factors for foal survival (P > 0.1). Further studies are required to determine if changing management procedures will be effective in reducing the incidence of neonatal foal mortality in this extensively managed herd.
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PMID:Risk factors associated with the incidence of foal mortality in an extensively managed mare herd. 864 Jun 55

"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

An epizootic of disease attributed to infection with Streptobacillus moniliformis occurred in a colony of Swiss white mice. The mortality rate among the 180 breeding females in the 6 affected pens was 100%, and most of the sucking young died from starvation. Acute septicemia, subacute septicemia, and polyarthritis were the 3 forms of disease observed. Clinically, septicemic mice either were found dead or were depressed and hunched for 1-2 days prior to death. About a half of these mice had brown skin crusts overlying the mammae. Pathologic findings in cases of acute septicemia were few; in mice with subacute septicemia, there was acute, multifocal, suppurative, embolic interstitial nephritis, and the arthritic form was characterized by many subcutaneous and periarticular abscesses. Severe, acute, diffuse neutrophilic dermatitis was responsible for the brown skin crusts. The S. moniliformis isolate conformed morphologically and physiologically to classical descriptions of the organism. The infection may have gained entry to the colony via wild rats.
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PMID:Streptobacillus moniliformis infection in Swiss white mice. 874 42

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

The purpose in this paper is to consider the importance of early nutrition for critically ill patients, briefly reviewing the effects of malnutrition, and the metabolic response to starvation and sepsis. Discussion includes assessment of nutritional status and nutritional requirements, with a suggested enteral feeding regime; and also the combined effect of enteral nutrition and glutamine on gut integrity and its relevance to nosocomial pneumonia, and the ability of the gut to accept food during critical illness.
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PMID:Nutrition and its importance to intensive care patients. 884 27

The development of malnutrition is often rapid in critically ill patients with sepsis and severe trauma. In such patients, a wide array of hormonal and nonhormonal mediators are released, inducing complex metabolic changes. Hypermetabolism, associated with protein and fat catabolism, negative nitrogen balance, hyperglycemia, and resistance to insulin, constitute the hallmark of this response. Critically ill patients demonstrate a marked alteration in the adaptation to prolonged starvation: resting metabolic rate and tissue catabolism stay elevated, while ketogenesis remains suppressed. The response to nutrition support is impaired. Substrate use is modified in septic and traumatized patients. Glucose administration during severe aggression does not suppress the enhanced hepatic glucose production and the lipolysis. This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. In addition, the elevated protein catabolism is difficult to abolish, even during aggressive nutrition support. Thus, in patients with prolonged aggression, these alterations produce a progressive loss of body cell mass and foster the development of malnutrition and it dire complications. In this review, the relevant physiologic data and the nutritional implications related to energy metabolism in septic and injured patients are discussed, while potential therapeutic strategies are proposed.
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PMID:Energy metabolism in sepsis and injury. 929 Jan 9

The daily turnover of protein amounts to 280 g in an adult weighing 70 kg but the metabolic processes responsible for protein turnover are only just beginning to be understood. In cells, the major pathway of protein degradation is the ubiquitin-proteasome pathway and protein flux through this pathway is precisely regulated. In catabolic conditions such as uremia, activity of the ubiquitin-proteasome pathway increases, resulting in degradation of muscle protein. In addition to increased protein degradation, gene transcription is activated, resulting in higher levels of the mRNAs encoding ubiquitin and proteasome subunits. The signals activating this pathway include metabolic acidosis and glucocorticoids but must be more diverse since the pathway is also activated in response to starvation, sepsis, cancer, muscle denervation, thermal injury, and acute diabetes. Understanding how the pathway is controlled could lead to the prevention of muscle loss in uremia and other conditions.
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PMID:Cellular mechanisms controlling protein degradation in catabolic states. 938 15

Bacillus thuringiensis is a Gram-positive bacterium, widely used in agriculture as a biological pesticide. The biocidal activity mainly resides in a parasporal protein inclusion body, or crystal. The inclusion is composed of one or more types of delta-endotoxins (Cry and Cyt proteins). Cry proteins are selectively toxic to different species from several invertebrate phyla: arthropods (mainly insects), nematodes, flatworms and protozoa. The mode of action of the insecticidal proteins is still a matter of investigation; generally, the active toxin is supposed to bind specific membrane receptors on the insect midgut brush-border epithelium, leading to intestinal cell lysis and subsequent insect death by starvation or septicemia. The toxin-encoding cry genes have been extensively studied and expressed in a large number of prokaryotic and eukaryotic organisms. The expression of such genes in transgenic plants has provided a powerful alternative for crop protection.
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PMID:Bacillus thuringiensis: from biodiversity to biotechnology. 941 60


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