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

The effect of major trauma and sepsis on skeletal muscle, central tissue and whole body nitrogen (N) metabolism was investigated in 5 patients before and during TPN (30 kcal, 0.30 g N kg-1 day-1). Fasting 3-methylhistidine (MEH) urinary excretion was elevated (407.9 +/- 67.6 mumol m-2 day-1), muscle and body N balances (NB) were markedly negative (-28.2 +/- 4.6 g m-2 day-1 and -15.7 +/- 3.1 g m-2 day-1), while central tissue NB was positive (13.0 +/- 2.4 g m-2 day-1). TPN effected a reduction in MEH excretion (261.8 +/- 27.5 mmol m-2 day-1 - p less than 0.05) and decreased the release of almost all amino acids from muscle tissue, some of them acting as catabolic markers. Muscle (-7.2 +/- 1.2 g m-2 day-1 - p less than 0.01) as well as body NB (-4.8 +/- 1.4 g m-2 day-1 - p less than 0.01) improved, whilst central tissue NB worsened, even though still positive (3.1 +/- 1.6 g m-2 day-1 - p less than 0.05). Gathering fasting and TPN data MEH excretion was significantly related to both body (r = 0.89) and muscle (r = 0.73) NB, that were highly related to each other (r = 0.93), being muscle always worse than body NB. In conclusion, the anticatabolic activity of TPN is confirmed, although our setting did not achieve muscle NB, it was consistently improved and seems to be the major determinant of body NB, in contrast central NB and central N utilization (46.4% +/- 5.4 vs 15.8% +/- 8.4 - p less than 0.05) worsened.
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PMID:Peripheral, visceral and body nitrogen balance of catabolic patients, without and with parenteral nutrition. 313 91

Gut malnutrition in patients with persistent hypermetabolism is hypothesized to be an important factor in postseptic multiple organ failure syndrome (MOFS). The hypothesis was made that enteral nutrition (EN) started at the onset of hypermetabolism could reduce the incidence of MOFS. Sixty-six patients with persistent hypermetabolism 4 to 6 days after onset of sepsis were prospectively randomized to receive either parenteral nutrition (PN) or enteral nutrition (EN) at 1.5 gm protein/kg/day and 30 nonprotein calories/kg/day; the EN and TPN were of the same composition. There was no reduction in either the incidence of MOFS or mortality attributable to the route of nutrition administration. The PN group tended to have better visceral protein support; the EN group had more gut complications. When analyzed, the type of formula given did have an effect on the nutritional outcome but not on the mortality rate. A formula with a nonprotein-calorie-to-nitrogen ratio of 100:1 was associated with more nitrogen retention, higher levels of visceral proteins, and better gut tolerance. The route of nutrition administration does not seem to affect the incidence of postseptic MOFS or mortality when hypermetabolism is already present and when commercially available nutritional formulas are used. The relationships among the route of nutrition, the type of enteral formula, and the disease process of hypermetabolism and MOFS appear to be complex and require much more investigation before the role of the gut and enteral nutrition can be defined.
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PMID:Enteral nutrition does not prevent multiple organ failure syndrome (MOFS) after sepsis. 314 Apr 3

Fat metabolism is a complex mechanism involving energy production as well as various physiological and biochemical effects involved in a large spectrum of both normal and pathological phenomena. Many different paths are currently being investigated by different medical and basic science disciplines. These include lipoproteins, prostaglandins, leukotrienes, and more. This chapter is limited to the energy related facets of fat metabolism, though in the future interrelations may be found between the different fields of fat research and serve not only for better understanding of the human organism, but also better treatment in hypermetabolic states. Much has been learned about fat metabolism both in normal and stressed man. The finding that, in most hypermetabolic states, fat is being oxidized and used as the main caloric source is definitely a cornerstone in improving nutritional therapy in such cases. The development of safe fat solutions, together with the studies showing that exogenous fat is efficiently utilized, has led to increased use of fat in TPN regimens as well as in enteral nutrition. The possibility of tilting the energy source in nutritional therapy from a 50:50 ratio of carbohydrates:fat to a fat-dominant regimen in the steady flow state (thus approaching the actual metabolic preference in stress) requires further studies and may prove to be beneficial. On the other hand, an increasing number of observations show that in late severe stress states--the so-called multi-organ failure syndrome--significant alterations in fat metabolism occur both in liver and in muscle. Recognizing the situations in which fat oxidation is decreased, leading to liver failure with fat accumulation, necessitates a different mode of treatment. Providing glucose or amino acids, and possibly more BCAA, is one method of treatment to be pursued. On the other hand, the prospect of new fat solutions containing medium chain triglycerides, may lead to improved nutritional support and decreased complications in these extreme situations. Other treatment modalities, like carnitine, need further research as well. Furthermore, if and when the relationship between fatty acids used in nutritional support and the various mediators involved in trauma and sepsis can be elucidated, better treatment of critically ill patients may be possible and offered in a more comprehensive way.
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PMID:Fat metabolism in injury and stress. 314 11

One hundred twenty-five infants underwent surgical intervention for necrotizing enterocolitis between 1972 and 1984. Sixty-three infants, who survived more than 30 days postoperatively, were evaluated for long-term complications. There were 28 girls and 35 boys (mean birth weight 1,725 +/- 890 g; gestational age 32 +/- 4 weeks). Associated problems included hyaline membrane disease (43), cardiac anomalies (25), and trisomy 21(2). Thirty-six survivors required long-term ventilatory support. Fifty-nine infants underwent bowel resection and enterostomy, 3 decompressing enterostomies without resection, and 1, exploratory laparotomy only. Enterostomies were closed at four months. Twenty four had short bowel syndrome. Fifteen infants subsequently died for a late mortality rate of 23%. Mortality was related to sepsis (3), respiratory failure (5), cardiac anomalies (3), cardio-respiratory arrest (2), and TPN related liver failure (2), and was common with gestational age less than 31 weeks and birth weight less than 1,000 g. Medical problems included cholestasis (17), TPN induced cirrhosis (3), meningitis (3), seizures (8), and nutritional rickets (6). Significant developmental and intellectual delays were observed.
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PMID:Long-term follow-up after surgical management of necrotizing enterocolitis: sixty-three cases. 372 6

The effect of lipid addition to TPN (Total Parenteral Nutrition) solutions on microbial growth was investigated. Staphylococcus epidermidis, which failed to grow or grew poorly in the absence of lipid, reached greater than 10(4) cfu/ml (colony forming units per ml), from an initial inoculum of approximately 50 cfu/ml after 24 h when lipid was added. Candida albicans grew more slowly in the presence of lipid, but nevertheless reached 10(4) cfu/ml after 40 h incubation. Klebsiella aerogenes grew readily in all solutions, whereas Escherichia coli failed to grow in any solution. Growth of S. epidermidis and K. aerogenes was improved when the inoculum consisted of starved cells; however, growth of starved cells of C. albicans lagged behind that of unstarved cells. The ability of S. epidermidis to grow in lipid-containing TPN mixtures is particularly important, since this organism is frequently associated with sepsis. In an infant surgical unit, where TPN is under the care of a nutrition team, samples of TPN fluids and giving sets were examined for microbiological contamination at the end of the 24 h administration period. Contamination was found in eight of the 98 systems examined from eight patients. The organisms were identified as coagulase-negative staphylococci and diphtheroids.
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PMID:Growth of microorganisms in total parenteral nutrition mixtures and related clinical observations. 392 44

TPN-associated cholestasis (TPNAC) is a common problem in neonatal surgical patients. Of the 222 infants admitted to the neonatal surgical intensive care unit between January 1982 and June 1983, 46 patients received parenteral nutrition for over 14 days. Cholestasis occurred in 16 of these patients (35%), while 30 patients remained jaundice-free. Clinical characteristics associated with the development of TPNAC, included primary diagnosis, low birth weight, duration of TPN administration, the interval before enteral feeding was initiated, sepsis, central venous catheter infection, and the number of operative procedures. Factors which did not appear significant in the development of conjugated hyperbilirubinemia were prematurity, sex, gestational age, average daily weight gain, and the specific components of the nutritional intake. Mortality was high in the children with cholestasis (31%) as compared to the "normal" neonates (3%) and two of the five deaths were directly related to progressive hepatic dysfunction. This report confirms the high incidence of TPNAC in the newborn surgical population and discusses the critical risk factors associated with development of the syndrome.
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PMID:TPN-associated hyperbilirubinemia: a common problem in newborn surgical patients. 393 Jun 93

Despite the fact that the clinical experience with TPN has been gathered from patients of all age groups suffering from a variety of underlying diseases running very different clinical courses and often complicated by a number of septic metabolic and therapeutic problems, certain points can be made with regard to predisposing factors. 1) Prematures and neonates are particularly at risk. 2) Cholestasis occurs earlier and has a greater chance of leading to chronic liver disease in surgical patients. 3) Hepatobiliary abnormalities are more likely to develop after a prolonged period of TPN and are less frequent in patients who are also receiving oral feedings. Definition of the mechanism of hepatobiliary complications remains a problem. Although calcium bilirubinate appears to be responsible for sludge and stones, there is as yet no explanation for the presence of large amounts of indirect-reacting bilirubin in gallbladder and hepatic bile in patients on TPN. The pathogenesis of cholestatic liver disease remains an enigma; the lack of normal gastrointestinal stimuli for bile formation, abnormalities of bile acid metabolism, and sepsis might play roles, but attention has recently been attracted to amino acid toxicity and this possibility deserves further study.
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PMID:Hepatobiliary complications associated with TPN: an enigma. 393 7

The effect of sepsis in modifying post-surgical fuel utilization in critically ill patients was determined from 374 observations (246 septic [S] and 128 nonseptic [N] in 12 intubated ICU patients studied serially. Patients received TPN (values/24 hrs: Septic, N2, 9.1 +/- 2.2 gm; glucose, 543 +/- 211 kcal/m2, Nonseptic, N2, 8.3 +/- 3.6 gm; glucose, 550 +/- 346 kcal/m2). In some periods, intravenous lipid (L) was given to raise total caloric intake to 826 +/- 223 kcal/ 24 hr/m2. The VO2, VCO2, respiratory rate, minute volume, and blood gas levels were measured, and respiratory quotient (RQ) and metabolic rate (MR) computed. Statistics were performed by 2-way ANOVA and analysis of covariance. Without lipid, mean VCO2 for S (126 ml/min/m2) and N (128 ml/min/m2) were not significantly different, but VO2 in S (146 ml/min/m2) and N (132 ml/min/m2), and the RQ values S (0.88) and N (0.97), were different (p less than 0.0001). In 360 studies RQ was shown to be increased by the total caloric intake, but reduced in the presence of sepsis: RQ = 0.00014 (kcal/m2) - 0.09 (sepsis effect + 0.878 N = 360; r2 = 0.304; F2,357 = 78; p less than 0.0001; but both administered glucose and lipid calories contribute to the RQ in sepsis: RQ = 0.00017 (glucose kcal/m2) + 0.266 X 10(-3) (lipid kcal/m2) + 0.732 n = 114; r2 = 0.260; F2,111 = 19.5; p 0.0001. Sepsis increased VO2 with little change in VCO2, thus RQ fell, suggesting increased use of lipid fuels for oxidation. During hypercaloric lipid infusion in septic patients (SL) VO2 and VCO2 increased but VO2 was still greater, so RQ remained low (SL RQ = 0.89). As sepsis worsened VO2 remained high but VCO2 fell producing RQ less than 0.8, while plasma glucose levels were increased. These data suggest that septic patients are more dependent than nonseptics on lipid fuels for oxidative metabolism, and that IV lipids can be used to increase oxidative metabolism in sepsis at a time when glucose metabolism appears reduced.
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PMID:Increased lipid fuel dependence in the critically ill septic patient. 642 May 77

The frequency of TPN in surgical infants was 242/686 (37.8%) in neonates and 260/2693 (9.7%) in older infants for the past 15 years. The frequent indications of TPN were intestinal atresia, Hirschsprung's disease and esophageal atresia in the neonatal period, and Hirschsprung's disease, pyloric stenosis and biliary atresia in infancy. The effectiveness of TPN was impressively indicated by better survival rate in the infants with massive intestinal resection received TPN. An amino acid solution (N1-2) was newly devised, based on the analysis of plasma aminograms in 36 infants received TPN with a commercial amino acid solution (Proteamin), and theoretical considerations. It was more useful solution for TPN in 12 young infants. Urinary phosphorus was a considerable parameter for the administration of Vitamin D in TPN. The incidence of TPN-induced hepatic dysfunction was significantly referred to the amount of amino acid in TPN. Closed infusion system with a soft bag and triple bacterial filters in the line was effective for the prevention of sepsis caused by central venous catheter. The nutritional care was important in the treatment of infants with biliary atresia, because generally they had some nutritional defects such as essential fatty acid deficiency, insufficient amino acid metabolism and zinc deficiency. The nutritional care in infants with advanced neuroblastoma favorably altered the course of the disease.
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PMID:[Total parenteral nutrition in surgical treatment of infants: recent progress and problems]. 643 80

In the past 10 years, the diagnosis of pseudoobstruction lasting more than two months was confirmed in 10 infants after sepsis, meconium ileus, and Hirschsprung's disease were excluded, and surgery or autopsy failed to demonstrate a site of mechanical intestinal obstruction. Four infants had undergone prior operation for another anomaly: gastroschisis (2) and ileal atresia (2). Five of the remaining infants also had megacystis. The lack of coordinated intestinal motility was best appreciated by radiocontrast small bowel studies, which showed degrees of aperistalsis or segmentation. Rectal manometric studies were not helpful. Histology of the intestine was normal in seven, while a gross deficiency of nerve fibres was noted in one patient and a myopathy of smooth muscle in another. A variety of drugs used to stimulate peristalsis were ineffective. Seven patients had 25 operations, often to exclude mechanical causes of obstruction. The mainstay of treatment was TPN and intestinal decompression. Six children survived; their ages ranged between 8 months and 9 years (median age, 16 months). There has been improvement in intestinal peristalsis in five children, three of whom now tolerate a regular diet and two of whom are on TPN and are currently increasing oral intake. Four infants died, two from sepsis, two from TPN-related hepatic failure. In contrast to previous reports, we conclude that intestinal pseudoobstruction may be self-limited in some neonates, including those with megacystis. Therapy should consist of long-term nutritional support and treatment of other anomalies that may be present.
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PMID:Neonatal intestinal pseudoobstruction. 644 Sep 67


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