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

In order to quantitate the effect of sepsis and skeletal trauma on gluconeogenesis, four septic and five skeletal trauma patients were evaluated for their ability to convert 14C-L-alanine to 14C-glucose while receiving 5% dextrose by peripheral vein. In the septic group, the mean glucose pool size increased by 35% and the glucose turnover rate increased by 85% over normal. The alanine conversion averaged 11.1% of the dose. The skeletal trauma group showed a glucose pool size increase of 61%, a 100% increase in glucose turnover rate and a 11.7% conversion of the alanine dose to glucose. The increased conversion of 14C-alanine to 14C-glucose in both sepsis and skeletal trauma in the face of an exogenous glucose infusion indicates an abnormal unsuppressible response. Each of the above parameters when compared to normal values was found to be significant at levels greater than 97.5%. The percentages of the dose expired as 14CO2 in three hours were not significantly different from the normals.
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PMID:Gluconeogenic response during glucose infusions in patients following skeletal trauma or during sepsis. 57 25

Hormonal and substrate profiles and urinary nitrogen and urea excretion were measured in 78 underweight patients admitted for surgical investigation, who were placed into either a normo- or a hyperketonemic group, depending upon their levels of acetoacetate and beta-hydroxybutyrate. The two groups were otherwise similar in terms of weight loss, arm muscle circumference, triceps skinfold thickness, and serum protein levels. Before surgery only one-quarter of them were hyperketonemic displaying mean glucose, insulin, and glucagon levels characteristic of starvation-adaption, and excreted significantly less urinary nitrogen than in normoketonemic group. Those patients who underwent surgery tended to retain their presurgery hormonal and substrate profile. The normoketonemic group excreted significantly greater amounts of urinary nitrogen, depleted body protein to a greater extent as evidenced by larger changes in arm muscle circumference and serum protein levels, and mortality was greater. Interference with insulin-glucagon balance by sepsis and disease is suggested as a possible explanation for the failure of three-quarters of the patients to become starvation-adapted. The implications of this finding on the parenteral feeding of undernourished patients are discussed.
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PMID:Ketosis and nitrogen excretion in undernourished surgical patients. 57 67

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

1. Hepatic carbohydrate metabolism was studied by an intravenous galactose test in control patients, malnourished non-septic patients, patients with prolonged severe sepsis and patients after recovery from sepsis. 2. Blood galactose half-life was not significantly increased in the septic group despite abnormal liver-function tests, whereas it was approximately doubled in the malnourished patients. 3. The rise in blood glucose after galactose injection was less in both the septic and malnourished groups, as compared with that in the control subjects. 4. Fasting blood glucose, lactate and pyruvate concentrations were similar in all groups, whereas blood ketone bodies were increased in the malnourished and septic groups, and blood alanine was decreased only in the septic group. 5. The changes in hepatic metabolism and function were reversible on recovery from sepsis. 6. It is suggested that alterations in hepatic blood flow and the metabolic fate of galactose within the liver may explain the changes in the metabolic response to galactose observed in malnourished or septic patients.
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PMID:Galactose and hepatic metabolism in malnutrition and sepsis in man. 67 28

Insulin glucose therapy can correct hyponatraemia and renal sodium retention in burns, sepsis and circulatory failure. A case of fulminant hepatic failure (F.H.F.) is described in which the same effect was observed. Insulin was thought to have corrected abnormal cell membrane permeability. The actions of insulin are discussed in relation to its possible role in the management of F.H.F.
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PMID:The effects of insulin glucose administration in fulminant hepatic failure. 69 Mar 22

An 85-year-old woman with the diagnosis of diabetic ketoacidosis developed septicemia during hospitalization. Cultures of the patient's blood revealed the presence of Gram-variable coccobacilli, later identified as Corynebacterium aquaticum. The microorganisms grew aerobically on blood agar plates after incubation overnight. The colonies were convex, non-hemolytic and slightly yellow-pigmented. No growth was observed on MacConkey and endo agar plates. The organisms were catalase-positive, oxidase-negative, motile, and oxidized glucose and mannitol. The morphologic and biochemical properties of Corynebacterium aquaticum should be considered for separation from related organisms such as Listeria monocytogenes, Corynebacterium species and oxidative Gram-negative rods that do not grow on MacConkey medium (Flavobacterium spp.).
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PMID:Corynebacterium aquaticum septicemia. Characterization of the microorganisms. 80 59

Long-term parenteral feeding in childhood must be adapted to the requirements of the young organism. The caloric requirements are mainly provided by glucose and fat emulsions; additional calories can be supplied by xylite and, with some reservations, by fructose. For neonates and young infants the combination and quantity of amino-acids is of particular importance: histidine, arginine, proline and tyrosine are essential amino-acids; glycine, glutamic acid, aspartic acid and cystine should form part of the unspecific sources of nitrogen. Addition of trace elements and vitamins is obligatory in long-term parenteral feeding. Complications may arise at the site of the catheter (sepsis, clotting). Late damage due to intravenous feeding is known to occurs; but a more detailed knowledge needs long-term investigations.
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PMID:[Problems of long-term parenteral feeding in childhood (author's transl)]. 82 14

Forty patients with a mean age of 56 yrs, all of whom required hemodialysis therapy, for mean of 32 days, were treated with a minimum of 2000 kilocalories of I.V. glucose, potassium orthophosphate with mulit-vitamins and 25 Gm of I.V. albumin. Patients were initially dialyzed daily and then every other day or 3 times/wk. Complications including pneumonia, GI bleeding, gram negative septicemia, shock, the need for tracheostomy and ventialtory assist were high. Overall survival rate was 33%. This survival rate we beleive to be high considering the complicated type of illness these patients had as well as our clinical experience prior to the use of total parenteral nutrition in the manner described in this report. Essential L-amino acids were not used based on our experience in 3 patients with hepatic and renal failure who developed worsening neurological findings with the use of this substance. We believe further that I.V. glucose and albumin may be preferred mode of hyperalimentation.
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PMID:Total parenteral nutrition in acute renal failure. 82 19

The application of parenteral nutrition in patients in intensive care units can be limited by shock, septicemia and metabolic disorders. Stress- or trauma-induced glucose intolerance sometimes makes it difficult to maintain the caloric requirements with glucose. Sugar substitutes seem to be of advantage in these cases. Meticulous care is essential to avoid severe complications arising from the use of the central venous feeding catheters.
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PMID:[Problems with hyperalimentation in intensive care units (author's transl)]. 82 90

Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
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PMID:Lactic acidosis. 87 61


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