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

The most appropriate nutriment for total parenteral feeding (TPF) must be nutritionally efficient, safe and easy to use. Glucose is the most used carbohydrate as it has most of these qualities, as well as a high rate of metabolism by all tissues. It has not been clearly demonstrated that the administration of exogenous insulin with glucose improves nitrogen retention. Substitutes for glucose, such as fructose, maltose, galactose or polyols (xylitol, surbitol, glycerol) are not really superior to glucose itself. On the other hand, they have major side-effects. Therefore, they are not much used as energy substrates for TPF, at least not for long term TPF. Intravenous fat emulsions have taken an important place as a source of energy during TPF. Fat emulsions containing long chain triglycerides (LCT) supply essential fatty acids (EFA) (linolenic and linoleic acids), thus preventing EFA deficiency. The metabolism of fat emulsions is influenced by various factors: age, metabolic and nutritional status, the amount of glucose intake, insulin deficiency, sepsis, heparin therapy. Recently, medium chain triglycerides (MCT) have been proposed as an alternative energy source. The latter are cleared more rapidly from the blood, and are therefore less liable to be deposited in the liver and adipose tissue; they are also oxidized more quickly and more completely. MCT are safe to use at a rate of less than 0.12 g.kg-1.h-1 and with a MCT/LCT ratio less than 3 to 1. The simultaneous administration of glucose prevents an acceleration of ketogenesis. MCT/LCT emulsions are a safe and effective source of calories. It is important that those patients for whom such nutriment may be of particular interest should be identified. Fat emulsions associated with glucose seem to be more efficient in terms of nitrogen sparing effect than glucose alone. They also avoid the problems due to the infusion of large amounts of glucose (excessive carbon dioxide production, fatty infiltration of the liver), while there is no EFA deficiency. If the infusion of TPF nutriment must be continuous in intensive care patients, or during the postoperative period, cyclic nocturnal parenteral nutrition over a 12 or 16 hour period may be used in patients who are not in a catabolic state, or only mildly so. This is a safe and efficient method of nutritional support, which reduces the incidence rate of TPF-induced cholestasis.
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PMID:[Energy substrates in parenteral nutrition]. 178 8

This study compares CO2 laser sterilization with iodine surgical scrub in infected pseudomonas wounds in the rabbit, and on frequency of wound breakdown secondary to sepsis. Thirty-three New Zealand rabbits underwent bilateral flank incisions and infection with a standard solution of pseudomonas aeruginosa. After 4 days of incubation, the wounds were randomized to receive laser sterilization and routine iodine surgical scrub respectively. Following sterilization, excision of the wound, and suturing was carried out. After 12 days, the wounds were assessed for evidence of residual infection as well as wound breakdown in a double blind fashion. Clinical observation, qualitative microbiology, and in some cases histology, were used to document the presence of infection. Statistical analysis of wound breakdown secondary to infection revealed a significant difference in breakdown rates. Three laser and 12 iodine treated wounds displayed breakdown secondary to sepsis. We conclude that the CO2 laser sterilization technique is more effective than routine iodine surgical scrub.
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PMID:Healing of infected wounds following iodine scrub or CO2 laser treatment. 181 84

Little is known of the endorphins' role in sepsis-induced respiratory distress and naloxone's effect as a treatment of it. Thirteen piglets were infused with live Escherichia coli at a rate of 2 to 10 x 10(8) colony-forming units per hour for six hours or until death and were divided into two groups: the septic control group (n = 8), and the naloxone-treated group (n = 5), which received 8 mg/kg/h of naloxone by continuous infusion. The results showed a significant reduction of QS/QT, VD/VT, and arterial carbon dioxide pressure at one hour and a significant increase of arterial carbon dioxide pressure and minute ventilation at 1, 3, and 4 hours in the naloxone-treated group, compared with the untreated septic group. None of the piglets in the naloxone-treated group developed ventilatory depression, while 75% of those in the untreated septic group did. Among the latter ficial effects of naloxone are likely related to its action on the central and peripheral respiratory regulatory mechanisms. A transient protection of the cardiac output and relatively decreased extravascular lung water with naloxone treatment may also, in part, improve the ventilation-perfusion maldistribution and secondarily reduce QS/QT and VD/VT.
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PMID:[Prevention of septic ventilatory depression with naloxone]. 181 74

Among 659 infants of 30 weeks' gestation or less born in a regional perinatal centre between 1983 and 1989, 195 were ventilated for four days or more and survived to 28 days, and 87 of these developed chronic lung disease. There was a sevenfold increase in the annual incidence of chronic lung disease over time. During the same period there were significant increases in the number of infants who survived, the incidence of septicaemia, and the use of parenteral lipid emulsions. Chronic lung disease was significantly associated with low birth weight, shorter gestation, duration of ventilation, vaginal delivery, sepsis, and the use of lipid. Respiratory and physiological measurements at 96 hours were significantly worse in infants who subsequently developed chronic lung disease. Initial logistic regression showed that gestation, arterial carbon dioxide tension (PaCO2), and ventilation rate at 96 hours; and birth in 1988 or 1989, were independently associated with chronic lung disease, but when septicaemia and use of lipid during the first 21 days were included, only gestational age (odds ratio 0.64, 95% confidence interval (CI), 0.49 to 0.81 for each week) and use of lipid (odds ratio 8.1, 95% CI, 2.32 to 28.0) remained significantly associated with chronic lung disease. The observed increase in incidence of chronic lung disease in this population was associated with earlier use of parenteral lipids in infants of very low gestation rather than with changes in population, survival, or ventilator treatment of respiratory distress syndrome.
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PMID:Factors associated with chronic lung disease in preterm infants. 173 38

The effect of group B streptococcal sepsis acquired in utero on umbilical cord gas values is not known. Hypothesizing that fetal acid-base balance may be affected, we sought to identify a pattern of cord gas values that might detect newborns at increased risk of group B streptococcal sepsis. This review encompassed all newborns from January 1, 1986 to March 31, 1990 who manifested group B streptococcal sepsis as confirmed by a positive blood culture. An increased-risk cord gas profile was identified as an arterial pH less than 7.18 with either an arterial carbon dioxide pressure less than 59 mmHg or bicarbonate level less than 19 mEq/L. This pattern was found in four of 11 newborns with group B streptococcal disease but in only 43 of 4290 controls, yielding a relative risk of 51.7 (95% confidence interval 13.1-224.9). Our results suggest that a mild metabolic acidosis characterized by these indices may serve as an indicator of increased risk of early-onset group B streptococcal disease.
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PMID:Cord blood gas patterns identifying newborns at increased risk of group B streptococcal sepsis. 192 95

Six full-term newborn infants are described who suffered from severe adult respiratory distress syndrome (ARDS). The triggering event was intrauterine/perinatal asphyxia in five, and group B streptococcal (GBS) septicemia in three. All had severe respiratory distress/failure and were ventilated mechanically with high concentrations of inspired oxygen and positive end-expiratory pressure. Radiography of the chest showed dense bilateral consolidation with air bronchograms and reduced lung volume. Persistent pulmonary hypertension (PPH) was documented in all cases. The coincidence of ARDS and PPH rendered respiratory management extremely difficult. For this reason high-frequency ventilation was instituted in all patients in order to improve CO2 elimination and induce respiratory alkalosis. Acute complications of respiratory therapy were encountered in five patients (pneumothorax, pulmonary interstitial emphysema, pneumopericardium). Three infants died (irreversible septic shock, progressive severe hypoxemia, and sudden cardiac arrest) after 17, 80, and 175 h of life. Histologic examination of the lungs was possible in all fatal cases and revealed typical changes of acute to subacute stages of ARDS. Three infants survived, the mean time of mechanical respiratory support being 703 h. Two patients were still dependent on oxygen after 1 month of life, and all survivors had increased interstitial markings and increased lung volumes on their chest roentgenograms at this time.
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PMID:The paradox of adult respiratory distress syndrome in neonates. 200 41

We studied 37 patients with severe sepsis and systemic hypoperfusion to assess changes in PvCO2. Before fluid administration, the cardiac index (CI) was 2.64 +/- 0.14 L/min.m2. The PvCO2 was 38 +/- 1 torr and mixed venous pH was 7.32 +/- 0.02. The venous-arterial CO2 tension gradient (P[v-a]CO2) was 6 +/- 1 torr. After fluid administration, the CI increased to 3.45 +/- 0.14 L/min.m2 (p less than .001) and the P(v-a)CO2 decreased to 5 +/- 1 torr. The correlation between the change in CI and the change in P(v-a)CO2 was r = .42, p less than .01. P(v-a)CO2 was elevated in 19 (51%) patients before fluid administration (P[v-a]CO2 greater than 6 torr) (hypercarbic group). The P(v-a)CO2 gradient in this group was 9 +/- 1 compared with 4 +/- 1 torr in 18 patients with a normal P(v-a)CO2 gradient (p less than .001) (normocarbic group). PvCO2 was 41 +/- 2 torr in the hypercarbic group compared with 35 +/- 2 torr in the normocarbic group (p less than .05). No difference was noted in PaCO2. Venous arterial pH and HCO3- gradients were of greater magnitude in the hypercarbic group, -0.05 +/- 0.003 and 2.4 +/- 0.3 mEq/L compared to -0.02 +/- 0.004 (p less than .001) and 1.1 +/- 0.2 mEq/L (p less than .001), respectively. CI in the hypercarbic group was 2.3 +/- 0.2 compared to 3.0 +/- 0.2 L/min.m2 in the normocarbic group (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Venous hypercarbia associated with severe sepsis and systemic hypoperfusion. 190 57

It has been suggested that lipid is a preferred fuel in stressed patients. We evaluated glucose oxidation in 20 patients (sepsis, cancer of the colon, multiple trauma, controls) while they received TPN (5.65 mg glucose/kg/min). Respiratory quotient (RQ) was measured by indirect calorimetry and the percent VCO2 arising from the oxidation of glucose was measured using [U-14C] glucose. Since RQs were 1.0 or greater in all patients, the nonprotein energy utilized by them was calculated to be derived completely from glucose. However, the kinetic data showed that glucose contributed only 55-60% of the VCO2. Protein oxidation contributed less than 20% of the VCO2, as calculated from urinary nitrogen. The difference must have been derived from fatty acid oxidation. The glucose turnover that was not oxidized was presumed to be converted to lipid at an RQ of 8.6. The net oxygen consumption and carbon dioxide production from this overall distribution resulted in an RQ of about 1.0 with only 60% coming from glucose oxidation. Since all patients responded in the same manner, it appears that the proper ratio of glucose and lipid was dictated on a physiologic basis and not on the type of disease.
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PMID:A physiologic basis for the provision of fuel mixtures in normal and stressed patients. 212 Apr 66

The sequential changes in lipid metabolism and in the fatty acid profile of liver lipids during fasting and sepsis were studied. Liver and blood specimens were taken from normally fed rats and from nonseptically and septically fasted rats at 5, 24, and 48 hr. Sepsis was induced by injecting live Escherichia coli bacteria intraperitoneally. Sepsis attenuated the fasting-induced increase in beta-hydroxybutyrate and reduced liver and serum triglycerides at 5 hr. There was a percentage decline in the most abundant fatty acids in neutral lipids, namely oleic (18:1w9) and linoleic (18:2w6) acids. This was seen throughout fasting and septic fasting. These results indicate that 18:1w9 and 18:2w6 are used as energy substrates and are oxidized to beta-hydroxybutyrate during fasting and mainly to carbon dioxide during septic fasting. On the contrary, the most abundant fatty acids in phospholipids, stearic (18:0), arachidonic (20:4w6), and docosahexaenoic (22:6w3) acids, accumulated in neutral lipids and in phospholipids throughout fasting. However, during sepsis this accumulation was reduced in neutral lipids and reversed to a level below that in the fed and fasted state in phospholipids. These results indicate that a disturbance in membrane integrity and function induced by septic fasting may have pathophysiological consequences for lipid metabolism and liver function during sepsis.
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PMID:Sequential changes in lipid metabolism and the fatty acid profile in liver lipids during fasting and sepsis. 219 Jul 12

To investigate why blood ketone bodies are depressed during sepsis, the production and utilization of ketone bodies was studied in fasted control, fasted, Escherichia coli-treated, fed control, and fed E coli-treated rats. Gram-negative sepsis was induced by intravenous (IV) injection of 8 x 10(7) live colonies of E coli per 100 g body weight. Food was removed from the fasted rats after E coli injection. Fed rats were infused intragastrically with a nutritionally adequate diet for 5 days before inducing sepsis. Twenty-four hours after E coli injection, blood ketone bodies were reduced in fasted septic rats and fed septic rats compared with their respective control rats. Ketogenesis and oxidation of labeled palmitate was not altered in hepatocytes from fasted E coli-treated rats. Yet, ketogenesis declined significantly in hepatocytes from fed E coli-treated rats. Oxidation of labeled palmitate was also significantly reduced in hepatocytes from fed E coli-treated rats. Utilization of ketone bodies as measured by the incorporation of [3-14C]beta-hydroxybutyrate into CO2, increased over threefold in the diaphragm, 12% in the heart, and 19% in the kidneys from the fasted E coli-treated rats. In the fed state, incorporation of [3-14C]beta-hydroxybutyrate into CO2 was elevated fivefold in the heart, fourfold in the diaphragm, and over threefold in the kidneys from the septic rats. These results suggest that in the fasted state, plasma ketone bodies remain low during gram-negative sepsis because peripheral tissues use more ketone bodies and because liver ketogenesis is not increased to compensate for the increased utilization. In the fed state, the reduction in blood ketone bodies appears to be attributed to both impaired ketogenic capacity and increased peripheral utilization.
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PMID:Altered ketone body metabolism during gram-negative sepsis in the rat. 223 76


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